Sunday, August 30, 2009


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Nisheeth Verma, MD*, Avinash Murthy, MD, Vinay Sood, DO, Konstantinos Linos, MD. Pathology, Gastroenterology, Internal Medicine, Albany Medical College, Albany, NY.

Purpose: To report a rare case and emphasize the significant association of AFAP with ampullary adenocarcinoma.

Methods: Literary Review and Clinical Vignette

Results: To report the various types of occurences in AFAP and highlight the need for further research in dealing with these presentations.

Conclusion: A 66-year-old male with a family history of colon cancer presented with a two week history of right upper quadrant pain, jaundice, and 4.5-kilogram weight loss. Initial laboratory values revealed a total bilirubin of 21.6 mg/dL with direct bilirubin 12.6 mg/dL, alkaline phosphatase 462 IU/L, aspartate transaminase 73 IU/L, alanine transaminase 85 IU/L, amylase 64 IU/L, lipase 32 IU/L, and white blood cell count of 8.8 thousand per cubic millimeter. Right upper quadrant ultrasound revealed a distended gallbladder with multiple gallstones, and a 1.1 cm stone in the common bile duct with severe intra and extra hepatic biliary dilatation. Subsequently an ERCP was performed which identified numerous gastric polyps and a large, fungating ampullary mass. Cholangiogram at the time of ERCP revealed multiple stones in the bile duct. Sphincterotomy and biliary stent placement were then performed to relieve the patient's biliary obstruction. Biopsies were taken from both the ampullary mass and the gastric polyps. Pathology revealed the gastric polyps to be fundic gland polyps and the ampullary mass biopsy showed adenomatous mucosa with focal high grade dysplasia. Follow up CT scan of the abdomen and pelvis revealed a 2.7 x 2.2 cm mass in the region of the ampulla/ pancreatic head. Further work up with endoscopic ultrasound identified the mass at the level of the ampulla, which was staged T2N0Mx by endosonographic criteria. Colonoscopy was then performed which revealed numerous 1-5 mm polyps in the ascending colon, hepatic flexure, and proximal transverse colon. Biopsies of these polyps were consistent with tubular adenomas. The patient was referred to surgery for Whipple resection of the ampullary mass and subtotal colectomy for resection of the multiple colonic adenomas. Surgical pathology revealed ampullary adenocarcinoma arising in association with tubulovillous adenoma and colectomy specimen identified numerous adenomas consistent with adenomatous polyposis syndrome. We present a rare case of attenuated familial adenomatous polyposis syndrome initially presenting as obstructive jaundice secondary to ampullary adenocarcinoma.


Gerald Arbour, MD*, Ankur Sheth, MD, Paul Jordan, MD, Kenneth Manas, MD. Gastroenterology, LSU Health Sciences Center - Shreveport, Shreveport, LA.

Purpose: Eosinophilic esophagitis (EE) is an esophageal disorder characterized by upper GI symptoms and associated with dense eosinophilic infiltration of the esophagus. The exact pathophysiology is unknown, but there is an association with food allergies suggesting an aberrant immune response is responsible. EE is increasing in prevalence, most likely due to increased recognition. Clinically, EE usually presents with dysphagia and food-bolus impaction is common. Endoscopically, linear furrows or mucosal rings are often observed in the esophagus. Histologically, greater than 15 eosinophils are present per high power field. We present a case of eosinophilic esophagitis presenting with a grape obstructing the esophagus and innovative management with removal of the grape using the barrell apparatus from a banding device.

Methods: A 26 year old male prisoner with no past medical history was brought to our emergency department with the complaint of dysphagia and inability to swallow his secretions after eating grapes. Malingering was initially suspected, but GI was eventually consulted. EGD revealed a fully intact grape obstructing the distal esophagus. A transient appearance of a ringed esophagus and persistent longitudinal furrows were observed as well.

Results: An attempt was made with a Roth net to retrieve the grape but was unsuccessful. Rat tooth forceps were then used to excise multiple pieces of the grape, however the grape maintained its integrity and we were unable to push the grape through the GE junction. The bands were then removed from the plastic barrell of a variceal ligation device. This cap was utilized to provide a larger area of forceful suction enabling us to remove the grape from its impacted location. Multiple biopsies were then taken along the length of the esophagus which revealed degranulated eosinophils and greater than 15 eosinophils per high power field confirming the diagnosis of eosinophilic esophagitis.

Conclusion: Eosinophilic esophagitis is chronic inflammatory disease of the esophagus and while there are many effective treatments, the optimal therapy has yet to be fully defined. As it is being recognized more frequently, different presentations and findings are being documented. This case is the first, to our knowledge, of eosinophilic esophagitis presenting with a grape as a food-bolus impaction. Another case of a grape causing esophageal obstruction has been described, but the primary pathology was a stricture. This case also demonstrates an alternative use for the barrell on banding devices, which may prove useful with foreign bodies such as in this case.


Nirmal Mann, MD, MS, PhD, DSc*. Gastroenterology, Univ. of Calif. Davis, Folsom, CA.

Purpose: It is well known that chronic use of laxatives containing natural herbal products such as Aloe vera, Senna, Cascara and other anthraquinone laxatives, results in pigmentation of the colonic mucosa called pseudomelanosis coli. The common herbal laxatives in this category are Chomper, Swiss Kriss and Supercleanse. Sometimes colonic enemas contaning such herbal products are used. The resulting pigmentation is usually patchy with areas of normal non-pigmented mucosa being present. Sometimes the colonic pigmentation is so dark that a satisfactory colonoscopy could not be performed (Am J Gastro2007;102:S200). Besides the colon, small bowel, gall-bladder, vagina, fallopian tubes and prostate may show pseudo-melanosis. We describe two cases where pseudomelanosis produced sharply circumscribed, regular, circular, unpigmented areas of normal mucosa resembling aphthous ulcers in the cecum & ascending colon.

Methods: Case 1.51 year old caucasian woman with medical problems such as lupus, chronic arthropathy had chronic constipation. She could not have a bowel movement without using a herbal laxative. For the last 10 years she had been using daily"supercleanse", a herbal laxative containing Cascara. She underwent screening colonoscopy. Starting from the rectum, the whole colonic mucosa showed dark pigmentation which worsened proximally. In the cecum and ascending colon, white sharply demarcated, circular areas ranging in size from 3 mm to 5 mm were seen. They resembled colonic ulcers with hyperemic margin. However on closer inspection, they were found to be areas of unpigmented normal mucosa; the brownish margin of pseudomelanosis resembled"hyperemic" margin of ulcers. Biopsy of the margin of these areas showed severe pseudomelanosis coli. Case No.2.53 Yr old caucasian woman with chronic depression had chronic constipation. She had been using the herbal laxative "Chomper" daily for 8 years. She underwent screening colonoscopy. The colonoscopic findings were similar to the first case."Chomper" contains senna.

Results: See methods

Conclusion: Chronic users of some herbal laxatives may have pseudomelanosis coli. The distribution of the pigmentation may be non-uniform and sometimes may leave circular, sharply demarcated areas of normal mucosa in the cecum and ascending colon superficially resembling aphthous ulcers of IBD.


Nirmal Mann, MD, MS, PhD, DSc*, Kanat Brahmanakul, MD. Gastroenterology, Univ. of Calif. Davis, Folsom, CA.

Purpose: After adenomatous polyps, lipomas are the second most common benign polyps of the colon. Most of the colonic lipomas are asymptomatic. However large lipomas especially in the sigmoid may cause colonic obstruction (Am J Gastro 1999;94:2683). Rarely they may ulcerate and bleed. During the evaluation & management of large colonic lipoma submucosal hemorrhage of the colonic mucosa has been reported (Am J Gastro 2007;102:S330). Small lipomas of the colon are usually left alone. However carcinoid tumors of the colon, because of their high lipid content may have yellowish appearance and may mimic lipoma. The presence of the pillow sign (indentation when pressed with biopsy forceps) may be helpful. Sometimes colonoscopic ultrasound may be needed to make a definitive diagnosis of submucosal lipoma (Am J Gastro 1999;94:2683). Snare removal of large sessile submucosal lipoma after creating a pseudostalk is possible but has the risk of colonic perforation. We describe a new, novel and safe method i.e. suction polypectomy to remove a sessile colonic lipoma.

Methods: Case report: 59 year old man with history of kidney stone, essential hypertension & organic impotence was evaluated for screening colonoscopy. His cardiac evaluation showed concentric LVH and tricuspid regurgitation. He had no colonic or gastrointestinal symptoms. There was no family history of colon cancer. The family history was positive for stroke & diabetes mellitus. The patient did not smoke and drank 14 oz alcohol per week. The physical examination and basic laboratory data were normal

Results: Screening colonoscopy to the cecum was successfully performed. In the descending colon a 2 cm sessile submucosal soft polyp was seen. The pillow sign was present. On biopsying this polyp, a sudden yellowish material protruded through the biopsy site (Naked Fat Sign). The biopsy site was gently enlarged. Suction on the colonoscope was increased to maximum and the lipoma was successfully sucked out. There were no complications.

Conclusion: We describe a new, novel and safe method i.e. suction polypectomy, for removing a sessile colonic lipoma.


Gopalan Badarinarayanan, MD, FACG*. Gastroenterology, A.V.B. Gastro Care Clinic, Tirunelveli, India.

Purpose: To analyze the cause of R.A.P in extensively Investigated cases of abdominal pain of unknown origin

Methods: A Three year study was conducted in all patients constituting of10,000 patients attendig our Gastroenterolgy Out Patient Departmemt located in Southern Rural Area Of Tamil Nadu. Of the above patients 2145 patients had the above problem had treatment in various places. All underwent O.G.D. Sccopy, M.RI of Skull, CT scan of abdomen, Opthol and E.N.T. Workup including colonoscopy and Metabolic workup

Results: Of the 21.45% we couldn't trace any organic pathology like ulcers. Mass leisions or H. Pylori Infection. Of these 21.45% 18.3% were children between 5 years and 15 years. Of them 12.7% were female Children. Hence we decided to give treatment after getting prior permission from the parents and the adults were explained about the disease and a written permission was got and treatment started with Tabs. Flunaricine, Propranolol and Divalproex Sodium according to the age For a period of Six months. Our center had no side effects.

Conclusion: Of the 2145 patients the R A P was fully under control in more than 78% of cases we tried. Hence we strongly reccommend a trial Treatment with the same regimen for abdominal pain of unknown origin. In all the cases female predominance was more than men. This can be attributed to the faily strains in adults and over workload in children.


Gopalan Badarinarayanan, MD, FACG*, Patchirajan Murugesan, MS, Muthukumarm, DDMRD. Radiology, Orthopaedic Surgery, Gastroenterology, A.V.B. Gastro Care Clinic, Tirunelveli, India.

Purpose: To analyze the cause of lower abdominal pain due to Non Abdominal Etiology.

Methods: In our outpatient department a four year trial was conducted in more than 3,675 patients who had lower abdominal pain. These patients had been getting treatment in various centers for the same and had undergone elaborate investigations including routine blood, urine, stools, X-ray analysis, Gynec, Urological and C-T Scan of abdomen, with even virtual colonoscopy.

Results: We examined all these patients with detailed Questionnaires including queries about their occupation and work activities. Of the 3,675 patients 80% ranged from 40 to 60 years of age with a female predominance of 78%, the females being mainly homemakers of medium income group family and the rest were males who were either farmers or with other occupations. The remaining 20% of the 3675 gave history of either fall from a medium high place or from a two wheeler or an accident 3 to 4 years earlier which was ignored. These were the main points of attraction from our questionnaires which was not revealed in any other centers where they underwent the earlier treatment.

Conclusion: All these patients were screened with the help of our orthopaedic surgeons and were submitted for a skeletal evaluation with M.R.I. Scan of mainly LumboSacral Parts. As per the scans all these patients had either Disc prolapse indending on the Thecal sac or severe Osteoporosis leading on to the anterior Radiclitis. They were given adequate bone traction, mild painkillers and advised change in life style. Most of the patients were free from symptoms after Eight weeks. The rest required a bone bracing for one year. Hence patients with Lower abdominal pain not responding to conventional treatment require an Orthopaedic evaluation.


Amitpal Johal, MD*, Robert Smith, MD. Gastroenterology, Geisinger Medical Center, Danville, PA.

Purpose: A 78 yo male with hypertension and CKD presented for evaluation of acute on chronic renal failure. A renal ultrasound incidentally revealed a large 4 cm x 6 cm x 10 cm infra-renal abdominal aortic aneurysm. He was evaluated by vascular surgery who planned an open repair in the near future. 4 days later the patient presented to the emergency department with abdominal pain, nausea and intolerance to po intake. Abdominal exam revealed tenderness, distention and a pulsatile abdominal mass. Significant findings upon work up included hypotension, a creatinine of 5.1 and ST segment changes on EKG. A NG tube was placed which drained 1700 cc fluid with symptomatic improvement. CT showed a proximal duodenum which was obstructed just below the superior mesenteric artery takeoff due to direct compression from the large AAA. The patient underwent cardiac workup for his acute MI. Prior to surgical repair of his AAA he underwent a CABG X 3. Approximately 2 weeks later, after aggressive nutritional support, he successfully underwent an open AAA repair with a tube graft. He is currently in a rehabilitation facility doing well.

Methods: -

Results: -

Conclusion: Aortoduodenal syndrome is a clinical entity rarely reported in the gastroenterology literature. It was first described in 1905 by William Osler in an article entitled "Aneurysm of the Abdominal aorta."1 There have been fewer than 30 cases reported in the literature. The AAA compresses the superior mesenteric artery or the transverse segment of the duodenal wall. Patients present with emesis, pulsatile abdominal mass, abdominal pain, weight loss, and electrolyte disturbances.2 The diagnosis should be suspected in a patient with known vascular disease, pulsatile abdominal mass and signs of gastric outlet obstruction. Initial workup should include CT, UGI barium study or EGD to rule out other causes of gastric outlet obstruction. Treatment is initially supportive with attention to nutritional status prior to surgical vascular repair. Osler W. Aneurysm of the abdominal aorta. Lancet 1905;166:1089-96. Deitch J et al. AAA causing duodenal obstruction: 2 case reports and review of the literature. J of Vasc Surg 2004;40:543-7.


Charles Koczka, MD*, Waqas Khan, MD, Adam Goodman, MD. SUNY Downstate Medical Center, Brooklyn, NY.

Purpose: Although the incidence of colorectal cancer in the child/adolescent population is quite low, a rising incidence has been reported. Furthermore, in the current literature, the behavior of this disease is not described in Afro-Caribbean youth.

Methods: A 20 year-old female presented with increasing abdominal girth and pain over 5 weeks. Her abdomen had been gradually growing, associated with dull non-radiating pain in the upper abdomen. Loss of appetite as well as weight loss of 20 lbs in 1 1/2 months was reported. She had been having bloody stools for the past 3 months. She denied fever, dysphagia, jaundice, night sweats, nausea or vomiting. She had emigrated from Trinidad to the United States three years ago. No prior medical history reported nor did she mention taking medications, smoking, alcohol, or illicit drugs. She had no familial history of cancer. On examination, she appeared cachetic with bitemporal wasting, but was in no acute distress. She was tachycardic at 130 bpm. There was mild conjunctival pallor but no scleral icterus or lymphadenopathy present. The abdomen was distended with tenderness elicited in right upper quadrant. The liver was firm, irregular, and palpable to almost 6-7 finger breaths below the costal margin. There was no shifting dullness or splenomegaly present. Rectal exam was limited secondary to pain however fresh blood was observed.

Results: CT of abdomen revealed massive hepatomegaly with innumerable hypodensities enlarging the liver. Focal thickening of rectosigmoid wall was recognized as a mucinous adenocarcinoma. CT chest showed multiple parenchymal and pleural based pulmonary nodules bilaterally. Laboratory evaluation was significant for anemia of chronic disease and a mild elevation in transaminases. Chemistry panel, AFP, and white blood cell count were unremarkable. CEA level was markedly elevated at 13,682 U/L as well as CA 19-9 of 37,761 U/L and CA-125 U/L of 233. A colonoscopy revealed a mass visualized 3 cm above the anal verge, obstructing the lumen and extending into the sigmoid colon. Colonoscope could not be advanced further, preventing full colonic examination. Pathological diagnosis of biopsies was consistent with high grade adenocarcinoma with signet-ring features. The patient was diagnosed with Stage IV rectosigmoid cancer with metastases to liver, peritoneum, and lungs. Treatment was begun with a regimen of Folfox (Folinic acid + 5 FU + Oxalplatin) and Bevacizumab. One year after the time of her diagnosis, she expired.

Conclusion: The aim of this report is to raise awareness of colorectal cancer in younger individuals especially in the Afro-Caribbean community which remains understudied compared to the rest of the U.S. population.


Fnu Deepinder, MD*, Andrew Albert, MD, Nkemakolam Iroegbu, MD. Gastroenterology and Hepatology, Internal Medicine, St. Joseph Hospital, Chicago, IL.

Purpose: To diagnose and manage Klippel Trenaunay Syndrome (KTS).

Methods: Case: A 27 year old white male presented with fatigue, pallor, and black stools for 4 months. Past medical history revealed varicosities of right lower extremity since childhood, urinary bladder hemangioma and hemorrhoids. Physical examination was mostly benign except for severe pallor and bluish-purple hemangiomas along with varicose veins of right lower limb. The stool test for occult blood was positive. Hb was 2.8 g/dL and Hct 10.1%. Following transfusion therapy, he underwent upper GI and small bowel follow-through. Multiple phleboliths were noted suggesting residual recurrent hemangiomas. Colonoscopy revealed large dilated veins in the rectosigmoid with hyperemic, edematous and friable mucosa that bled easily on manipulation of the scope. Rectal prolapse with wide rectal dilatation was also noted. The procedure was aborted due to risk of precipitating further bleeding and causing perforation. An emergent CT scan revealed hepato-splenomegaly with prominent hepatic veins. The inferior vena cava and common iliac veins were markedly dilated. Walls of the recto-sigmoid and urinary bladder were tremendously thickened and had multiple calcified phleboliths. Scattered varicosities were also seen throughout the fatty tissue of the retroperitoneum. X-ray showed soft tissue hypertrophy on the lateral aspect of the femur and proximal portion of the lower leg. The constellation of findings including port wine stain, venous abnormalities, and unilateral limb hypertrophy were consistent with the diagnosis of KTS.

Results: Bleeding subsided spontaneously and was accompanied by a gradual rise in Hb to 9.4 gm/dL.

Conclusion: KTS is a nonhereditary congenital disorder in which GI involvement may lead to life threatening bleeding. It can often be misinterpreted as internal hemorrhoids, as in our patient. The associated hemangiomas may sequester platelets leading to consumptive coagulopathy further worsening the bleeding. Melena with hepatospleenomegaly in our patient may indicate elevated portal venous pressure and gastric varices due to underlying vascular abnormalities. Conservative management and iron supplementation may be sufficient in those having occasional non-life threatening bleeding. Transfusion dependency and life threatening bleeding episodes necessitate definitive surgical therapy. Debilitating disease localized to the colon can be treated by resection of the involved segment and either a colo-anal anastomosis or permanent colostomy. Endoscopic laser therapy using argon and Nd:YAG lasers may be useful in localized hemangiomas and post-operative residual disease. Vascular embolization can be considered if a distinct bleeding site is encountered with visceral angiography.


Gopalan Badarinarayanan, MD, FACG*. Gastroenterologist, A.V.B. Gastro Care Clinic, Tirunelveli, India.

Purpose: We have already made an elaborate study on Oesophagial Candidiasis (O.C.) in Non Immunocompromised Patients during the scientific meeting in 2000. Keeping this in our mind we wanted to study about Duodenal Candidiasis in our part of the country which has not been evaluated earlier. This study showed that patiens who had Duodenal Candidiasis suffered from two main diseases either Impaired Glucose Tolerance (I.G.T.) or from severe Depression.

Methods: We in the past three years took a survey of 10,300 patients who attended Outpatient Dept for various complaints. Of them 2,200 patients required O.G.D. Scopy for multiple Upper G.I Symptoms. Amongst these patients 242 patients had suspected D.C. They underwent culture test with sterile biopsy forceps and 92 were positive for Candidiasis. Patients who were Immunocompromised, Diabetic, on long term P.P.I or Steroid therapies and H.I.V were excluded from this study.

Results: We evaluated all these 92 patients. None of them had Diabetic family history and routine blood glucose (random) was normal. All these patients were requested to undergo G.T.T. 72% Of these had Impaired Glucose Tolerance. The remaining 28% of the patients underwent a psychoanalysis and were declared to have severe depression by the Psychiatrist. All these patients were given a course of oral Flucanazole of 150 mg per day for 21 days along with diabetic control and antidepressants suggested by the diabetologist and Psychiatrist respectively. All these patients recovered from their Gastro Intestinal Problem successfully.

Conclusion: Since our study shows 4.18% of the patients who underwent O.G.D. Scpoy had D.C which is really significant and showed evidence of I.G.T and marked depression we strongly recommend that patients with Duodenal Candidiasis may be be potent diabetics or hidden depressed patients who require earlier medical guidance to avoid any long term complications and hence can be taken as markers for Diabetes and Depression.


Kyoung Ae Kim, MD*, Kong Peng Yap, MD, Dennis Moseley, MD. Internal Medicine, UCSF Fresno, Fresno, CA, Gastroenterology, pathology, VA Central California Health Care System, Fresno, CA.

Purpose: Amyloidosis (below AM) is characterized by extracellular deposition of abnormal protein with multiple systemic manifestations. Since AM clinical findings, especially GI symptoms, are broad and nonspecific, making a primary diagnosis by colonoscopy is challenging if the patient does not have an established diagnosis.

Methods: A 75-year-old male presented in GI clinic with non-specific abdominal pain and recent onset of rectal bleeding. History was significant for CAD, non-DM renal failure on hemodialysis since 2007, and a colonic polypectomy in 2002. The prior colonoscopy only showed a benign polyp. Physical exam was nonspecific. The laboratory finding was noted to have normocytic anemia, elevated ALP, and a negative SPEP. A repeat colonoscopy revealed diffuse petechiae, ecchymosis and ulceration in the sigmoid descending colon region (Figure 1).

Results: Biopsies were obtained and the pathology revealed amyloid deposition in the muscularis mucosa on Congo Red staining showing the apple green biferengent appearance under polarized light (Figure 2). Further immunostaining proved Amyloid P, confirming the diagnosis of primary AM. A kidney biopsy confirmed the diagnosis. A bone marrow biopsy showed amyloid deposition and plasmocytosis. The patient is now on chemotherapy and his GI clinical symptoms have resolved.

Conclusion: The initial clinical diagnosis of primary AM by non-specific GI symptom is difficult and requires a high index of suspicion. The colonoscopic findings of ulceration and mucosal petechiae in the left colon with a clinical history of non-DM nephropathy, cardiomyopathy or hepatomegaly with abnormal LFT should prompt AM evaluation. Biopsies with amyloid staining is critical for making the diagnosis, as early diagnosis reduces risk of critical systemic end organ damages.

Colonoscopic picture of petechial lesion

Congo Red stain of biopsy lesion in colon


Matthew Tsushima, MD*, Deborah Anghesom, MD, Bruce Runyon, MD. Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA.

Purpose: Budd-Chiari syndrome (BCS) is a rare, heterogeneous group of disorders characterized by obstruction of the hepatic venous outflow tract. The presence of hypercoagulable states, both hereditary and acquired, predisposes patients to the development of BCS. We report a rare case of BCS in a patient with sickle cell trait.

Methods: A 33-year-old African-American male with a presumed diagnosis of alcoholic liver disease cirrhosis complicated by ascites, on furosemide and spironolactone, presented with a chief complaint of mid-abdominal pain for four days. He also noted increased abdominal girth and lower extremity edema. He reportedly had been compliant with his diuretics and was on a low salt diet. He denied any fever or chills. On admission, he had a temperature of 98.8[degrees]F. Physical examination revealed icteric sclera with large, non-tense ascites and prominent abdominal wall and dorsal collaterals. Mild lower extremity edema was observed. Laboratory examination revealed a white blood cell count of 6.18 x 10.sup.3/[mu]L [4.8-11.8 x 10.sup.3/[mu]L], BUN 12 mg/dL [7-20 mg/dL], creatinine 1.0 mg/dL [0.7-1.3 mg/dL], total bilirubin 2.3 mg/dL [0-1.3 mg/dL], and lipase 66 U/L [12-35 U/L]. His calculated MELD score was 16. An abdominal CT scan revealed a 2.4 x 2.9 cm lobular area of increased density in the medial segment of the left lobe of the liver, multiple collateral vessels, and extensive ascites. No contrast was seen within the inferior vena cava (IVC) above the level of the right renal hilum. Alpha fetoprotein was 1.8 ng/mL [0.0-8.7 ng/mL]. Transjugular liver biopsy by interventional radiology was unsuccessful due to inability to cannulate any hepatic vein. A chronic appearing thrombosis of the IVC was noted 1.5 cm below the right atrium. Ultrasound guided liver biopsy was performed and paracentesis revealed a SAAG of 3.06. Pathology results showed benign hepatic parenchyma with central hepatocyte dropout, hemorrhage and sinusoidal dilation consistent with BCS.

Results: The patient was started on enoxaparin. Procoagulant workup including prothrombin gene mutation 20210A, factor V, thrombin time, protein C and S, and anticardiolipin antibody were all within normal limits. However, the patient, along with his father, had a history of sickle cell trait. Due to psychosocial contraindications, the patient was not a candidate for liver transplantation. He was discharged home with enoxaparin, furosemide, and spironolactone.

Conclusion: A review of the literature revealed only two other case reports of BCS with sickle cell disease. One case involved hepatic vein thrombosis in sickle cell anemia. The second case involved IVC obstruction in sickle cell trait. We now present a third case of BCS in a patient with sickle cell disease.


Perry Hookman, MD, FACG*, Gloria Weinberg, MD, Michele Pato, MD, Richard Gelfand, MD, Bernard Rosof, MD, FACG, Jamie Barkin, MD, MACG. Gastroenterology, Medicine, MT. Sinai Medical Center, Miami Beach, FL, Medicine, North Shore Medical Center, Huntington, NY, Psychiatry, USC, Los Angeles, CA, gastroenterology, metro gastroenterologists, Washington, DC.

Purpose: The purpose of this multicenter study was to evaluate the use of medical malpractice risk reduction seminars in the form of short bursts of e-mailed seminars [SBS].

Methods: SBS to teach medical malpractice reduction strategies [1] were designed for hospital trainees and practicing physicians at several institutions and private practices centers in the Northeast, Southeast & West coasts of the U.S. SBS was e-mailed to coordinators in gastroenterology, internal medicine, psychiatry & other specialties who targeted their audience of students, trainees and practicing physicians. The target audience, performed the sequence of pre test, seminar, post test, and returned the testing on an anonymous basis to the coordinators. One answer on the post-test required a short written response to a medical malpractice case study. Pre and post-tests were graded by the change of post-test answer scores compared to pre test total scores.

Results: Post-test scores showed significant improvements & documented the benefits of an e-mailed medical malpractice/risk reduction seminar. SBS was well accepted by medical students, gastrointestinal trainees and practicing physicians. Residents [2] and department chiefs learned how to teach medical malpractice reduction techniques which provides a potential pool of new teachers. Actual medical malpractice cases were useful as documented by responses given to a case study.

Conclusion: SBS: 1. Offers more convenience, reduces time away from patient care, schedules learning around busy schedules, and can be an ongoing resource to refresh seminar knowledge retention when filed in each participant's e-mail folder. 2. Can be provided in a consistent fashion and specifically tailored to certain levels of training for each specialty. 3. May be delivered in each specialty either as online CME or in a classroom setting by medical schools, teaching hospitals, & medical professional liability insurance companies. 4. Teaches how to teach medical malpractice/risk reduction. 5. More easily connects physicians with risk management specialists with short turn around time to customize contemporaneously in changing risk areas of hospitals and/or different clinical specialties. 6. A medical malpractice case history increases seminar lesson retention. [1] Hookman P. "Medical Malpractice Expert Witnessing: Introductory Guide for Physicians and Medical Professionals" (Hardcover) 592 pages Publisher: CRC; Boca Raton, Fl. ISBN-10: 1420058959; Price $239.95 [2] Aiyer M. et al. "Change in Residents Perceptions of Teaching: Following a One Day "Residents as Teachers"[RasT] Workshop", Southern Medical Journal 2008 101[5]:485


Joseph Yarze, MD, FACP, FACG, FASGE, AGAF*, Michael Chase, MD, FASGE, Charles Lowe, MD, Edward Orris, MD. Gastroenterology Associates of Northern New York, Glens Falls, NY, Department of Medicine, Glens Falls Hospital, Glens Falls, NY, Albany Gastroenterology Consultants, Albany, NY.

Purpose: To report a rare cause of hemosuccus pancreaticus

Methods: CASE REPORT: An otherwise healthy 77 yo female presented in 4/08 with subacute fatigue, iron deficiency anemia and a few day history of low-volume melena. After informed consent was obtained, colonoscopy (performed given IDA) revealed no abnormality, and terminal ileal intubation was negative for gross blood or mucosal pathology. EGD using a standard video gastroscope (performed for evaluation of IDA and low-volume melena) disclosed bleeding from the region of the second portion of the duodenum. A side-viewing duodenoscope was immediately passed, which allowed rapid visualization of a steady ooze of bright red blood from the major papilla. A small incidental periampullary diverticulum was also seen. Abdominal CT scanning was unremarkable, and mesenteric angiography was negative for overt pathology or contrast extravasation. The patient underwent abdominal MRI/MRCP which suggested the possibility of a 1.2 cm nonspecific lesion in the uncinate process of the pancreas. ERCP showed no overt biliary or pancreatic ductal abnormality and cholangioscopy confirmed that despite blood continuing to ooze from the major papilla, there was a "clear" biliary effluent. The patient underwent pancreaticoduodenectomy (Whipple resection) uneventfully. Pathology revealed a benign side-branch intraductal papillary mucinous tumor (IPMT) of the pancreatic head. Resection margins were clear of tumor and multiple peripancreatic lymph nodes showed only reactive changes. The patient recovered uneventfully.

Results: In this unusual case, IPMT of the pancreas caused hemosuccus pancreaticus.

Conclusion: IPMT of the pancreas can rarely present as hemosuccus pancreaticus.


Joseph Yarze, MD, FACP, FACG, FASGE, AGAF*. Gastroenterology Associates of Northern New York, Glens Falls, NY.

Purpose: To describe 2 cases of chronic hepatitis C where a sustained virologic response (SVR) occurred after an ultra-short, attenuated course of antiviral therapy.

Methods: CASE REPORTS: A 52 yo male with chronic hepatitis C (serum viral load = 1,760,000 IU/ml; genotype 3a; A2/F2 disease by liver biopsy) underwent a trial of weight-based antiviral therapy. Pegylated interferon (alpha-2b) 150 mcg sq qwk and ribavirin (1200 mg po qd) were begun (in 3/04) and after the initial dose of PEG-IFN, severe myalgia, arthralgia, headache and lightheadedness ensued. Hospital emergency room evaluation (including routine bloodwork) showed no abnormality of concern. The symptoms were intolerable (despite use of acetaminophen and reassurance) and after 2 weeks, the dose of PEG-IFN was lowered to 50 mcg sq qwk. Medication discontinuation was required due to escalation of symptoms at day 18 of the treatment regimen. Symptoms resolved rapidly after antiviral therapy was withdrawn. The patient was followed clinically and was on no subsequent antiviral, immunomodulatory or other treatment. He was transiently incarcerated and again presented in 11/07, at which time he requested another trial of HCV antiviral therapy. Pre-treatment assessment revealed that HCV was undetectable by both quantitative (in 12/07) and qualitative (3/08) PCR determinations. A 48 yo female with chronic hepatitis C (serum viral load = 219,000 IU/ml; genotype 1; A4/F4 disease by liver biopsy) underwent a trial of weight-based antiviral therapy. Pegylated interferon (alpha-2b) 120 mcg sq qwk and ribavirin (1200 mg po qd) were begun (in 1/07) and after 35 days of treatment, the medication was withdrawn due to a severe exacerbation of underlying depression with associated medical noncompliance. No other subsequent antiviral, immunomodulatory or other treatment (except for antidepressant therapy) was prescribed. The patient was to be followed clinically and she was seen in follow-up on multiple occasions over the ensuing year. She desired another attempt at HCV antiviral therapy and pre-treatment assessment (done >8 mos after her last dose of PEG-IFN/ribavirin) revealed that HCV was undetectable by both quantitative (in 12/07) and qualitative (in 4/08) PCR determinations.

Results: In these 2 cases, SVR was achieved after an ultra-short, attenuated course of anti-HCV therapy.

Conclusion: These 2 anecdotal cases confirm that in rare instances (and even with cirrhotic stage, type 1 infection), an ultra-short, attenuated course of antiviral therapy can be associated with a SVR. This suggests that when planning to re-treat patients in whom antiviral therapy was previously discontinued prematurely, reassessing for prior unsuspected HCV eradication is crucial.


Shanthi Sivendran, MD*, Nicole Swallow, MD, Ian Schreibman, MD. Medicine, Pennsylvania State University-Hershey Medical Center, Hershey, PA.

Conclusion: This case illustrates the need for fungal prophylaxis during invasive gastrointestinal procedures in patients at high risk for endocarditis. A 53 year old man with two previous episodes of bacterial endocarditis resulting in aortic valve replacement and repair was admitted for evaluation of hematemesis. Several days after endoscopy, he developed shortness of breath and a progressive palpable purpuric rash. Studies revealed hypocomplementemia, anemia, thrombocytopenia, elevated creatinine and pleural effusions. Blood cultures revealed Candida parapsilosis. Echocardiography showed vegetations on the native mitral valve and prosthetic aortic valve. Due to the patient's previous valve replacement, he was a poor surgical candidate. Despite aggressive antifungal treatment, the patient's fungemia continued leading to valvular destruction and subsequent death. Fungal endocarditis is a rare, serious disease that often requires cardiac surgery and carries a poor prognosis. The updated American Heart Association guidelines do not address fungal prophylaxis and they no longer recommend routine bacterial prophylaxis for gastrointestinal procedures except in high risk patients. Recent reports show an association between Candida parapsilosis, nosocomial infections, invasive procedures and prosthetic devices. As Candida is normal flora in the upper gastrointestinal tract, endoscopy may lead to a transient fungemia which could seed the cardiac valves. In our high risk patients, prophylaxis for fungal infections during endoscopy may be beneficial. Animal models demonstrated that two doses of fluconazole prevented experimental endocarditis caused by Candida. Amphotericin B has also shown to be successful in preventing fungal endocarditis in animal models. Newer generation echinocandins may be able to achieve the same result with fewer side affects. Guidelines should be interpreted within a clinical context. Fungal prophylaxis of high risk individuals for invasive procedures may prevent unnecessary death.


Marty Meyer, MD*, Edward Levine, MD. Gastroenterology, Hepatology, and Nutrition, The Ohio State University Medical Center, Columbus, OH.

Purpose: Crohn's Disease (CD) rarely presents with life-threatening massive hematochezia. Conservative treatment frequently results in recurrent bleeding only controlled by surgery. Infliximab rapidly induces mucosal healing and can prevent further hemorrhage without need for surgery. We aim to present a case of hemorrhagic Crohn's Disease and the successful management with infliximab.

Methods: We report a case of hemorrhagic Crohn's Disease subsequently controlled with infliximab.

Results: A 19-year-old female with a 6 year history of ileocolonic CD presented with acute recurrent hematochezia. Her remission was induced by prednisone and mesalamine and she otherwise felt well. She presented with mild tachycardia and hypotension and was subsequently admitted. An admission hemoglobin of 9.1 g/dL dropped to 6.8 g/dL after ongoing hematochezia. The patient required four units of packed red blood cells for resuscitation. Infectious etiologies were ruled out and abdominopelvic computed tomography with contrast demonstrated terminal ileitis and right lower quadrant lymphadenopathy consistent with active CD. The patient was placed on intravenous steroids but continued to demonstrate hematochezia. Upper endoscopy showed Los Angeles Grade A esophagitis and no other acute findings. Colonoscopy revealed numerous ulcers in the terminal ileum with fresh blood. In addition, clotted blood filled the entire colon. No active disease was visualized 10 cm proximal to the terminal ileal ulcers. General Surgery evaluated the patient given the extent of the hemorrhage. A small bowel follow through demonstrated terminal ileum irregularity consistent with active CD and no other diseased segments. After a non-reactive tuberculin skin test and normal chest film, a 5 mg/kg infliximab infusion was given. The patient's bleeding promptly ceased and she did not require surgical intervention or additional blood transfusions. She was discharged 4 days after infliximab infusion with repeat doses given at 2 and 6 weeks. The patient successfully responded to infliximab and has demonstrated no further hemorrhage 2 months since initiating this therapy.

Conclusion: Hemorrhagic CD is a rare entity with a high risk for life-threatening complications. Previous patients with this presentation were relegated to conservative management versus surgery as CD specific therapy was suboptimal. Given the advantages of mucosal healing, infliximab should be considered immediately for hemorrhagic CD patients instead of waiting for corticosteroids to fail. The ongoing discourse regarding top-down versus step-up therapy may be influenced by outcomes such as these reported here. Longer follow up will be required to demonstrate the lasting effects of infliximab for the treatment of hemorrhagic CD.


Marty Meyer, MD*, Edward Levine, MD. Gastroenterology, Hepatology, and Nutrition, The Ohio State University Medical Center, Columbus, OH.

Purpose: Esophageal injuries typically present after direct intraluminal trauma by foodstuffs, the mechanical shearing forces caused by retching, ingested foreign bodies, or iatrogenesis. Injuries range from the mucosal tears of Mallory-Weiss syndrome to the transmural rupture of Boerhaave's syndrome. Esophageal intramural hematomas (EIH) are exceedingly rare types of esophageal injury. These hematomas typically involve the distal esophagus; thus their discovery in the proximal esophagus deserves special mention. We aim to present a case of an EIH at the cricopharyngeus and review the appropriate management strategies.

Methods: We report a rare case of a cricopharyngeal intramural hematoma following anterior cervical decompression presenting only with dysphagia.

Results: An 87-year-old male with a history of Billroth-II gastrojejunostomy sustained an injury to his cervical spine. Computed tomography (CT) and magnetic resonance imaging demonstrated significant cervical stenosis with cord injury. The patient received corticosteroids and ultimately underwent an anterior cervical decompression. Postoperatively, the patient complained of dysphagia. Nasogastric tube placement failed even under fluoroscopic guidance. An upper endoscopy demonstrated a cricopharyngeal intramural hematoma. No other esophageal abnormalities were noted, and the patient's gastrojejunostomy was widely patent. A nasojejunal feeding tube was placed under endoscopic guidance. Repeat CT demonstrated marked soft tissue swelling with many high density collections consistent with hematomas. The patient was managed conservatively and discharged to our rehabilitation hospital with ongoing enteral nutrition through a nasojejunal tube. Repeat upper endoscopy two weeks later showed that the hematoma had resolved.

Conclusion: Esophageal injuries, including EIH, range from Mallory-Weiss tears to Boerhaave's syndrome. These entities are a rare cause of chest pain, dysphagia, odynophagia, and hematemesis, but should always be considered in those patients with certain risk factors. Recent endoscopic or cervical spine procedures as well as direct intraluminal trauma predispose patients to esophageal injuries, including EIH. Physicians may utilize endoscopy or contrast imaging to make the diagnosis. After one confirms an EIH, conservative management should follow, as 80% of patients will demonstrate spontaneous resolution. In contrast, some groups have successfully punctured hematomas for immediate drainage. EIH and Mallory-Weiss tears both carry a favorable prognosis. Physicians should have a high index of suspicion for an EIH in those patients with typical risk factors.


Natalie Bowser, MBBS*, Vincent Ho, MBBS, Andrew Pascoe, MBBS, FRACP. Gastroenterology, Princess Alexandra Hospital, Brisbane, QLD, Australia.

Purpose: C. septicum gas gangrene is well documented in the literature, typically in the setting of trauma or immunosuppression. We report a unique case in the English literature of spontaneous clostridial myonecrosis in a patient with Crohn's disease and sulfasalazine-induced neutropaenia.

Methods: A 26 year old man presented after a few hours of vomiting, diarrhoea and severe left anterolateral thigh pain. His background history included asthma and Crohn's colitis, diagnosed by colonoscopy two months prior. He was given sulfasalazine, though this was ceased two weeks prior to presentation due to 'ineffective' relief of symptoms. He was tachycardic (150 bpm) but normotensive and afebrile. Respiratory and abdominal exams were unremarkable. Initially the left thigh was extremely tender to palpation, but two hours later he was febrile (38.7[degrees]C) and a marked erythema of the left thigh developed. Laboratory investigations demonstrated a profound neutropaenia (neutrophil count 0.2 x 10.sup.9/L, WCC 1.6 x 10.sup.9/L) and myoglobinuria. MRI scan showed extensive necrotizing myositis of quadriceps and adductors. The patient underwent an emergent left hip disarticulation and laparotomy. Two days later a right hemicolectomy was performed after abdominal CT scan showed free gas in the caecal wall. Initial blood cultures grew C. septicum. Antibiotic treatment was with IV meropenem, lincomycin and penicillin.

Results: There was no further progression of necrotising myositis. The patient was discharged after three weeks, on oral penicillin. Two weeks after the four-week antibiotic course was completed, the patient returned with pain and erythema over the right pectoral muscle. CT scan showed an enlarged right pectoralis major muscle with intramuscular gas and inflamed overlying subcutaneous fat. Necrotic pectoralis major was debrided, C. septicum was cultured from the intraoperative specimen. High dose IV benzylpenicillin was used in the perioperative period and recovery was uneventful. The patient now remains on lifelong oral ampicillin prophylaxis.

Conclusion: C. septicum is uncommonly found in healthy human intestinal flora. It is a motile, gram positive bacilli capable of rapidly producing tissue necrosis and systemic shock. C. septicum seems to have a predilection for the caecum as a portal of entry and most cases complicate haematological or colon cancer. Sulfasalazine is a common drug treatment in inflammatory bowel disease, less so in Crohn's disease, and not infrequently causes agranulocytosis in the first weeks. This case highlights the need for physicians to be aware of the potentially life-threatening adverse effects of sulfasalazine and the need for early laboratory monitoring and emergent management if symptoms of sepsis manifest in the neutropaenic state.


Amitpal Johal, MD*, Robert Smith, MD. Gastroenterology, Geisinger Medical Center, Danville, PA.

Purpose: A 34 yo WM with past medical history of seasonal allergies on Allegra (fexofenadine) developed abdominal cramping, whole body erythematous rash, chills and dark urine. He denied any sick contacts, over the counter medication use, and active alcohol consumption. However, he does admit to heavy alcohol use in college. The patient presented to his primary care doctor and was found to be afebrile with stable vital signs. Physical exam was significant for mild scleral icterus but no stigmata of chronic liver disease. Laboratory investigation showed total bilirubin of 5.7, AST 93, ALT 248 and AP 218. A CBC showed 12% eosinophilia with normal total WBC count. A work up for viral hepatitis, autoimmune hepatitis, hemochromatosis and other hereditary liver conditions were unremarkable. A right upper quadrant ultrasound did not show evidence of cholelithiasis or biliary duct dilation. He subsequently underwent a liver biopsy which revealed eosinophilic hepatitis with focal bridging fibrosis. The only medication he was taking, fexofenadine, was held and over the next few weeks his liver function tests returned into normal range. The patient saw an allergist who, upon skin prick testing, found common aeroallergens to tree, grass, dust, cat, and ragweed. The testing failed to demonstrate any food allergies. The allergist felt that a drug effect was a more likely explanation for his presentation. He is currently doing well with no further episodes 6 months after the event off all medications. Discussion The eosinophilic gastrointestinal disorders are increasingly seen of late. Eosinophilic hepatitis is rarely described in the literature. There have been three case reports of this entity being associated with hypersensitivity to certain drugs, including Trovafloxacin1, Cefonicid2 and Lamotrigine3 Eosinophilic hepatitis, in past case reports, was treated by discontinuation of the suspected offending agent and initiation of systemic steroids. In this case discontinuation of fexofenadine was done with improvement in liver function tests. In rare cases Allegra has been associated with hypersensitivity reactions manifested by angioedema, chest tightness, dyspnea, flushing and systemic anaphylaxis4. This is the first report to our knowledge in published literature of eosinophilic hepatitis with fexofenadine use. 1. Chen H, Bloch K. Acute Eosinophilic Hepatitis from Trovafloxacin. N Engl J Med. 2000;342:359-360. 2. Famularo G, Bizzarri C et al. Eosinophilic hepatitis associated with Cefonicid therapy. Ann of Pharm 2001;35: 1669-1671 3. Oren K, Marion G et al. Eosinophilic hepatitis Caused by Lamotrigine. Clin Gastro and Hep 2006: 4; xxvi 4.; sanofi-aventis U.S LLC


Charles Koczka, MD*, Adam Goodman, MD. Gastroenterology, SUNY Downstate Medical Center, Brooklyn, NY.

Purpose: Amyloidosis is commonly systemic, occasionally organ-limited, and rarely a solitary localized mass. The latter, commonly referred to Tumoral Amyloidosis, is described occurring in every organ/tissue. Only a few reports of gastric amyloidosis exist today.

Methods: A 72 year-old black male from Barbados presented with 3 days of diffuse abdominal pain. He described the pain severe, non-radiating, and worse with seating upright. A 60 lb weight loss over one year as well as loss of appetite for several months was noted. The patient reported early satiety for 8 months. He denied dysphagia, odynophagia, nausea, or vomiting. There was no change in bowel habits or character of stool. Colonoscopy and EGD six years ago were unremarkable. His medical history included Non-Hodgkin's Lymphoma diagnosed five years ago, status-post six rounds of CHOP chemotherapy, and currently was in remission. He gave no familial history of gastrointestinal disorders or malignancy. He had been a life-long smoker and consumed a moderate amount of alcohol daily. On examination, the patient was thin with mild pallor but no scleral icterus or jaundice. Abdominal exam revealed generalized tenderness with guarding, but no abdominal masses were felt. Complete blood count and iron panel revealed anemia of chronic disease. Electrolyte and hepatic panels were unremarkable.

Results: On CT scan of the abdomen, thickening and calcification of the gastric wall was noted along with pneumatosis. A 1 cm pedunculated mass in the proximal duodenum was noted. No focal hepatic masses or biliary ductal dilatations seen. On EGD, a large circumferential friable mass was seen from the GE junction to the body. The mass was ulcerated, nodular, edematous, and bled easily on contact. A large non-bleeding 3 cm polyp was also seen in post bulbar area of duodenum. Biopsies were stained with Congo red and gave green birefringence under polarized light, consistent with tumoral amyloidosis. PET scan revealed diffuse gastric mucosa uptake compatible with gastric malignancy without metastatic foci. After medically controlling his abdominal pain, the patient was discharged with plan of action being observation.

Conclusion: Tumoral amyloidosis exists as a rare disease entity in today's literature. There are no reports to support that this presentation represented a relapse of his prior disease process. Treatment for gastric amyloidomas has presently been one of observation or, at most, resection of the amyloid mass. It is not known if our patient required the same approach or if this warranted the re-institution of chemotherapy for NHL? Until more reports of tumoral amyloidosis are made known, treatment as well as prognosis remain uncertain.


Thuc Quyen Nguyen, MD*, Adrien Mazer, BS, James Lewis, MD, FACG. Gastroenterology, Medicine, Georgetown University, Washington, DC.

Results: A 50 yr WF was admitted at 3 pm for abdominal pain, nausea, vomiting and bloody diarrhea. She awoke at 3 am with LLQ pain, diaphoresis and tenesmus, and subsequently had 6 bowel movements which progressively became more bloody. The pain was continuous, crampy, non-radiating with pain 8/10, requiring narcotics. She denied GI symptoms like this in the past. She has a PMH of migraine and had been using sumatriptan tablets for about 15 yrs, usually once every other month. She had not used the IM form until 8 days prior to the onset of these symptoms, a one time 6 mg injection. On abdominal exam, she was tender in the LLQ without guarding or rebound; bowel sounds were hyperactive. The rest of her physical exam was normal. WBC was 16,700 with 92% neutrophils. A colonoscopy performed the next morning showed a normal rectum and sigmoid colon. In the upper descending colon, a colonic "stripe sign" (an area of broad exudate) was noted, beyond which were changes of severe colitis consistent with ischemia at the splenic flexure. Bx was consistent with acute IC. An IC scoring system (developed for IC cases associated with alosetron-Ringle et al Gastroenterology 2005;128 (No 4 suppl 2):A-467) gave a score of 15 out of 17, indicating a very high probability of IC. She was started on mesalamine, pentoxyfylline, Cipro, and metronidazole. Stool studies were negative. An MRI/MRA was consistent with IC, with edema and colonic wall thickening from the hepatic felxure to distal sigmoid colon, with no vascular abnormalities. A 2-D echo was normal with an EF of 60% and no thrombus. Over the next few days her pain and nausea diminished, she tolerated a regular diet, and her WBC normalized and was discharged. A repeat colonoscopy 6 weeks later showed complete healing of the mucosa, with some residual scarring at the splenic flexure. The rest of the colon, including the terminal ileum, was normal. There have been only two previous reports of IC caused by sumatriptan; one being a case report and the 2nd a series of 7 cases reported to the FDA. In our pt, despite having used oral sumatriptan for years, her presentation after the IM form was classic for IC. No other causes were found



Lawrence Chan, MD*, Paul Arnold, MD. Division of Gastroenterology, Virginia Commonwealth University Health System, Richmond, VA.

Purpose: To describe a rare complication of prostate cancer therapy infrequently encountered by gastroenterologists.

Methods: Adenocarcinoma of the prostate is the most common malignancy in American men and carries significant consequences. There are many surgical or radiation-based treatments; the combination of EBRT with brachytherapy carries significant risk of rectal toxicity. This rectal toxicity can manifest as hematochezia or rectal bleeding. There are rarer but more serious complications from radiation treatment such as recto-urethral fistulas (RUF), but one must be astutely aware. We describe a patient with previously treated prostate cancer who had a solitary rectal ulcer with fistulous tract from rectum to urethra.

Results: A 70 year old African American male presented complaining of rectal pain and intermittent hematochezia. He also reported tenesmus and occasional drainage of clear liquid suspected to be urine via rectum with passage of feces. Two years previously, he underwent combination prostatic seed implants and external beam radiation for prostate cancer. Physical examination described pain on palpation of the anterior rectal wall at the level of the prostate and the presence of occult blood in the stool. There were no other pertinent findings. Laboratory data was unremarkable except for urinalysis findings consistent with cystitis. Colonoscopy revealed friable rectal mucosa and a deep, 1.5 cm ulcer in the distal rectum on the anterior rectal wall. Biopsy specimens noted chronic inflammatory changes; there was no evidence of infectious or neoplastic processes. Computed tomography of the pelvis described air and contrast between the urinary bladder and the rectum indicating a recto-vesicular fistula.

Conclusion: Prostate cancer is a serious disease, and radiation treatment can carry significant gastrointestinal effects. Radiation proctitis can require repeated hospitalizations, procedures, and blood transfusions. Endoscopic therapy with argon plasma coagulation (APC), can provide substantial symptomatic relief over several sessions. Surgery is reserved for those patients with no other therapeutic options. The endoscopic approach for a patient with suspected radiation-induced injury to the rectum should be cautious. On encountering a rectal ulcer, one should carefully sample the affected tissue to exclude an alternate etiology; other diagnostic modalities including radiographs and cystoscopy should be pursued to confirm the diagnosis. RUF is not usually discovered by a gastroenterologist. Upon encountering the male patient previously treated with radiation to the prostate, one must be aware of the possibility of this phenomenon and exercise appropriate caution.


Ilan Weisberg, MD, MSc*, Cavell Lianne, MD, Doug Weine, MD, Ellen Scherl, MD. Gastroenterology and Hepatology, New York Presbyterian Hospital - Weil Cornell Medical Center, New York, NY.

Purpose: To highlight a rare cause of overt upper gastrointestinal bleeding successfully controlled with endoscopic hemoclip placement.

Methods: N/A

Results: Patient: A 90 year old woman presented to an outside hospital with one day of melena and hematemesis. She had no previous history of gastrointestinal disease. Her medical history was significant for hypertension, diabetes, and end-stage renal disease on hemodialysis. At initial presentation to the outside hospital she was hemodynamically stable with a hemoglobin of 9.8. Endoscopy revealed a bleeding duodenal diverticulum which was injected with epinephrine, though hemostasis was not confirmed. She was transferred to our institution for either selective arterial embolization or surgical intervention. On arrival, she was orthostatic with a 20 mmHg drop in blood pressure. She was mildly lethargic with normal cardiopulmonary exam and a soft, nontender abdomen. Several hours after arrival, she had an episode of hematochezia and bright red blood was lavaged from her nasogastric tube. Laboratory data revealed a hemoglobin drop of 4 grams (from 11 to 7.2). Emergent endoscopy was performed which revealed a large wide-mouthed diverticulum in the third portion of the duodenum. There was an actively bleeding arterial vessel within the diverticular sac, though no associated mucosal defect was identified. Complete hemostasis was achieved with injection of 9 cc of 1:10,000 epinephrine followed by placement of two hemostatic clips across the bleeding vessel. Afterwards the area was irrigated with saline with removal of residual clot and without evidence of further bleeding. The remainder of her hospital stay was uneventful and she was discharged home after a 5 day hospital course.

Conclusion: Discussion: Duodenal diverticula are commonly discovered on routine evaluation of the upper gastrointestinal tract. Though typically asymptomatic, these diverticula have been associated with duodenal or biliary obstruction and diverticulitis. Additionally they represent a rare and often overlooked source of gastrointestinal hemorrhage. No consensus currently exists to guide management of bleeding duodenal diverticula. Traditional methods have included surgical diverticulectomy or selective arterial embolization. In this elderly patient with multiple comorbidities, rapid endoscopic diagnosis with successful hemostatic clipping offered a less invasive and safer alternative. This case highlights an atypical source of overt gastrointestinal hemorrhage managed effectively with therapeutic endoscopy.


Hua Chen, MD*, Joseph Hancock, MD, Grace Sun, FNP. Gastroenterology, Texas Tech Health Sciences Center, Lubbock, TX.

Purpose: Clinical Vignette

Methods: A 64 year old Hispanic male reported to the ER November 2007 complaining of abdominal pain in the upper bilateral quadrants for the past week. Symptoms also included nausea and vomiting which worsened with meals. Over the past week, patient had also noticed "growth" of the abdomen, yellowing of his skin and eyes, increasing fatigue and loss of appetite. The patient denied any similar episodes in the past. Past medical history was significant for a history of lung cancer and with continued smoking. The remainder of the review of systems was non-contributory. Physical exam abnormalities included jaundice, icterus, ascites, and abdominal tenderness in the right upper quadrant and epigastric areas. There was no abdominal guarding or rebound tenderness. The remainder of the physical exam was unremarkable. Abnormal laboratory studies included elevated LFT's with markedly elevated alkaline phosphatase, mildly elevated ALT/AST, and CA 19-9 greater than 10,000. AFP was within normal limits. The remainder of the laboratory values were within normal limits. Imaging studies done during the hospital course included an abdominal ultrasound, CT, MRCP, ERCP, and liver biopsy. The results of the studies indicated cholelithiasis and choledocholithiasis with a questionable intra-hepatic obstructive process. No dilatation was seen at the common bile duct. Brushings from the ERCP and percutaneous biopsy of the liver was negative for ductal carcinoma.

Results: Initial impressions included cholelithiasis and choledocholithiasis. However, when ERCP failed to reveal an acute pathology, cholangiocarcinoma was suspected and the patient was informed of his grim prognosis. Even though biopsies were negative for malignancy, the patient was recommended for palliative percutaneous transhepatic cholangiography (PTC) with no further surgical treatment. A second opinion was obtained and exploratory laparoscopy revealed an unresectable, hard mass at the liver hilum. A PTC was performed and brushings obtained were negative for malignancy. The working diagnosis was changed to intra-hepatic lithiasis. Surgery was performed to remove the stones under direct visualization via choledoschoscope. A choledochododenostomy was also performed.

Conclusion: Intra-hepatic lithiasis is a rare western disease. However, it is commonly reported by doctors in China and Japan with literature published to date detailing evidence-based diagnosis and treatment. It is possible to prematurely doom patients to a grim diagnosis of cholangiocarcinoma. This case voices the importance of both a thorough approach towards medicine and highlights the need and benefits of international cooperation in furthering medical knowledge.


Hua Chen, MD*, Joseph Hancock, MD, Diana Vega, MD, Grace Sun, FNP, Dixon Santana, MD. Gastroenterology, Texas Tech Health Sciences Center, Lubbock, TX, Surgery, Texas Tech, Lubbock, TX.

Purpose: Clinical Vignette

Methods: A 46 year old African American woman presents to ER with nausea, vomiting, and abdominal pain. She is known to have ESRD secondary to SLE diagnosed in 10 years prior. The patient woke up one day prior feeling nauseous and threw up six times. As episodes progressed, vomitous became green and soft in consistency. She had not been able to eat since the episode began. Past medical history is significant for CVA x 2 (1997 and 2005), Lupus nephritis (2004), nonischemic cardiomyopathy, and ESRD (2005). Medications included a tapering dose of prednisone for a recent lupus flare. The remainder of the history and review of systems were noncontributory except as described above. On admission, vital signs were stable and physical exam was unremarkable with the exception of a positive Murphy's sign. Significant findings on CBC included microcytic anemia and increased poly-morphonuclear neutrophils. CMP abnormalities included elevated amylase, lipase, AST, ALT, and CRP. BUN and creatinine were also elevated. Imaging studies performed included an abdominal ultrasound which revealed a mass-like structure in the gallbladder fossa postulated to be a necrotic mass 4.1 by 6.7 centimeters reconfirmed by CT scan. An ERCP was done and revealed a dilated CBD with an abscess / inflammatory complex cavity found in the region of the gall bladder with a haziness postulated to be a leak.

Results: The patient underwent a laporoscopic cholecystectomy with successful resection and evacuation of gall bladder fossa. Findings at surgery included perforation of gall bladder into liver along with a severely inflamed gall bladder. Pathology reported acute and chronic cholecystitis with fibrinoid necrosis of blood vessels in gall bladder wall consistent with severe acute inflammation of systemic vasculitis. There were no signs of malignancy on frozen section.

Conclusion: The coexistence of lupus and cholecystitis is rare and literature concerning this condition is sparse. This presentation is not a random coincidence but rather a progression of SLE resulting in a dangerous gall-bladder pathology. To date, this is the only case report in literature where SLE vasculitis resulted the direct compromise of the gall bladder wall. Current treatment options include cholecystectomy and corticosteroid administration. Additional studies searching for anti-phospholipid antibodies and abnormalities in phospholipid-dependent tests of coagulation would also be recommended as anti-phospholipid syndrome (APS) can result in other catastrophic organ failures. Finally, a follow up with rheumatology for further management of SLE would be appropriate and long term anticoagulation should also be considered at that time.


Maria Westerhoff, MD*, Stanley Cohen, MD, Joseph Ahn, MD, MS. Hepatology, Rush University Medical Center, Chicago, IL, Pathology, University of Chicago, Chicago, IL.

Purpose: Bosentan is an orally administered endothelin-1 receptor antagonist used in the treatment of pulmonary arterial hypertension (PAH). It is known that bosentan can cause increases in liver aminotransferases and total bilirubin in up to 10% of cases. In rare cases, unexplained hepatic cirrhosis can occur with prolonged duration of therapy. The FDA has approved bosentan for the treatment of primary pulmonary hypertension despite the risk of liver function test abnormalities. Here we present a patient who developed autoimmune hepatitis following bosentan treatment.

Methods: A 69 year old male with PAH was treated with bosentan with regular liver function test (LFT) monitoring.

Results: The patient had no known previous liver disease or LFT abnormalities prior to bosentan initiation. After 2 months of bosentan treatment, the patient presented with an AST of 916 U/L, ALT of 1060 U/L, and alkaline phosphatase of 185 U/L. Bosentan was discontinued. The patient was asymptomatic and on examination had no stigmata of chronic liver disease. ANA, SSA, LKM, ASMA were negative. Serologies for viral hepatitis were negative. An ultrasound revealed a normal liver and gallbladder. A liver biopsy revealed severe grade 3 autoimmune hepatitis and centrilobular fibrosis (Figure). The patient was started on prednisone 40 mg daily. Within a month, his LFTs normalized and he has been followed for the last two years without further hepatic sequelae on azathioprine maintenance therapy.

Conclusion: We report the first case of autoimmune hepatitis associated with bosentan. Prompt discontinuation of bosentan and treatment with corticosteroids resulted in normalization of LFTs. The etiology of unexplained cirrhosis in patients undergoing treatment with bosentan may be from the development of autoimmune hepatitis. Patients on bosentan who develop LFT abnormalities should be evaluated for autoimmune hepatitis.


Charles Farr, MD*. Gastroenterology, St. Agnes, Fresno, CA.

Purpose: Barrett's Esophagus is seen in 3-12% of patients with chronic reflux symptoms. This is a study of three family members (father, son, and daughter) all of whom had long-segment Barrett's esophagus that rapidly progressed from low grade dysplasia (LGD) to high grade dysplasia (HGD) within a year. This study demonstrates that there is a genetic component to this disease, and that, in familial cases, there can be rapid histological progression suggesting that the biological behavior is distinct from that seen in sporadic cases of Barrett's esophagus.

Methods: A 77 year old male with chronic acid reflux was found to have long-segment Barrett's esophagus with LGD that progressed to HGD within a year. A laparoscopic esophagectomy was performed with the finding of HGD. The pstient's son and daughter were both subsequently diagnosed with long-segment Barrett's esophagus that rapidly progressed from LGD to HGD within a year. Both son and daughter had laparoscopic esophagectomy with finding of HGD. The patient's grandson was found to have short segment Barrett's esophagus without dysplasia. The patient's wife has erosive esophagitis as does a granddaughter.

Results: A 77 year old male, his daughter and son all were found to have long-segment Barrett's esophagus that rapidly progressed from LGD to HGD within a year. The patient's grandson was found to have short segment Barrett's esophagus without dysplasia and is under close surveillance.

Conclusion: Barrett's esophagus is felt to be an acquired condition resulting from chronic acid reflux. This report suggests that there is a genetic component to this disease, and, where there are familial clusters, the biological behavior can be more aggressive with rapid progression to HGD emphasizing the need to consider some modification of endoscopic screening strategies for this group of patients. Early intervention with ablation of Barrett's tissue might be considered in patients with a strong family history of Barrett's esophagus.


Kristen Robson, MD*, John Coller, MD. Colorectal Surgery, Gastroenterology, Lahey Clinic, Burlington, MA.

Purpose: Inversion of the appendix can be seen incidentally at the time of colonoscopy and can be caused by a variety of factors. We present a case of an inverted appendix that was identified during a colonoscopy and that was due to endometriosis based on histologic examination after surgical resection.

Methods: Case report.

Results: A 51 year old woman with a history of endometriosis and menorrhagia presented for colonoscopy at the request of her primary care physician. She had a history of right lower quadrant pain. Surgical history included the removal of an endometrioma ten years prior and laparoscopic cholecystectomy five years prior to presentation. During colonoscopy, a smooth, soft, polypoid lesion was identified in the caput cecum. The lesion seemed to be extruding from the appendiceal orifice. Sigmoid diverticulosis was noted but the colonoscopy was otherwise unremarkable. A computed tomography scan revealed no abnormality in the pericecal region. A laparoscopic cecectomy was performed. At operation, the appendix was not clearly evident, but the mesoappendix appeared to be protruding into the caput cecum. Endometrial implants were not observed. When the specimen was examined, the appendix was inverted into the cecum. The histopathologic examination demonstrated endometriosis within the substance of the inverted appendix. This was supported by positive cytokeratin 7 and negative cytokeratin 20 staining.

Conclusion: Most cases of inverted or intussuscepted appendix have been identified at the time of surgery. An inverted appendix may be caused by appendiceal carcinoma, carcinoid tumor of the appendix, mucocele, appendicitis, polyp or endometriosis. The condition may present with symptoms such as abdominal pain or may be asymptomatic. Although endometriosis of the appendix is well described, inversion of the appendix secondary to endometriosis is unusual and only 22 cases have been reported. Approximately 200 cases of appendiceal intussusception due to various causes have been described in the literature, and there are few cases of identification of an inverted appendix at the time of colonoscopy. The underlying etiology of an inverted appendix is typically established upon histologic examination of the surgical specimen as biopsies of the overlying mucosa and radiologic imaging of the region tend to yield non-diagnostic results. The development of a standardized approach to the evaluation of an inverted appendix found during colonoscopy would be helpful for clinicians.


Jeffrey Lewis, MD*, Brian Gehlbach, MD, Oto Aytekin, MD, Jennifer Chennat, MD, Smruti Mohanty, MD. Gastroenterology, Radiology, Pulmonary and critical care, Internal Medicine, University of Chicago Medical Center, Chicago, IL.

Purpose: Trans-arterial chemoembolization (TACE) is used as a bridge to liver transplantation in patients with hepatocellular carcinoma (HCC). Adverse events following TACE including infection and bleeding have been well documented in the literature. However, bilio-pleural fistula (BPF) following TACE has not been reported. We present a case of BPF in a patient with HCC following TACE. The patient is a 66-year old male with cryptogenic cirrhosis complicated by a 3.5 x 2.7 cm HCC who was listed for liver transplantation. He underwent successful pre-operative TACE in August and November of 2007. However, in March 2008, he presented with a productive cough and pleuritic, right-sided chest pain. A chest x-ray revealed a large, right-sided pleural effusion and a thoracentesis revealed bilious, exudative fluid with a neutrophilic predominance. The pleural fluid bilirubin level was 18.4 mg/dL with a pH of 6.8. These findings were suggestive of BPF and required chest tube placement. A subsequent MRI/MRCP revealed a significant dilatation of the right biliary duct without visualization of the liver capsule in segments VI and VII. These findings further confirmed BPF, suggesting tracking of bilious fluid from the liver into the pleural space. He underwent an ERCP-guided sphincterotomy with biliary stent placement and a thoracotomy with decortication which resulted in improvement of BPF. It appears that BPF in this case resulted from TACE-related rupture of HCC into the pleural space. A potential mechanism for the development of BPF is tumor necrosis and capsular destruction following TACE leading to a communication between the biliary system and pleural space through pre-existing diaphragmatic defects. Furthermore, tumor encasement of biliary structures and subsequent increases in retrograde biliary flow may serve to maintain flow into the pleural space.


Seth Sweetser, MD*, Louis-Michel Wong Kee Song, MD. Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.

Purpose: A rare case of GI bleeding from a post-splenectomy splenic artery pseudoaneurysm fistulizing to the colon is presented.

Methods: Case Report: A 79 y/o male awoke with abdominal pain and rectal bleeding. Past history was notable for a splenectomy 6 yrs ago for immune thrombocytopenic purpura. He denied aspirin or NSAID use. Evaluation revealed a significant drop in hemoglobin (13 g/dL to 6.9 g/dL) and resuscitative measures were undertaken.

Results: An emergent upper endoscopy was performed and was negative. At colonoscopy, a large 3-4 cm pulsatile lesion with ulceration and overlying adherent clot was seen in the proximal descending colon (Fig. 1). CT angiogram was performed which revealed a large hematoma in the splenic bed and visualization of the splenic artery coursing into this location with contrast extravasation. The patient declined surgery and subsequently underwent successful angiographic embolization of a large pseudoaneurysm at the distal splenic artery stump (Fig. 2). Repeat colonoscopy 6 weeks later revealed complete healing at the site of the eroding pseudoaneurysm.

Conclusion: GI bleeding from splenic artery pseudoaneurysm (SAP) is an uncommon but potentially life-threatening condition. Risk factors for SAP include pancreatitis, posttraumatic, peptic ulcer disease, and iatrogenic. Lower GI bleeding due to erosion or fistulization of SAP to the colon is a very rare event that requires a high index of suspicion and appropriate endoscopic/imaging studies to arrive at a correct diagnosis. This case highlights the fact that SAP should be considered in the differential diagnosis of GI bleeding in individuals who have undergone splenectomy.


Chethra Muthiah, MD*, Joseph Ahn, MD, MS, Stanley Cohen, MD. Internal Medicine, Section of Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Patients with cirrhosis are at risk for hepatic decompensation in case of superimposed acute liver damage. Surgical procedures in cirrhotics can also precipitate hepatic decompensation. We present a case of a stable cirrhotic patient who developed hepatic failure after acquiring acute hepatitis A (HAV) infection, and undergoing surgical procedures.

Methods: A clinical vignette case report is presented.

Results: A 54 year old male with no known liver disease presented with right upper quadrant pain. Laboratory data showed only a mild increase in his transaminases. Right upper quadrant ultrasound showed gallstones. He underwent an uneventful laporascopic cholecystectomy without mention of liver morphology. He presented eight days later with jaundice, malaise, lethargy, and ascites. Laboratory tests revealed bilirubin of 18.8 mg/dl, INR of 1.7, and creatinine of 4.2. No viral serologies were obtained. Imaging studies were inconclusive and the patient underwent exploratory laparotomy for possible retained biliary stone or iatrogenic bile duct damage. Operative findings included a grossly cirrhotic liver, but no biliary obstruction. Biopsy revealed micronodular cirrhosis with extensive acute necrosis. The patient was transferred for liver transplant evaluation. The patient had recently traveled to the Caribbean and his wife had contracted acute HAV infection. Serology confirmed acute HAV infection in our patient. Despite supportive care he did not improve, and subsequently underwent successful liver transplantation.

Conclusion: This case illustrates several important points relating to the care of cirrhotic patients. First, acute HAV infection can have devastating effects in a cirrhotic patient. The overall case-fatality rate of acute HAV is 0.01% to 0.3%, but can reach up to 11.6% in patients with underlying chronic liver disease. Fulminant hepatic failure secondary to superinfection with HAV has been well-documented in patients with cirrhosis and chronic viral hepatitis. The CDC recommends widespread vaccination for HAV in patients with known chronic liver disease. Second, cirrhotic patients undergoing emergent intra-abdominal surgery have a high risk of morbidity and mortality. Prior data has shown peri-operative mortalities in the 10%, 30%, and 70% range for patients with Child's A, B, and C cirrhosis, respectively. Finally, there can be significant mortality (approximately 10%) in any patient undergoing surgery in the face of acute viral hepatitis. In conclusion, patients with chronic liver disease should be vaccinated against hepatitis A and B. Also, clinicians should recognize the high risk of morbidity and mortality in cirrhotic patients and patients with acute viral hepatitis undergoing surgical procedures.


Douglas Weine, MD*, Ketan Kulkarni, MD, Ilan Weisberg, MD, Robert Schaefer, MD, Kunal Jajoo, MD, Christine Frissora, MD. Gastroenterology and Hepatology, New York Presbyterian Hospital - Weill Cornell Medical Center, New York, NY.

Purpose: Gastric bezoars are a rare cause of abdominal pain that can be seen on endoscopic evaluation. Phytobezoar formation usually occurs because of ingestion of foods rich in cellulose and other indigestible solids in patients with poor mastication and delayed gastric emptying. There are a few case reports in the literature using Coca-Cola or diet Coca-Cola in large quantities to break up phytobezoars. Many patients with phytobezoars have gastroparesis secondary to diabetes and should not injest large quantities of regular soda or find it unappealing to have a large volume lavage of soda instilled through a nasogastric (NG) tube. All previous case reports utilize Coca-Cola or diet Coca-Cola. We present the first case of phytobezoar dissolution using diet Pepsi.

Methods: A 54 year old woman with a history of poorly controlled diabetes leading to end stage renal disease requiring renal transplant presented with abdominal pain. She described a burning midepigastric pain, epigastric fullness, nausea and severe reflux. An esophagogastroduodenoscopy (EGD) was performed and revealed two large phytobezoars. On the basis of reports of the efficacy of cola lavage for the treatment of phytobezoars, nasogastric (NG) lavage with 3L of cola over 12 hours was recommended, but she declined the NG tube.

Results: The patient was given three 20 oz bottles of diet Pepsi to drink over an eight hour period, and she was made NPO after midnight. An EGD was performed the following morning which demonstrated complete dissolution of the phytobezoar. The remaining food particles were suctioned through the endoscope (Olympus GIF-2T160, 3.7 mm aspiration channel), and the endoscope's irrigation port was connected to a bottle containing diet Pepsi for further lavage and suctioning. The patient tolerated the procedure well and reported resolution of abdominal pain the following day.

Conclusion: This case demonstrates a novel approach for the treatment of gastric bezoars. The treatment of gastric bezoars can either be conservative or surgical. The efficacy of large dissolution of gastric bezoars with large volumes of Coca-Cola and direct endoscopic infusion of bezoars has been reported in the past but we propose a less aggressive use of cola as being just as effective. The mechanisms of cola dissolution is not well understood, but it has been proposed that it is a combination of the mucolytic effect of NaHCO3 and the penetration of CO2 bubbles into the surface of bezoars. Thus, in diabetic patients, it is unnecessary to use regular cola beverages that contain high sugar content. In addition, our case is the first reported use of diet Pepsi brand cola for this purpose.


Alfonso Waller, MD*, Conrad Jablonski, MD, Yomaris Pena, MD, Anand Srinivasan, MD. Medicine, UMDNJ - New Jersey Medical School, Newark, NJ, Medicine, Veterans Affairs New Jersey Health Care System, East Orange, NJ.

Conclusion: Pancreaticopleural fistula is a rare complication of pancreatitis, with an incidence rate of 0.4% to 4.5% of patients with pancreatitis. Awareness of this entity by clinicians is essential because only 20% of patients complain of abdominal pain, and the diagnosis is often delayed because respiratory symptoms may predominate. We report the case of a 61-year-old man with chronic alcoholism and pancreatitis was admitted for respiratory distress. Physical examination revealed an oxygen saturation of 90% on room air, dullness to percussion and egophony over the entire left chest, minimal air entry in the left with breath sounds heard in the upper left chest and clear breath sounds on the right chest. An electrocardiogram (EKG) revealed low voltage, which was a new finding compared to his old EKG. Chest x-ray demonstrated a new left sided pleural effusion, and a thoracentesis yielded bloody fluid with an amylase level of 5241 U/L. Computed tomography (CT) scan showed a large pleural effusion with near complete left lung collapse and coronal reconstruction revealed a small subpulmonic collection adjacent to the pancreas. Magnetic resonance cholangiopancreatography (MRCP) was suspicious for possible sinus tracts extending from the proximal pancreatic duct. Initial management was conservative; the patient was on bowel rest with intravenous hydration and placement of chest tube which allowed serial drainage. However, because of a persistent pleural effusion thoracotomy with evacuation of blood and clots, and lung decortication was performed. The patient recovered well. Though a pancreaticopleural fistula is rare, it should be considered in a patient with a history of pancreatitis or alcohol use presenting with a unilateral pleural effusion.


Saman Ahmed, MD*, Leelavathi Kasturi, MD, Henry Safier, MD, FACG. Internal Medicine, Queens Hospital Center, Jamaica, NY.

Purpose: Abstract: Liver abscess is the most common manifestation of systemic amebiasis. Common in endemic areas like Mexico, India, South and East Africa, with increased travel, the incidence is increasing in USA. We present an interesting case of massive amebic liver abscess involving both lobes.

Methods: Case Report:48 year old Guyanese male with history of seizure disorder was admitted with the chief compliant of RUQ abdominal pain for one week, with three to four loose stools per day. Pain was worse on coughing and was accompanied by nausea, anorexia and occasional shortness of breath. Patient had a history of alcohol, smoking and was HIV negative. He was taking Dilantin and Ibprofen and had no allergies. Review of systems was unremarkable. On admission patient was afebrile but drowsy with incomprehensible speech. Physical exam was unremarkable except mild RUQ tenderness, with a liver of 2 cm below right costal margin. Stool was positive for occult blood. Lab studies were unremarkable except Hb 11.5, hct 35.2, WBC 42K with 65% toxic bands. LFTs revealed alk phos 277, AST 51, GGT 191, Albumin 2.1, t.bil 1.7, conj. bil 0.8 and LDH 183. On CT was a 16 cm liver mass with surrounding edema, perihepatic fluid and a nonspecific multifocal colitis involving right colon, hepatic flexure, sigmoid and rectum. Patient underwent CT guided drainage of liver abscess, yielding about 800 cc of brown colored thick fluid without evidence of bacteria, mycobacteria, but with presence of ova. Serology was positive for entamoeba histolytica. Subsequent CT revealed decrease in the size of the abscess and patient improved clinically. Colonoscopy revealed ulcerations with overhanging edges, throughout colon, with areas of normal intervening mucosa. Patient was placed on flagyl, zosyn and paramomycin was added as a luminicidal agent. With drainage and treatment, his lab data improved with resolution of colitis and sepsis.

Results: Discussion:Ameba is more prevalent in areas of overcrowding and poor sanitation and spread from person to person by fecal oral route. Risk increases with old age, pregnancy, immunosuppression, malnutrition, homosexuality, alcoholism and travel to endemic areas. Cyst ingestion releases trophozoites which adhere to the wall of the large intestine, causing ulceration with subsequent passage into the blood stream. Amebiasis may be acute or chronic, causing symptoms of epigastric pain, jaundice, encephalopathy and sepsis. Abscess is usually solitary involving right lobe with only 10-15% cases revealing multiple small abscesses.

Conclusion: Small liver abscess can be successfully treated with antiamebics only, but the larger abscesses, especially those involving the left lobe are more effectively treated with amebicides and aspiration.


Joshua Goldman, MD*, Francis Farraye, MD, MSc, FACG. Section of Gastroenterology, Boston University School of Medicine, Boston, MA.

Purpose: Hollow visceral myopathy (HVM) is a form of chronic idiopathic intestinal pseudo obstruction (CIIP). It rarely involves other systems including the urinary tract.

Methods: A 45 year old female was transferred to our hospital with 3 months of nausea, vomiting and watery diarrhea. She had a tender, distended abdomen on physical exam. CT enterography demonstrated thickening and distension of the large and small intestines without a transition point. Bilateral hydroureter/nephrosis was noted.

Results: EGD and colonoscopy were grossly and histologically normal. Ureteral stents were placed without resolution of her hydronephrosis. Laparotomy did not reveal a mechanical obstruction. A full thickness rectal biopsy showed vacuolar smooth muscle degeneration with loss of a majority of muscle fibers c/w HVM. A PET scan and testing for amyloid, scleroderma and HIV were negative. A venting gastrostomy was placed and TPN started with resolution of symptoms. She was discharged to a rehabilitation facility.

Conclusion: Secondary chronic intestinal pseudo obstruction (CIP) is usually due to a paraneoplastic syndrome, scleroderma, amyloidosis or HIV. In contrast, CIIP is due to either a HVM or hollow visceral neuropathy. Involvement of other visceral smooth muscle including the urinary tract and gallbladder has been reported. Although CIIP is usually seen as a familial syndrome, rare sporadic cases have been reported. Treatment of CIIP is primarily supportive with venting, surgical resecton and TPN as needed. Chronic nausea, vomiting and diarrhea with small intestinal dilation and hydroureter should prompt consideration of CIIP.


Bryan Ong, MD*, Manmeet Padda, MD, Don Rockey, MD. Internal Medicine, University of Texas Southwestern, Dallas, TX, Digestive and Liver Disease, University of Texas Soutwestern, Dallas, TX.

Purpose: Background: Despite their ubiquity, bottle caps are seldom ingested and few published cases exist. Because of their size and shape, bottle cap extraction presents a management challenge.


Results: Case Report: A 23 year-old, healthy male presented with severe throat pain, nausea, and retching after accidentally swallowing a bottle cap three days prior to admission while he was inebriated. He opened a beer bottle with his teeth and the beverage's compressed gas propelled the metal top into his mouth, forcing him to swallow it. Esophagogastroduodenoscopy (EGD) at an outside hospital identified the bottle cap in his esophagus. After unsuccessful retrieval, the cap was pushed into his stomach to allow a chance for it to pass. The patient presented to our facility one day later complaining of nausea, vomiting, and food intolerance. We performed an EGD and identified the bottle cap in his stomach; there were no signs of esophageal, stomach, or duodenal injury. Initial attempts to retrieve the cap using a 16.7 mm inner-diameter oval overtube by grasping the cap with rat tooth forceps were unsuccessful because the forceps slid off the cap's metal surface. The cap was finally retrieved with a Roth net but was too wide to pass through the overtube. Consequently the endoscope, bottle cap, and overtube were gently removed as a unit under direct vision. The patient had no post-procedure complications and was discharged on the same day.

Conclusion: Discussion: We report our attempt and difficulties encountered with metal bottle top extraction. Endoscopic removal of wide objects such as bottle caps may be better facilitated with wider diameter or more malleable overtubes. We reviewed five previous reports of bottle cap ingestion, the earliest dating 1988. Four cases presented with esophageal obstruction. In two cases, caps were surgically removed while the rest were endoscopically removed. Unlike other blunt items, the serrated edges of metal bottle tops pose a hazard of luminal injury and hinder passage through narrower spaces like the esophagus or pylorus. Bottle caps should thus be treated as sharp objects and prompt removal with a protective covering is recommended.


Charles Koczka, MD*, Ovidiu Platica, MD. Medicine, SUNY Downstate Medical Center, Brooklyn, NY, Medicine, Brooklyn Campus of VA New York Harbor Healthcare System, Brooklyn, NY.

Purpose: Gastrointestinal Stromal Tumors (GIST) represent one percent of primary cancers of the gastrointestinal tract. GISTs are differentiated from other spindle-cell tumors by expression of the CD 117 antigen, which serves as part of the KIT transmembrane receptor tyrosine kinase. Traditionally treated with surgery if over 2 cm in size, stromal tumor management was revolutionized in 2001 by tyrosine kinase inhibitors. However, refractory GIST still remains a problem.

Methods: A 63-year-old male presented with abdominal cramps of two days duration, in a band-like distribution over the umbilicus. He denied nausea, vomiting, association with meals, hematochezia, or melena. Unintentional weight loss was noted. A colonoscopy ten year prior had been unremarkable. There was no history of malignancy or gastrointestinal disease in his family. On presentation, his abdomen was distended but soft, diffusely tender to palpation, positive for rebound tenderness. No masses appreciated on rectal examination but stool was positive for occult blood. Laboratory analysis was significant for microcytic anemia. Amylase and lipase were within normal limits and liver function was intact. CT scan of his abdomen revealed a 24 cm x 10.4 cm necrotic mass along the mesentery extending to the anterior abdominal wall. No hepatic masses or small bowel obstruction noted. He received palliative resection of his mesenteric mass along with small bowel resection and primary anastomosis. Pathologic interpretation of mass was significant for spindle cells being brightly positive for CD117, consistent with GIST. Given the size of the mass, peritoneal involvement, as well as high mitotic count, he was started on Imatinab 400 mg daily. Five months later, he returned with similar abdominal pain of four days. Compliance with daily Imatinib reported. On examination, a well healed surgical scar was seen across the abdomen. He was diffusely tender, with normoactive bowel sounds appreciated. While a repeat CT scan noted resolution of his previous large mass, there were multiple loops of small bowel with wall thickening, adherent to the anterior abdominal wall. An upper GI series failed to reveal bowel obstruction.

Results: Diagnosed with GIST refractory to surgery and Imatinib, he was instructed to stop Imatinab and was started on Sunitinib 50 mg.

Conclusion: Tyrosine kinase inhibitors, have been integral in treatment of GIST. By binding to an ATP-binding pocket, KIT signaling is halted. Resistance to Imatinib has been attributed to secondary mutations of the KIT receptor. Sunitinib has emerged as second-line treatment, but progression within 6 months poses a problem. Furthermore, patients on Sunitinib need close follow up for thyroid dysfunction.


Naim Alkhouri, MD*, Christine Carter-Kent, MD, Vera Hupertz, MD, Bijan Eghtesad, MD, John Fung, MD, PHD, Kadakkal Radhakrishnan, MD. Department of General Surgery, Liver Transplant Center, Pediatric Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, OH.

Purpose: A 2 year-old female was referred for abnormal liver function tests, diarrhea and low albumin. As an infant, she had idiopathic cholestatic jaundice that resolved spontaneously. Family history was significant for abnormal transaminases in her 2 older brothers. On physical exam the patient was at the 50% for weight and height. She had periorbital and lower extremity edema and her liver span was 8 cm. Her initial labs revealed albumin 2 g/dL (3.5-5.0), total protein 3.7 g/dL (6.0-8.4), AST 181 U/L (10-55), ALT 194 U/L (0-45), ALP 253 U/L (80-340), INR 0.9 (0.9-1.2), total bilirubin 0.1 mg/dL (0-1.5) and absolute lymphocyte count of 810/ uL (1500-8000). Further work up showed stool alpha-1-antitrypsin (A1AT) 459 mg/dL (0-54), IgG 105 mg/dL (423-1090) and no proteinuria. Evaluation for A1AT deficiency, Wilson's disease, autoimmune hepatitis, celiac disease and bile acid abnormalities was negative. An EGD showed dilated lacteals in the duodenum that was confirmed by wireless capsule endoscopy. Histology was consistent with lymphangiectasia. Hepatic venogram showed a corrected sinusoidal pressure of 5 mmHg with no evidence for portal hypertension. Liver biopsy demonstrated cirrhosis and ductular proliferation. Evaluation for congenital disorders of glycosylation by isoelectric focusing of transferrin and by genetic testing for type Ib was negative. Our patient was started on low-fat, high-MCT oil and low-salt diet in addition to spironolactone. She required multiple hospitalizations for albumin transfusions and she did not respond to octreotide. Her symptoms improved on oral prednisone; however, at the age of 4 years she presented with worsening diarrhea, ascites and low albumin refractory to higher dose of steroids. Because of her poor quality of life from protein-losing enteropathy (PLE) and her chronic liver disease with cirrhosis, she underwent liver transplantation (OLT) with a cadaveric split left segment. She recovered quickly and she had resolution of her diarrhea, ascites and edema. Her labs 4 months post-transplant revealed albumin 4.8 g/dL, absolute lymphocyte count of 1500/ uL and normal transaminases. To our knowledge, this is the first pediatric case of reversal of PLE after OLT. In patients with cirrhosis and normal synthetic function, a disproportionately low albumin level should alert to the possibility of PLE and lymphangiectasia. OLT should be considered in patients with cirrhosis and PLE unresponsive to medical treatment.


Jennifer Primeggia, MD*, James Lewis, MD. Internal Medicine, Georgeotown University, Washington, DC.

Purpose: While no longer listed in the Physicians' Desk Reference, PTU is still commonly used in the management of hyperthyroidism around the world. Serious complications of PTU include agranulocytosis, vasculitis, and hepatotoxicity. We report a case of PTU-associated ALF in a patient whose liver tests were not monitored while on therapy, reflecting U.S. guidelines written in 1995.


Results: A 19 year old female was diagnosed with Graves' disease in August 2007 and treated with PTU. Pre-Tx CBC and LFTs were normal, but no further LFTs were obtained. Three months later she presented with nausea, vomiting, abdominal pain and jaundice. LFTs now revealed a total bilirubin 6.5 mg/dL, AST 1747 IU/L and ALT 1589 IU/L. After 6 days at the outside hospital, she was transferred in acute liver failure with coagulopathy and stage II encephalopathy. Liver transplant evaluation was promptly initiated and she was listed as status 1. PTU was the only medication she had taken and all serologic, autoimmune, and metabolic studies were negative. She demonstrated rapid clinical deterioration while awaiting transplant, requiring intubation and CNS pressure monitoring. On our hospital day 7, she underwent orthotopic liver transplant, but succumbed to tonsillar herniation immediately after surgery. Pathology from her explanted liver revealed marked necrosis and fibrosis, consistent with drug-induced liver injury (DILI) (Fig. 1). ALF from non-acetaminophen DILI often has a poor prognosis with a mortality rate as high as 75%. PTU-associated hepatotoxicity has been a well-recognized phenomenon in the clinical literature for >50 years. However, as deaths related to PTU DILI are rare, routine monitoring of LFTs was considered unnecessary in national thyroid society guidelines, although monitoring WBC levels was advised (JAMA 1995;273:808)

Conclusion: Given the wide spectrum of PTU related DILI, ranging from asymptomatic elevations in ALT to fatal ALF, we agree with the advice to obtain baseline and surveillance LFTs to prevent irreversible liver damage, as is being recommended by several non-U.S. groups (Am J Gastro 2001;96:165), and call for a reappraisal of LFT monitoring guidelines in the U.S.


Jason Swoger, MD, MPH*, Edward Loftus, MD. Miles and Shirley Fiterman Center for Digestive Diseases, Mayo Clinic, Rochester, MN.

Purpose: Crohn's disease (CD) and carcinoid tumors commonly affect the terminal ileum (TI). Clinical, radiographic and pathologic findings in these conditions may be difficult to distinguish, and patients often undergo surgery for bowel obstruction before a diagnosis is confirmed. We report a case of coexisting CD and TI carcinoid tumor which highlights some of the diagnostic difficulties.

Methods: Case Report: A 38 year old woman with a 10-yr history of CD ileocolitis presented for routine follow-up. She had been maintained in asymptomatic remission on 2.4 g/d Asacol for 4 years. Recent episodic epigastric pain, nausea and vomiting led to an ultrasound showing a 1.0 cm liver lesion. CT enterography showed a liver FNH, along with a focal nodular area of enhancement in the TI. Concern was raised for a carcinoid tumor, but ileocolonoscopy showed only TI ulceration. Biopsies showed mild active chronic ileitis. She returned for reimaging after 4 months of budesonide. While TI mucosal hyperenhancement improved, a 0.9 x 0.8 cm nodular area remained. A 24-hr urine collection for 5-HIAA was normal. Octreoscan showed activity at the 24-hr images in the anterior ileal wall, but 48-h images showed resolution of this uptake. This was thought to represent physiologic excretion of the tracer, and not be consistent with carcinoid.

Results: Based on continued presence of the nodular mass with resolved TI inflammation following budesonide therapy, surgery was recommended for definitive diagnosis. She underwent laparoscopic-assisted right hemicolectomy with en-bloc lymphadenectomy. Histology showed a carcinoid tumor with invasion into the surrounding adipose tissue, along with 3 ulcerated strictures (min. diameter 3 mm), not present on radiographic imaging. Sixty regional lymph nodes were negative for tumor.

Conclusion: Despite careful endoscopy with biopsy, CT scans, and nuclear imaging, the diagnosis of a carcinoid tumor in the background of CD was not made until surgical excision. CD and carcinoid can both coexist and mimic each other, with up to 2.3% of TI carcinoids being initially misdiagnosed as CD. Furthermore, an incidental carcinoid diagnosis is made in 3.6% of CD resections. Most cases require surgical intervention for diagnosis, as in our case. An unexpected finding was significant ileal stricturing disease, which was not appreciated on CT enterography. Due to symptomatic, radiographic, and even histologic similarities between CD and carcinoid, accurate diagnosis remains challenging. Clinical suspicion for these diagnoses should remain high when the clinical picture remains unclear.


Gordon Liss, MD*, Stanley Benjamin, MD. Gastroenterology, Georgetown University Hospital, Washington, DC.

Purpose: Complications of colonoscopy (CLN) are frequently reported and studied. We report a unique scenario of post CLN hemoperitoneum without perforation or splenic rupture.

Methods: 44 yo female with h/o of Meckel's diverticulum s/p resection as a newborn underwent uneventful CLN and upper endoscopy (EGD) for the evaluation of diarrhea. EGD was normal. The CLN involved a 1 cm pedunculated polypectomy via hot snare. Post procedure the patient complained of abdominal pain. Physical exam was normal except for LLQ abdominal tenderness. Due to the pain, CT was performed demonstrating an intraperitoneal bleed without perforation or splenic rupture. Post procedure labs included hematocrit 35.7 (baseline 42.8) with normal platelets, PT/PTT. Decision was made to admit patient for observation. Surgery was consulted. Serial CBCs and abdominal exams were performed. Patient's hematocrit fell to 28.8 on day 2.

Results: Repeat CT was performed on day 3 showing improvement in the size of the hemoperitoneum. During the hospital stay, patient received IV then PO narcotics once able to tolerate PO diet. She was discharged on day 5.

Conclusion: Many complications relating to CLN with and without polypectomy have been reported. Post procedure bleeding manifesting as rectal bleeding has been well documented. Intraperitoneal bleeding is less common, but still reported in the setting of splenic rupture. Our patient is unique in that she exhibited hemoperitoneum without perforation or splenic rupture. Her history of prior surgery and presumed adhesions is likely her risk factor for this unique presentation.


Anupam Mohanty, MD*, Eugene Schiff, MD. Hepatology, University of Miami, Miami, FL.

Purpose: A 20-year-old previously healthy fisherman presented with one week of asymptomatic jaundice. He denied any past medical or family history, and denied use of medications, alcohol, drugs, or supplements. He consumed fresh fish up to three times per week for years and mentioned that he was exposed to permanent marker ink. Vitals and physical exam were unremarkable except for jaundice. Labs revealed normal CBC and BMP. LFT's showed AST 2597, ALT 2306, AP 188, TP 5.2, Albumin 2.6, TB 31.3, DB 24.3. INR was 1.3 with PT of 13.8. Urine drug screen, duplex ultrasound of the liver, CT of the abdomen, and MRCP were normal.

Methods: Other labs were normal including infection (Hepatitis A, B, and C, HIV, EBV, CMV, HSV), iron and TIBC, autoimmune markers (ANA, AMA, anti-smooth muscle antibody, and quantitative immunoglobulins), and alpha-1 antitrypsin. Copper studies were normal including ceruloplasmin, serum copper, and estimated serum free copper. The 24-hour urinary copper test returned elevated at 347 ug/day (normal 3-50). Ophthalmologic exam reported Kaiser-Fleisher rings with 60% confidence.

Results: Over the next four days, the INR rose to 2.3 and decision was made for emergent liver transplant. The patient tolerated the procedure well without complication. The liver was noted to be cholestatic and noncirrhotic. Explanted liver biopsy showed 40-50% panacinar and confluent necrosis with multifocal lymphocytic infiltration. Hepatic copper returned normal.

Conclusion: This case presents the dilemma of idiopathic fulminant hepatic failure in identifying the cause and deciding when transplant is warranted. FHF carries a high mortality rate and affects up to 2,000 person per year. 20% of cases are attributed to idiopathic causes, likely unknown environmental or infectious etiologies. Despite extensive workup, no cause was found. Elevated urine copper levels are found in Wilson disease but also in any disease with extensive hepatocellular necrosis. Other hepatotoxins include mercury in fish, microcystin found in blue green algae, toluene or xylene found in permanent marker, or drugs such as MDMA (ecstacy). The patient later admitted he may have been exposed to MDMA. This drug is not included in standard urine drug screening. This case also demonstrates that clinical judgment is important in determining candidacy for transplant. Although King's College criteria were not fulfilled, liver biopsy confirmed extensive necrosis. The advent of orthotopic liver transplantation has reduced the mortality rate of acute liver failure from 80% to 40%. Our patient's worsening coagulopathy and associated high mortality rate warranted emergent transplant which most likely saved this fisherman's life.


Anupam Mohanty, MD*, David Elijah, MD, Patrick Brady, MD, FACG. Division of Hepatology, University of Miami, Miami, FL, Division of Digestive Diseases, University of South Florida, Tampa, FL.

Purpose: A 49-year-old male with chronic anemia, hypertension, and gastresophageal reflux presented with three months of worsening fatigue and dyspnea. Over the past two years, the patient had several positive fecal occult tests with hemoglobin levels as low as 7.6. Multiple upper, lower, and capsule endoscopies revealed a large hiatal hernia and erosive gastritis in the fundus and proximal body. He required 22 units of blood and intermittent intravenous iron supplementation over the two years. His TSH, serum chemistries, and cardiac workup had always been normal.

Methods: The patient denied any surgical, family, tobacco, alcohol, or drug history. He had no allergies and took lansoprazole and lisinopril daily. The patient denied any chest pain, or change in color or caliber of stool.

Results: Physical exam revealed blood pressure of 157/104, heart rate of 113 bpm, and conjunctival pallor. He was not orthostatic. His hemoglobin was 11.8, hematocrit 35.3, and MCV was 76. WBC and platelets were normal, as were basic metabolic profile, liver-function tests, coagulation studies, cardiac-enzyme measurements, and urinalysis. CT scan of the abdomen revealed a large hiatal hernia. Upper endoscopy was performed revealing a large, 6 cm sliding hiatal hernia. Upon retroflexion of the endoscope, several linear erosions were visualized at the diaphragmatic hiatus with some dried blood but no active bleeding. He was advised to continue his acid-suppressing medication and was referred for surgical correction of the hiatal hernia as the endoscopic findings were characteristic of "Cameron lesions."

Conclusion: In 1986, A.J. Cameron described linear gastric erosions associated with hiatal hernias as a cause for chronic blood loss. These lesions are attributed to mechanical irritation of the hiatal hernia as it rides over the crux of the diaphragm with possible concomitant microvascular changes. These lesions may bleed intermittently causing iron deficiency anemia. Due to their transient nature, "Cameron lesions" may elude visualization by even the most skilled endoscopists. In this case, the lesions were absent on several endoscopies or misinterpreted as erosive gastritis. Standard therapy includes acid-suppressing medication, iron repletion, and blood transfusions when necessary. However, surgical correction of the hiatal hernia is the definitive therapy by eliminating the mechanical stress of the hernia allowing the lesions to heal and bleeding to cease. This case illustrates that awareness of Cameron lesions by internists and gastroenterologists may prevent years of undiagnosed chronic blood loss, and the repetition of multiple endoscopic and radiological procedures, and transfusions.


Lokesh Jha, MD*, Nabin Timilsina, MD, Michel Bidros, MD, Shaila Nupur, MD, Frederick Fallick, MD, Jeremiah Kurz, MD, Michelle Dahdouh, MD. Department of Infectious Disease, Department of Gastroenterology, Department of Medicine, St. Barnabas Hospital, Bronx, NY.

Purpose: A 40 year old African American male with h/o AIDS (CD4 count of 0/[mu]L), h/o pulmonary MAC infection with dissemination, non-compliance with medical treatment came to ED for evaluation of gradually worsening abdominal distension for a month associated with weight loss. On admission, he was afebrile, normotensive, but slightly tachycardic. Laboratory examination showed WBC of 21.8 per mm.sup.3 with 89.6% neutrophils, and albumin of 1.4 g/dl. CT scan of abdomen/ pelvis showed massive ascites with retroperitoneal and retrocaval lymphadenopathy. Abdominal paracentesis revealed cloudy fluid with WBC of 1800 per mm3, 78% neutrophils, and SAAG was 0. Patient was given antimicrobial coverage for spontaneous bacterial peritonitis; and empiric intensive treatment for MAC peritonitis was started with rifabutin, azithromycin, ethambutol, amikacin, and ciprofloxacin. Antiretroviral therapy was restarted. Microbiological analysis of the peritoneal fluid showed acid-fast bacillus and blood culture grew mycobacterium species confirmed to be MAC by DNA probe. Three weeks later, patient's CD4 count improved to 34/[mu]L, however he developed worsening ascites and fever with repeat CT scan showing loculated pocket of ascites. Repeat paracentesis showed chylous peritoneal fluid with WBC of 375 per mm3, 56% neutrophils, and triglycerides level of 780 mg/dl. Antiretroviral therapy was discontinued and steroids were added to intensive MAC treatment for suspected IRIS. Patient's stool, sputum, blood as well as ascitic fluid culture grew MAC. Patient's ascites and fever resolved, steroids tapered, and antiretroviral therapy was resumed. Three weeks later, repeat CT scan of abdomen showed no loculation of ascites with minimal improvement. He was treated with ciprofloxacin and amikacin for 28 days and discharged to rehabilitation facility for intense nutrition support, on azithromycin, rifabutin, ethambutol, bactrim, and antiretroviral therapy. At three months post admission, patient had repeat CT scan that showed no ascites and improvement in adenopathy. In the literature, there are only four reported cases of chylous ascites as a complication of disseminated MAC infection in adult patients to our knowledge, and two reported cases complicated by immune reconstitution inflammatory syndrome (IRIS). Though chylous ascites is a rare complication of disseminated MAC infection, it should be considered in the differential diagnosis of ascites in patients with AIDS.


Maqsood Khan, MD*, Joseph Ahn, MD, Nikunj Shah, MD, Shriram Jakate, MD, Ajay Patel, MD, Burns Meredith, BS, Stanley Cohen, MD. Internal Medicine, West Suburban Medical Center, Oak Park, IL, Hepatology, Rush University Medical Center, Chicago, IL, Medicine, Loyola University Medical Center, Maywood, IL.

Purpose: Giant cell hepatitis (GCH) is most often found in neonates and rarely seen in the adult's. We present an adult with GCH who progressed to fulminant hepatic failure (FHF), requiring liver transplantation. Case Report A 56 year old male with hemolytic anemia and idiopathic thrombocytopenic purpura (ITP) who had been managed with splenectomy and corticosteroids presented with jaundice. On physical exam, the patient was jaundiced without other stigmata of chronic liver disease. Hemoglobin was 13.9 mg/dl, platelet count 170,000/cmm, total bilirubin 13.2 mg/dl, direct bilirubin 9.5 mg/dl, albumin 3.0 g/dl, alkaline phosphatase 246 U/l, AST 435 U/L and ALT 758 U/L. Serological markers for viral hepatitis, HIV, parvovirus, CMV were negative. ANA, ANCA, ASMA, and LKM were negative. A liver biopsy showed periportal and lobular grade 3 hepatitis, with lymphoplasmacytosis and rosetting. The patient was treated with prednisone 40 mg daily and mycophenylate mofetil 1 g BID for autoimmune hepatitis. The patient subsequently developed renal failure, ascites, and hepatic encephalopathy. He underwent liver transplantation for FHF on hospital day 13. The explanted liver revealed on microscopic exam, giant cell transformation of hepatocytes suggesting a giant cell hepatitis variant of autoimmune hepatitis. The patient was discharged 9 days after transplantation and is doing well currently. Discussion GCH is a condition characterized by inflammation and large multinucleated hepatocytes. In newborn livers, various insults may cause GCH. In adults GCH comprises less than 0.25% of all hepatic diseases, and cases are variable in presentation and etiology. Adult GCH has been associated with autoimmune disorders, paramyxovirus, viral hepatitis, and medications. Corticosteroids have been found to improve the clinical picture in those individuals who are seropositive for autoimmune markers. Our patient had a history of hemolytic anemia and ITP but negative autoimmune markers. This case of FHF due to GCH highlights the extremely rare presentation of adult GCH with negative autoimmune markers requiring liver transplantation. Figure Legend High magnification microphotograph showing giant cell hepatitis with multinucleated hepatocytes and focal necrosis with inflammation (arrows) [Hematoxylin & Eosin stain, x 400 magnification].


Sunana Sohi, MD*, Stanley Cohen, MD, Nikunj Shah, MD, David Van Thiel, MD, Joseph Ahn, MD. Gastroenterology and Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Graft versus host disease (GVHD) is most commonly seen after allogenic bone marrow transplantation. We present a rare case of GVHD occurring after liver transplantation.

Methods: A 66-year-old man with non-alcoholic fatty liver disease presented with fever and dysuria one month after undergoing an orthotopic liver transplant (OLT). He was treated with levofloxacin for a presumed urinary tract infection, but continued to have fevers. Subsequently, the patient developed pancytopenia, with a WBC of 1.24 x 10.sup.3/mcL, hemoglobin of 8.3 g/dL, and platelet count of 19 x 10.sup.3/mcL. Two days after admission, he developed a generalized erythematous to violaceous macular skin eruption on his back and lower extremities. Punch biopsy of the skin lesions demonstrated lymphocytic infiltrates and basal epidermal cell vacuolization consistent with GVHD. He received high-dose steroids followed by three doses of basiliximab (20 mg) and one dose of daclizumab (16.5 mg). Antimicrobial prophylaxis was initiated with voriconazole, acyclovir, aztreonam, and daptomycin. G-CSF was administered for neutropenia.

Results: The patient's fever, rash, and diarrhea transiently improved, though he remained pancytopenic. Despite antimicrobial prophylaxis, the patient developed an influenza pneumonia requiring intubation. Oseltamivir was initiated but he subsequently suffered a cardiopulmonary arrest and expired.

Conclusion: The incidence of GVHD after OLT is estimated to be 1-2% based on case series, but the mortality is quite high at 85%. GVHD in this population is thought to occur when 10.sup.9-10 donor lymphocytes within the liver graft successfully mount an attack before the recipient is able to reject the organ. Diagnosis of GVHD can often be made on biopsy of affected organs (skin, GI tract, bone marrow), but if biopsy is non-specific, HLA typing can be performed for confirmation. Risk factors for the development of GVHD after OLT are not well elucidated, but may include closely matched HLA status, older age of the recipient, and relative immunodeficiency of the recipient. Treatment protocols have not been standardized, but have included modification of immunosuppression, corticosteroids, anti-lymphocyte agents, and interleukin-2 antibodies. As most patients succumb to death from sepsis, prevention of infection with antimicrobial prophylaxis is of the utmost importance. Clinicians should be aware that GVHD is a rare but serious complication of OLT. Every attempt should be made to diagnose and treat promptly when symptoms arise.


Dimple Raina, MD*, Aberrahim Khomani, MD, Fadi Rahhal, MD, Arvind Movva, MD, Sherman Chamberlain, MD. Section of Hematology Oncology, Section of Gastroenterology and Hepatology, Medical College of Georgia, Augusta, GA.

Purpose: Glanzmann's thrombasthenia (GT) is a rare autosomal recessive bleeding syndrome characterized by absent platelet aggregation secondary to abnormal Glycoprotein IIb/IIIa complex. We report the first case of endoscopic management of large polyps in a patient with GT.

Methods: A 52-year-old African American female with GT underwent four sequential colonoscopies over 9 months as enumerated below.

Results: Colonoscopy 1: Performed for heme-positive stools, no blood products given. It revealed multiple sessile polyps, the 2 largest (13 and 14 mm) in the right colon. The 13 mm one was removed using saline-assisted technique in combination with Endoloop and standard cautery. Immediate post-polypectomy bleeding was observed and successfully controlled with placement of 2 Triclips. Further polypectomies were deferred. The polyp was a sessile serrated adenoma. A surgical opinion recommended endoscopic surveillance. Colonoscopy 2: Preprocedure platelets and aminocaproic acid were given. Hot biopsy polypectomies were done to remove ten smaller 4-5 mm polyps in left colon. The 14 mm polyp was left in place to help localize potential post-polypectomy bleeding. No immediate or delayed bleeding occurred. Colonoscopy 3: Preprocedure platelets and aminocaproic acid were given. The remaining 14 mm polyp was removed by saline-assisted technique. A single Quick Clip placed at the polypectomy site. Two other smaller polyps (7 and 9 mm) were also removed from the left colon using standard electrocautery, with no clips applied. Three days later patient was admitted with delayed post-polypectomy bleeding. Colonoscopy 4: Hematochezia persisted despite daily replacement of red blood cells, platelets, recombinant factor VIIa, and prothrombin concentrate complex over a period of 10 days prompted the fourth colonoscopy. Active bleeding was identified in the right colon at the 14 mm polypectomy site. Dual therapy with epinephrine injection and placement of 4 Resolution clips achieved hemostasis. No further episodes of colonic bleeding have been reported to date.

Conclusion: Polypectomy in GT patients is complicated by immediate and delayed bleeding. The single previous GT case report suggested a protective effect of platelet transfusion and aminocaproic acid, to retard fibrinolysis, in preventing post-polypectomy bleeding. However, we conclude that for polyps 10 mm or larger the addition of mechanical therapy, with multiple clips, after standard cautery polypectomy, is more effective in preventing immediate and delayed post-polypectomy bleeding in patients with GT. The cost of preemptive multiple clips at the post-polypectomy site may be offset by a reduction in the need for blood products and by averting or shortening potential hospitalizations.


Lesley Andrews, MD*, Sherri Yong, MD, Khondker Islam, MD. Medicine, Loyola University Medical Center, Maywood, IL.

Purpose: This is an unusual case of microcytic anemia in a 52 year old female with malignant melanoma (T3N2M0) who presented to the hospital with hip pain after a fall. A CT of the pelvis did not show any hip abnormalities, but revealed asymmetric wall thickening of the rectum and a right posterolateral 17 x 13 mm perirectal lymph node. The patient had no hematemesis, melena or hematochezia. Her physical exam was unremarkable. Subsequent colonoscopy revealed a 3-4 cm necrotic, friable mass located on the inside of the ileocecal valve extending into the cecum. No other gross abnormalities were seen throughout the colon. Biopsy results of the colonic mass were consistent with melanoma with tumor cell staining positive for S100, HMB45 and melanin. The tumor cells failed to stain with CK7, CK20 and CDX2. Upper endoscopy revealed no abnormalities except mild antral erythema. Melanoma is one of the more uncommon types of malignancies, yet it is one of the most common tumors to metastasize to the gastrointestinal (GI) tract. Most often, melanoma of the GI tract is in the form of metastasis, although rare occurrences of primary melanoma in the GI tract have been reported. Although melanoma will most commonly metastasize to the lung and lymph nodes, any organ can be affected by the disease. The most common site of metastasis to the GI tract is the liver and small intestine, followed by the colon in which metastasis can also be seen 20-28% of the time. Metastases to the GI track often times go undiagnosed. If symptoms do occur, they are often symptoms typical of any type of tumor in the GI tract including hematemesis, abdominal pain, small bowel obstruction, melena and tenesmus. When patients with metastatic melanoma to the GI tract are symptomatic, it often correlates with more severe disease and a worse prognosis. Select symptomatic patients can be treated with surgery for palliation and some studies show it may in fact improve survival. Our case demonstrates a patient with melanoma metastatic to the lung, brain and omentum, who presents with new onset anemia and now found to have new metastasis to the colon. Metastatic melanoma to the colon is relatively uncommon and patients are frequently asymptomatic and, therefore, often undiagnosed. If symptoms do occur, they are often obvious in the form of hematemesis, melena, and severe abdominal pain. In patients with metastatic melanoma with even mild signs and symptoms, the physician should have a high suspicion for metastases to the GI tract. Endoscopic evaluation should be considered in all patients with melanoma who present with microcytic anemia in order to rule out gastrointestinal metastasis.

Methods: N/A

Results: N/A

Conclusion: N/A


Matthew Tsushima, MD*, Michael Walter, MD, Snorri Olaffson, MD. Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA.

Purpose: Hyperemesis gravidarum (HEG) is a severe form of nausea and vomiting during pregnancy. We report the use of percutaneous endoscopic gastrostomy for nutrition support in a patient with HEG.

Methods: A 25 year old G2P1 Caucasian female with a history of HEG presented at 7 6/7 weeks gestation with weight loss and persistent nausea and vomiting. After failing management with ondansetron, pyridoxine, and bland diet, she was admitted for persistent nausea and vomiting. On admission, she was afebrile and in mild distress. A weight loss from 128 lbs to 119 lbs since becoming pregnant, with a BMI of 21.1, was noted. Physical examination revealed dry oral mucous membranes. Laboratory examination revealed a transthyretin level of 19 mg/dL [11-53 mg/dL], white blood cell count of 6.84 x 10.sup.3/[mu]L [4.8-11.8 x 10.sup.3/[mu]L], BUN 12 mg/dL [7-20 mg/dL], creatinine 0.7 mg/dL [0.7-1.3 mg/dL], albumin 4.7 mg/dL [3.8-5.2 mg/dL]. Urinalysis revealed ketones >80 mg/dL. She was managed conservatively with intravenous fluids and ondansetron. A nasojejunal feeding tube was placed and enteral nutrition was initiated with prompt relief of symptoms. Osmolite 1.2 at 60 mL/hour was tolerated at goal rate. However, three days later, the feeding tube became clogged and she again complained of nausea and vomiting. A second feeding tube was placed with the end coiled in the stomach and enteral nutrition was restarted. However, the patient was unable to tolerate gastric feedings and TPN was initiated. She continued to complain of nausea and vomiting on TPN.

Results: After discussion with the patient, OB/GYN and Nutrition services, a percutaneous endoscopic gastrostomy tube with a 12 Fr J (PEG-J) tube extension was placed without difficulty. Enteral feedings resumed with improvement of symptoms and TPN was discontinued. Three days later, she again complained of nausea and vomiting. An upper endoscopy was performed which revealed jejunostomy tube tip in the gastric fundus. Using a guidewire, the jejunostomy tube was advanced further into the jejunum. She was discharged home tolerating enteral nutrition near goal rate. Occasional clogging of the jejunostomy tube at home resolved with flushes. One month later, the PEG-J tube was removed and a larger 22 Fr, 45 cm transgastric jejunal feeding tube was placed over a guidewire. At 26 weeks gestation, she weighed 165 pounds tolerating oral feeding, and the PEG-J tube was removed.

Conclusion: Enteral feeding is the preferred route of nutrition for a patient with a functional gastrointestinal tract. It also appears to be a safe and highly effective means of providing symptom relief in HEG. If patients are unable to tolerate nasogastric or nasoduodenal tubes, PEG placement may be an alternative to TPN.


Ketan Kulkarni, MD*, Doug Weine, MD, Charles Maltz, MD, PhD. Department of Gastroenterology and Hepatology, Weill Cornell Medical Center, New York, NY.

Purpose: To increase awareness among physicians of antibiotic-associated hemorrhagic colitis caused by Klebsiella oxytoca.

Methods: N/A

Results: Case 1: A 30 year-old man with no significant past medical history presented with right-sided abdominal pain and bloody diarrhea one week after receiving amoxicillin following a routine dental procedure. The patient's labs were significant for a mildly elevated WBC count and a CT scan demonstrated wall thickening of the entire colon, sparing the sigmoid colon and rectum, but most pronounced in the right hemicolon. Multiple stool studies were negative for the presence of Clostridium difficile toxin. However, Klebsiella oxytoca was isolated from stool cultures and the patient's symptoms resolved with supportive care. Case 2: A 67 year-old man with a history of AML who underwent induction chemotherapy followed by autologous stem cell transplantation complicated by MRSA bacteremia requiring linezolid began complaining of bloody diarrhea and abdominal pain two weeks following completion of his antibiotic course. Stool studies were negative for the presence of Clostridium difficile toxin; however Klebsiella oxytoca was isolated from stool cultures. The patient's diarrhea resolved after three days of supportive care.

Conclusion: Colitis following administration of an antibiotic is a well-recognized complication, with Clostridium difficile traditionally implicated as the most common culprit. However, increasingly C. difficile negative antibiotic-associated colitis is being diagnosed and infection with Klebsiella oxytoca has been identified as a cause of antibiotic-associated hemorrhagic colitis. Antibiotic-associated hemorrhagic colitis caused by Klebsiella oxytoca is a separate entity from C. difficile colitis and typically occurs in young, healthy patients after administration of penicillins. However, we also report here, for the first time to our knowledge, K. oxytoca infection after linezolid use in a hospitalized patient. The colitis associated with Klebsiella oxytoca usually displays an abrupt onset and involves the right colon. The colitic symptoms are typically self-limited and resolve after discontinuation of the offending antibiotic without the need for additional treatment. Our series of patients emphasize the importance of pursuing specific studies for the diagnosis of K. oxytoca among patients with the classic presentation (case 1) in addition to individuals with C. difficile negative colitis following antibiotics (case 2). Greater awareness of Klebsiella oxytoca associated colitis is needed among gastroenterologists and primary care physicians in order to avoid misdiagnosis and unwarranted therapy.


Ravi Juluri, MD*, Raj Vuppalanchi, MD. Medicine-Gastroenterology, Indiana University, Indianapolis, IN.

Purpose: Noni juice is a popular complimentary alternative medication often consumed for its wellness effects and is recommended for consumption at a dose of 1 oz (30 ml) per day. To our knowledge this is the first reported case of idiosyncratic drug induced liver injury (DILI) from United States that occurred after high dose consumption of Noni juice.

Methods: A 49 -year-old African American female with underlying liver disease presented with new onset jaundice. She had history of chronic consumption of Noni juice for several years at the recommended dose. However, two months prior to the presentation she had increased her daily consumption to 8 oz. Six weeks after increasing her dose, she developed mild constitutional symptoms eventually progressing to fatigue and jaundice.

Results: Her workup revealed elevated liver tests (ALP 247, AST 365, ALT 145 and total bilirubin 3.9 gm/dL), negative titers for viral and autoimmune hepatitis and imaging studies significant only for fatty infiltration of liver. She gave a history of occasional alcohol and acetaminophen use (4-6 grams/day). She had no exposure to any other xenobiotics. Extensive biochemical work up performed excluded all competing etiologies. Upon discontinuation of consumption of Noni juice at the onset of her jaundice, she had normalization of her liver tests over a period of 4 months. She did not receive any therapy with steroids.

Conclusion: This is the first reported case of idiosyncratic DILI after exposure to Noni juice from the United States. While a few cases reported from Europe showed a hepatocellular pattern of injury, this case presented with a cholestatic pattern of liver injury. The potential for toxicity caused by noni juices remains under surveillance by the food safety authorities in Europe currently and physicians in United States should be aware of this possibility.


Fouad Moawad, MD*, Todd LaRock, DO, Michael Biondi, MD, Brooks Cash, MD, Jayde Kurland, MD. Gastroenterology, Walter Reed Army Medical Center, Washington, DC, Radiology, Gastroenterology, National Naval Medical Center, Bethesda, MD.

Purpose: Obscure gastrointestinal (GI) bleeding creates a diagnostic challenge for gastroenterologists. Modern imaging techniques improve the detection and characterization of small bowel tumors and provide important guidance for treatment options.

Methods: A 28 year-old woman presented with symptomatic anemia. She denied abdominal pain, melena, or hematochezia. Her medical history was unremarkable and she denied the use of NSAIDs. Her examination was normal except for a positive FOBT. Initial laboratory values indicated a hemoglobin level of 3.8 g/dl (normal 12-16 g/dl). Upper and lower endoscopy with ileal intubation failed to reveal a bleeding source. Video capsule endoscopy (VCE) demonstrated red blood in the small intestinal lumen 5 hours after swallowing the pill without an apparent source. She subsequently underwent a Meckel's scan and RBC scintigraphy; both were negative studies. A Magnetic Resonance Enterography (MRE) was performed which revealed a 2.9 cm x 3 cm distal jejunal wall mass. While it demonstrated an intraluminal component, the mass was predominantly extramural. She underwent successful laparoscopic resection of the tumor, which stained strongly for C-117 (c-kit) consistent with a diagnosis of gastrointestinal stromal tumor.

Results: The evaluation of obscure GI bleeding can be a challenging task for the gastroenterologist. The majority of cases arise from the small bowel. Its free intraperitoneal location, extensive length, and vigorous contractility make the diagnosis of bleeding difficult. The etiology of obscure bleeding is dependent on the patient's age. In patients under the age of 40, the most common cause is tumors. While intraluminal extension of small bowel tumors may cause symptoms of obstruction, such tumors may also extend extraluminally into the peritoneum and be missed on VCE. Magnetic resonance imaging provides many unique properties and advantages over other imaging modalities to include enhanced visualization of soft tissues without superimposition of loops of bowel, the ability to screen for mural and extraluminal involvement and the lack of exposure to ionizing radiation.

Conclusion: MRE may have a role in the evaluation of patients with obscure GI bleeding and should be considered as a diagnostic option, especially in those under the age of 40 in whom no source can be clearly identified.


Joshua Hall, MD*, Arvind Movva, MD, Subbaramiah Sridhar, MB, BS, FACG, Sherman Chamberlain, MD, FACG. Section of Gastroenterology and Hepatology, Medical College of Georgia, Augusta, GA.

Purpose: A 42-year-old female was referred to us following an abnormal PET scan one month after a right breast lumpectomy for intraductal carcinoma. The PET scan used 18F fluorodeoxyglucose (FDG) with tandem computed tomography (CT) and demonstrated increased activity in the ascending colon, especially in the cecum, most of which appeared to be intraluminal. No other area of abnormal uptake in the abdomen was seen (Image 1). The patient had no family history of colon cancer or bowel symptoms.

Methods: The colonoscopy revealed a large wad of pink bubble gum adherent to the proximal right colon wall. The gum was piece-meal snared and removed with 2 Roth baskets (Image 2). Otherwise, the colon appeared normal. A follow up CT scan demonstrated that the intraluminal defect had resolved.

Results: This is a case of a false positive PET caused by adherent bubble gum in the colon. PET scans detect malignancy by demonstrating alterations in metabolic and molecular activity. FDG-PET evaluates changes in glycolysis. This leaves PET scans subject to false positive results by any process that increases glucose metabolism or alters the rate of glycolysis, as would occur with mucosally adherent sugared gum.

Conclusion: To our knowledge, this is the first case report of sugared gum in the colon causing abnormal uptake on PET scan. There was one previous case report of abnormal uptake of the tongue during FDG-PET because the patient had chewed gum prior to the PET scan. This case differs from other previous false positive PET scan cases due to foreign bodies, because it details a foreign body causing abnormal FDG uptake, as opposed to a foreign body causing granulomatous reactions, which then secondarily cause alterations in glycolysis resulting in the false positive result. This case teaches us to consider alternate diagnoses and even foreign bodies when dealing with abnormal PET imaging. Finally, it reinforces us to follow what our mothers said: "Don't swallow your gum."


Ami Behara, MD, MS*, Daniel Deziel, MD, Michael Brown, MD. General Surgery, Gastroenterology and Nutrition, Rush University Medical Center, Chicago, IL.

Purpose: Enteric duplication cysts are rare congenital malformations that can occur anywhere from the mouth to the anus. Cystic duplications are endothelium lined and share a common muscular wall and blood supply with the adjacent gastrointestinal tract. We present the unique case of a foregut derived duplication cyst presenting as abdominal pain and elevated inflammatory markers in an adult patient.

Methods: A 26 year-old Caucasian female presented to our gastroenterology clinic with 3 weeks of constant, non-radiating, epigastric abdominal pain. She denied weight change, nausea, emesis or dysphagia and had no past medical or surgical history. Medications only included lansoprazole 30 mg daily started 2 weeks prior by her primary care physician which provided no relief. She had moderate tenderness to palpation in the epigastrium and an otherwise normal physical exam. Laboratory tests were significant for WBC of 11, 300, CRP of 40.2 mg/L, and gastrin level of 156 pg/mL. Upper endoscopy revealed mild antral erythema and biopsies were consistent with non-specific gastritis. An abdominal CT demonstrated a cystic structure anterior to the gastro-esophageal junction and posterior to the left hepatic lobe measuring 1.7 x 1.6 cm (Fig. 1). The patient was then referred for exploratory laparoscopy which showed a smooth mass protruding through the gastrohepatic ligament. The mass was removed and grossly appeared to be a 2.7 x 2.5 x 1.5 cm cyst. The histology was consistent with a foregut derived duplication cyst of either bronchogenic or esophageal origin. Two weeks post-operatively her symptoms had resolved and laboratory values had normalized.

Results: This case is a unique presentation of a foregut derived duplication cyst presenting as epigastric abdominal pain and elevated inflammatory markers, suggesting that duplication cysts be included in the differential diagnosis of abdominal pain.

Conclusion: As the potential complications of enteric duplications include gastrointestinal bleeding and rarely malignant transformation, the recognition of duplication cysts must lead to prompt surgical evaluation.


Purna Kashyap, MBBS*, Lawrence Szarka, MD, Robert Cima, MD, Gianrico Farrugia, MD. Surgery, Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.

Purpose: Mitochondrial mutations affect several organ systems including the gastrointestinal tract. These mutations usually manifest before the 4th decade of life. The most common mitochondrial disorder affecting the gut is MNGIE (Mitochondrial Neuro GastroIntestinal Encephalomyopathy) associated with a thymidine phosphorylase gene mutation. Other mitochondrial diseases associated with GI disease include MIDD (maternally inherited diabetes and deafness) and MELAS (myoencephalopathy, lactic acidosis, stroke like episodes). In these diseases the commonest mutation is with a substitution of A with G at position 3243 in the mitochondrial DNA. We describe two older patients presenting with dysmotility that was associated with the mitochondrial mutation A3243G. Case 1: A 64 year old Caucasian male with history of deafness, diabetes and cardiac dysrhythmia presented with 3 month history of abdominal distention. Imaging studies revealed markedly distended colon with no evidence of mechanical obstruction. He was on TPN for nutritional support. Tests for secondary causes of intestinal dysmotility including connective tissue disorders, amyloidosis, spinal lesions and paraneoplastic dysmotility were negative. Colonic motility testing revealed megacolon with an absent contractile responses to a meal and to intravenous neostigmine. He underwent subtotal colectomy with primary anastomosis and is doing well at 9 months, off TPN and maintaining his weight with oral intake. Full thickness biopsies did not reveal any histological abnormalities Case 2: A 48 year old female with history of diabetes for 20 years, myoclonic epilepsy, lactic acidosis and chronic abdominal pain presented with gastroparesis and constipation. She had a history of a failed pancreatic transplant and brittle diabetes. Her family history was significant for a sister with hearing loss, diabetes, cardiomyopathy and short stature and mother with diabetes and stroke. She was unable to tolerate oral nutrition. She was treated with CoQ10, thiamine and an enterostomy tube was placed for nutritional support. Conclusion: Patients with mitochondrial diseases may have delayed onset of gastrointestinal symptoms. Therefore this needs to be considered and tested for regardless of age in all who present with gastrointestinal dysmotility, diabetes and other features of mitochondrial disease. The phenotypic presentation of mitochondrial disease varies, even with the same mutation. The first patient likely has MIDD while the second patient has MELAS. In carefully selected patients surgical treatment may be appropriate, though one needs to carefully balance the increased surgical risks of malignant hyperthermia and lactic acidemia in patients with MELAS.


Warren Finkelstein, MD*. The Gastroenterology Group of New Jersey, Glen Ridge, NJ.

Purpose: Rifaximin is a minimally-absorbed broad-spectrum antibiotic successfully used in the treatment of traveler's diarrhea. Multiple clinical studies have suggested clinical benefits of rifaximin in Crohn's disease. I previously presented two case reports of the successful induction of clinical remission by rifaximin in two patients with medically refractory Crohn's disease. The following case reports demonstrate the effectiveness of rifaximin as long-term maintenance therapy for these two patients.

Methods: Case Reports

Results: Case Report No. 1: A 39-year-old man with an 11-year history of Crohn's ileocolitis presented 31/2 years ago with severe non-bloody diarrhea. The patient had previously failed to respond to high-dose mesalamine, ciprofloxacin, metronidazole and multiple courses of prednisone. He developed severe pancytopenia on 6-mercaptopurine requiring hospitalization. He failed to respond to infliximab (5 mg/kg i.v.). Colonoscopy showed moderate pancolitis and mild ileitis. Treatment with rifaximin (400 mg bid) resulted in complete resolution of diarrhea within 10 days. Colonoscopic improvement was confirmed 2 months after initial rifaximin therapy and was sustained on a recent colonoscopy 31/2 years later which showed only mild colitis. The patient has remained fully asymptomatic on rifaximin (800 mg/day) for the past 31/2 years. No adverse effects of therapy occurred. Case Report No. 2: A 44-year-old woman with a 22-year history of Crohn's colitis presented with a 2 month history of bloody diarrhea and lower abdominal pain. The patient had previously failed to respond to high-dose mesalamine, ciprofloxacin, metronidazole and was steroid-dependent after many courses of prednisone. She could not tolerate 6-mercaptopurine or azathioprine. She failed to respond to methotrexate. She developed optic neuritis while on infliximab. Colonoscopy showed patchy colitis of the left colon with many ulcerations. Treatment with rifaximin (400 mg bid) resulted in complete resolution of diarrhea within 3 weeks. A colonoscopy 3-months later showed no active colitis. The patient has remained fully asymptomatic on rifaximin (800 mg/day) for the past 3 years. No adverse effects of therapy occurred.

Conclusion: Rifaximin effectively and safely induced and maintained long-term clinical remission for 3-31/2 years in two patients with refractory Crohn's disease. Double-blind randomized placebo-control trials are needed to determine the role of rifaximin as maintenance therapy for Crohn's disease.


Ami Behara, MD, MS*, Joseph Ahn, MD, Nikunj Shah, MD, Shriram Jakate, MD, Allison Howard, MD, Stanley Cohen, MD. Pathology, Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Parvovirus B19 is a single-stranded DNA virus that affects mainly children. Hepatic manifestations of parvovirus B19 infection range from liver chemistry abnormalities to fulminant hepatic failure. We report a unique case of Parvovirus B19 associated hepatitis and aplastic anemia in an immunocompetent, adult patient.

Methods: A 41-year old man with a history of hypertension presented with two weeks of fevers, headaches, and lethargy. He reported spelunking in bat caves while visiting Mexico three weeks prior to admission. There was no history of hepatotoxin exposure, previous liver disease, or alcohol abuse. Physical exam showed fever and splenomegaly but no stigmata of chronic liver disease. Initial laboratory evaluation revealed AST 4124 U/L, ALT 937 U/L, AP 190 U/L, total bilirubin 3.4 mg/dL, WBC 1,260/[mu]L, Hgb 8.7 g/dL, INR 1.5 and platelet count 27,000. The patient was admitted to the intensive care unit and empirically treated with imipenem, doxyxycline, and amphotericin. Ultrasound revealed increased echogenicity of the liver and splenomegaly. Serologies for viral hepatitis, HIV, CMV, EBV, lyme disease, urine histoplasma antigen, and blood cultures were negative. Liver biopsy revealed macrovesicular steatosis with grade 2-3 steatohepatitis, stage 2 fibrosis, and lipogranulomas (Fig. 1). Bone marrow analysis was positive for parvovirus B19 by PCR DNA and showed a hypercellular marrow with trilineage hyperplasia. The patient was treated with granulocyte macrophage colony stimulating factor and intravenous immune globulin, with resolution of his fever, liver function test and blood count abnormalities.

Results: Parvovirus B19 can cause hepatitis associated aplastic anemia and may be an underappreciated hepatotoxic virus.

Conclusion: Aplasia can be fatal in up to 88% of cases with no correlation between the severity of hepatitis and the interval to aplasia. However, as with our patient, medical management of aplasia can lead to good results. This case underlines the importance of considering parvovirus B19 infection in the differential diagnosis of hepatitis associated aplastic anemia in adults.


Arvind Movva, MD*, Shannon Marek, MD, Dimple Raina, MD, Subbaramiah Sridhar, MB, BS, FACG. Section of Gastroenterology and Hepatology, Medical College of Georgia, Augusta, GA.

Purpose: Sixty-seven cases of splenic hematoma after colonoscopy have been reported in the literature. This complication is rare, however it is associated with significantly increased morbidity and mortality. We report a case of a large splenic hematoma following colonoscopy, highlighting a delay in the diagnosis of this complication.

Methods: A 46-yr-old woman with a family history of colon cancer underwent an elective outpatient screening colonoscopy. She did not use anti-platelet or anti-coagulant agents prior to the procedure. The procedure was uneventful with intubation of the cecum. The patient tolerated the procedure well. Numerous colonic diverticula and a single 5 mm polyp in the rectosigmoid region were noted. Polypectomy was performed using cold biopsy forceps.

Results: She presented to her family practitioner 8 days following the procedure with a sharp left upper quadrant pain radiating to the sternum and left shoulder tip. The pain was worse with deep inspiration and unchanged with movement of the left shoulder joint. The physical examination was unremarkable except for mild diffuse abdominal tenderness. A 12 lead electrocardiogram was normal. She was treated with omeprazole 20 mg po daily for presumed gastroesophageal reflux disease. Musculoskeletal pain due to faulty sleep position was thought to be the cause of her shoulder pain and she was therefore instructed not to lie on the affected shoulder. Six weeks later, she presented to the Emergency Department with similar complaints, which had been continuous with no improvement after the empirical therapy. A chest x-ray showed blunting of the left costophrenic angle. The blood tests revealed normal complete blood count, metabolic profile, liver enzymes, serum amylase and serum lipase levels. She was treated with levofloxacin for presumed pneumonia. A subsequent contrast enhanced chest and abdominal CT found a large (9 x 6.3 x 11 cm) subcapsular splenic fluid collection, which was confirmed by an ultrasound exam. A total of 360 ml of old blood and fluid were drained percutaneously with ultrasound guidance. The patient made an uneventful recovery with resolution of her symptoms. A 4-week follow-up ultrasound showed complete resolution of the splenic hematoma.

Conclusion: To our knowledge, the delay to diagnosis from the colonoscopy is the longest reported in a patient with continuous symptoms. This case highlights the need for a high index of suspicion for splenic injury after colonoscopy in order to avoid a delayed or missed diagnosis. With the higher number of colonoscopies performed each year in the United States, it is likely that this complication is significantly under recognized and reported.


Bradley Shepherd, MD*, Christen Klochen, MD, Elizabeth Harris, MD, Roman Perri, MD. Division of Gastroenterology, Vanderbilt University, Nashville, TN.

Purpose: Fibrosing cholestatic hepatitis is a rare, aggressive, and usually fatal form of viral hepatitis found in immunosuppressed patients. It has been reported in solid organ and bone marrow transplant recipients. We report a case of acute hepatitis C related FCH in a post-lung transplant patient.

Methods: A 72 year old man who underwent a right lung transplantation nine months prior, came to the emergency department with jaundice. He reported 3-4 weeks of fatigue and one week of jaundice and tea-colored urine. He noted pruritis and easy bruising. Past medical history included COPD status post a single-right lung transplantation. His post-transplant course was complicated by CMV treated with valgancyclovir, and one episode of acute cellular rejection treated with solumedrol. His medications included tacrolimus, mycophenolate sodium, prednisone, bactrim, pravastatin, and valganciclovir.

Results: His examination revealed a thin, frail man with normal vital signs, scleral icterus, jaundice, and multiple ecchymoses. He had no asterixis or spider angiomata. His jugular venous pulse was not elevated. His mental status was normal. Admission labs showed a bilirubin of 16.1 mg/dL, alkaline phosphatase 442 U/L, AST 175 U/L, and ALT 115 U/L. Serologies including HAV, HBV, HCV, and EBV were normal. CMV PCR showed undetectable virus. Contrasted CT showed ascites without vascular obstruction and no biliary ductal dilation. Liver biopsy showed a mild mixed portal infiltration consisting of lymphocytes, neutrophils, and rare plasma cells. Bile ducts showed mild distortion. There was focal interface hepatitis and mild bile ductular proliferation. Mild lobulitis was present with scattered hepatocyte apoptosis. Multiple foci of bile plugs, intracanalicular and hepatocyte cholestasis, perivenular fibrosis and hepatic venular dilation were noted. These findings were consistent with acute hepatitis C with a suggestion of fibrosing cholestatic hepatitis. All hepatotoxic medications were stopped and immunosuppression was minimized. His condition continued to deteriorate. He developed hepatic encephalopathy and progressive jaundice despite the administration of lactulose and aggressive supportive care. On day 13 of his hospitalization Hepatitis C quantitative PCR revealed over 5,000,000 copies/mL. His clinical status continued to worsen and he died after being transitioned to hospice care.

Conclusion: Acute hepatitis C and fibrosing cholestatic hepatitis is a rapidly progressive form of hepatic dysfunction. There is no effective treatment of FCH in immunosuppressed patients. Reduction of immunosuppressive medications is the only feasible option. This case represents a rare presentation of acute Hepatitis C and FCH in a post-lung transplant patient.


Yasser Shaib, MD, MPH*, Jason Hou, MD. Gastroenterology, Baylor College Of Medicine, Houston, TX.

Purpose: Purpose: To present a case of low-pressure cryoablation for the treatment of radiation proctitis.

Methods: Methods: A 74 year old man who one year earlier was treated with radiotherapy for prostate cancer presneted with rectal bleeding. Colonoscopy showed erythema and inflammation in the distal 3 cm of rectum consistent with radiation proctitis. Bleeding persisted despite local therapy with steroid suppositories and hemoglobin progressively dropped from 14 g/dL to 9.4 g/dL. Low pressure cryoablation (CSA Medical) was performed using a cryoablation catheter passed through an endoscopic channel. The catheter was directed under direct visualization to three areas of the rectum most involved with proctitis. Liquid nitrogen spray was injected through the catheter in 10 second applications. A total of 4 applications were used for each area of proctitis. During cryoablation, a cryo decompression tube was placed in the rectum to prevent over insufflation.

Results: The patient denied any adverse effects after cryoablation. He reported a decrease in amount and frequency of rectal bleeding. Follow up sigmoidoscopy 6 weeks after cryoablation showed decreased erythema and inflammation with exudative material on treatment areas. Sigmoidoscopy at fifteen weeks follow up showed near normal mucosa throughout the rectum. His hemoglobin increased from 9.4 g/dL to 11.7 g/dL over the same time period.

Conclusion: We present the first case of mucosal healing and symptomatic resolution of radiation proctitis using low-pressure cryoablation in a patient who previously did not respond to medical therapy


Thomas Dunzendorfer, MD*, Sarah Wilkins, MD, Rebecca Johnson, MD, Srikanth Mansani, MD. Pathology, Gastroenterology, Berkshire Medical Center, Pittsfield, MA.

Purpose: To draw attention to mucosal tears as an unusual but important endoscopic presentation of collagenous colitis.

Methods: Case report of patient with collagenous colitis and mucosal tear on colonoscopy.

Results: A 60-year-old woman with a history of constipation presents with a complaint of rectal pain, watery, non-bloody diarrhea, and a 6-pound weight loss over one year. Physical exam, stool and blood tests were unremarkable. She did not use NSAID's, enemas or other rectal manipulations. Colonoscopy showed a 3-cm linear, raised mucosal sigmoid tear (Fig. A). The remaining colon and terminal ileum were normal. Random colon biopsies showed diffuse, irregular thickening of the subepithelial collagen table accompanied by focal denudation of the surface epithelium and increased intraepithelial lymphocytes, diagnostic of collagenous colitis (Fig. B, right). Biopsies of the mucosal tear showed granulation tissue with acute inflammation consistent with a nonspecific ulcer (Fig. B, left). The patient was treated with Pepto-Bismol, budesonide, mesalamine enemas, metronidazole, and ciprofloxacin. After three days, the diarrhea and rectal pain resolved and after three weeks, all medications, except budesonide, were stopped. At two years, the patient remained asymptomatic with normal colonoscopy and biopsies.

Conclusion: Mucosal tears have been reported previously in 12 patients with collagenous colitis. The cause is unclear but may be related to underlying inflammation with mucosal friability. In microscopic colitis, the mucosa is endoscopically normal, but histology shows characteristic abnormalities. We propose that mucosal tears may be a characteristic and significant endoscopic abnormality in collagenous colitis. Standard treatment for collagenous colitis appears adequate for management of mucosal tears.

Endoscopy showing linear raised mucosal tear in sigmoid

Left panel: H&E 20x, histology of tear, granulation tissue with acute inflammation Right panel: H&E 20x, random colon biopsy showing thickened subepithelial collagen layer (arrow).


Stacy Tong, MD*, Cynthia Lau, MD, Joseph Ahn, MD, Hector Ferral, MD, Nikunj Shah, MD, Stanley Cohen, MD. Interventional Radiology, Gastroenterology and Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Transjugular intrahepatic portosystemic shunt (TIPS) is an accepted treatment for complications of cirrhosis. Common complications of TIPS include stenosis of the stent and hepatic encephalopathy. An infrequent complication is stent migration into the portal vein or right atrium, reported in 2-9% of cases in the literature. We report a rare case of stent migration into the pulmonary artery after TIPS.

Methods: A 50 year-old man with Child-Pugh class C, MELD score of 19, alcoholic cirrhosis presented to an outside hospital with ascites and esophageal variceal bleeding refractory to band ligation. He underwent a successful TIPS placement with a nitinol (Zilver) stent. Six weeks later, the patient presented with recurrent ascites. Evaluation of the TIPS revealed a portosystemic gradient of 22 mmHg and narrowing in the hepatic venous end of the stent. Angioplasty of the stent was performed followed by placement of a second nitinol (Zilver) stent, resulting in a lowering of the gradient to 12 mmHg. One week later, the patient was transferred to our center for liver transplant evaluation.

Results: A routine chest x-ray demonstrated the stent projecting over the pulmonary hilum. Pulmonary angiogram confirmed the stent to be in the pulmonary artery. Based on the orientation of the stent in the pulmonary artery, removal was not attempted due to the high risk of pulmonary artery perforation. Subsequent chest x-rays showed stable stent position. The patient continued to remain asymptomatic.

Conclusion: An infrequent complication of TIPS is stent migration. Our case of pulmonary artery involvement has been rarely described. Technical aspects of stent placement, such as inappropriate size or type, or inadequate overlap, may contribute to the likelihood of stent migration.


Fedele DePalma, MD*, Jeffrey Gellis, DO, James Kovacs, DO, Joshua DeSipio, MD. Department of Radiology, Department of Gastroenterology, Department of Internal Medicine, Cooper University Hospital, Camden, NJ.

Purpose: Intrahepatic portosystemic venous shunts are rare and not well recognized. We report the case of a patient with a spontaneous intrahepatic portosystemic venous shunt.

Methods: A 48 year old Hispanic woman was referred for a 1.6 cm enhancing lesion of unclear etiology in the right lobe of the liver identified on a CT scan that was performed by her primary care physician for evaluation of her abdominal pain. At her initial office visit she reported mild abdominal discomfort. Physical exam was revealed tenderness in her right upper quadrant. Laboratory evaluation was unremarkable, including normal LFTs, a normal Alpha-fetoprotein, and negative viral hepatitis serologies. MRI of the liver was performed and demonstrated a vascular malformation in the right lobe of the liver being fed by a branch of the portal vein and drained by a tributary of the hepatic vein. This lesion is compatible with a rare spontaneous intrahepatic portosystemic venous shunt.

Results: Spontaneous intrahepatic portosystemic venous shunts are rare, described mostly in small series or case reports. More commonly these shunts are acquired in the setting of trauma or developed in chronic liver disease, and are generally due to an abnormal communication between the portal circulation and an extrahepatic systemic vein. The clinical significance and treatment of these shunts remains controversial. Instances of intrahepatic portosystemic venous shunts causing encephalopathy and larger fistulas adversely effecting systemic hemodynamics as well as causing liver fibrosis from longstanding diversion of portal flow have been reported. Treatment options include conservative management, surgery, or transcatheter embolization in symptomatic patients. IPSVS found in asymptomatic patients without liver disease are not thought to require treatment.

Conclusion: We report a case of an asymptomatic spontaneous intrahepatic portosystemic venous shunt. The long term sequelae of this anatomic abnormality are not well described.


Thanigaiarsu Thiyagarajan, MD*, Uma Sundaram, MD, Vijay Mahajan, MD. Internal Medicinie, St. Vincent Mercy Medical Center, Toledo, OH, Gastroenterology, West Virginia University, Morgantown, WV.

Purpose: 54-year-old Caucasian man had nausea, vomiting and right upper quadrant pain for 2 weeks. His significant past history includes hepatitis B and C, umbilical herniorhhapy and bilateral knee arthroscopies. He takes insulin, lisinopril, metaprolol, neurontin and prilosec. He is an ex-smoker, denies alcohol intake and used marijuana remotely in the past.

Methods: On examination pertinent positive findings include morbid obesity, body full of tattoos, BP 154/86, bilateral pedal oedema, distended abdomen with Murphy's sign positive. His significant labs include total bilirubin 6.4, direct bilirubin 4.9, alkaline phosphatase 196, ALT 70, AST 98, albumin 2.8, Hb 10 and chest x-ray showed multiple bilateral diffuse non-calcified pulmonary nodules. Gall bladder echo revealed multiple gallstones. HIDA scan findings were consistent with chronic cholecystitis. CAT scan of chest confirmed bilateral diffuse pulmonary nodules and of abdomen revealed multiple enlarged retro crural, perihepatic, pericaval and cardiophrenic lymphnodes with significant ascites. Ascitic fluid analysis revealed portal hypertension related ascites caused by porta hepatis lymphadenopathy rather than grade 2 liver fibrosis on metavir scores, and negative for infection and malignancy. The day following paracentesis, he was aggressive and confused. His labs were Hb 9, ammonia 320, BUN 33, creatinine 1.6 (baseline 0.5) and INR 1.7. EGD showed non-bleeding distal grade 1 oesophageal varices. Hepatic encephalopathy and hepatorenal syndrome was diagnosed and treated accordingly with good improvement. Hepatitis serology revealed positive HCV IgG antibody, genotype 1b, HCV RNA level of 4 million IU/mL and immune to hepatitis B. CAT scan guided perihepatic lympnode biopsy revealed B cell lymphoma.

Results: Diagnosing his hepatitis C associated B cell lymphoma was really a challenge as such lymphoma presenting as bilateral diffuse pulmonary nodules and multiple enlarged retro crural, perihepatic, pericaval and cardiophrenic lymphnodes is a rare entity. He was started on antiviral therapy (pegylated interferon and ribavarin) while waiting for liver transplantation.

Conclusion: This case report illustrates the challenge of diagnosing a lymphoproliferative disorder in a patient with unexplained anaemia and lymphadenopathy. According to AASLD guidelines, antiviral therapy for hepatitis C with decompensated cirrhosis can be individualized based on other co-morbidities. The role of combination therapy for HCV associated B cell lymphoma has not been well studied to know the success rates, as only limited data are available regarding the effects of antiviral therapy on rearranged B cell clones. This is one of the research areas that need to be explored in future.


John Petersen, DO, FACG, FACP*. Borland-Groover clinic, Jacksonville, FL.

Purpose: Clinical Vignette: Sarcoidosis is a multisystem granulomatous disease of unknown etiology that presents most often in young adults with hilar adenopathy, pulmonary infiltrates, skin or eye lesions. Hepatobiliary involvement is asymptomatic in most, with non-caseating granulomas seen often. Cholestatic hepatitis with liver chemistry resembling PBC or PSC has been described. Intra-hepatic cholestasis, hepatosplenomegaly, pre-sinusoidal portal hypertension, portal fibrosis, and cirrhosis may be seen. Abnormalities of the large bile ducts and extra-hepatic tree is rarely seen, and we describe a Klatskin-like biliary confluence granulomatous obstruction that responded to balloon dilation, stenting, and corticosteroid therapy. Case: A 38 yr. old caucasian female presented with painless jaundice. She complained of pruritus, weakness, fatigue, dark urine and malaise. Initial labs: Bilirubin 11, AST-107, ALT-92, GGT-431 (Nl 15-85), Alk. Phos-635, CEA-1.2, Nl p-ANCA, Nl Ig's, ACE-28 (Nl 8-21); ANA, AMA, copper, Ferritin were WNL. U.S. revealed intra-hepatic duct dilations; CT and MRCP with confluence region mass effect with marked proximal ductal dilation. A 3 cm portacaval node was noted; ERCP with Spyglass cholangioscopy displayed a tight confluence stricture, with extension into the right hepatic system; After balloon dilation of both right and left ducts, cholangioscopy revealed a nodular duct wall and brushings and directed biopsy bites were collected. Histology from the confluence revealed non-caseating granulomas with chronic cholangitis; No malignancy was detected. A 10 F stent was placed into the dominant right system and the bilirubin fell from 17 to 11 mg/dl overnite. The pateint was treated with Urso and 40 mg of Prednisone. Follow-up 2 weeks later: Bili.-1.5, GGT-135, ALT-48. Conclusions: Sarcoidosis is a chronic granulomatous disease that may present in young adults as a hepatocellular or cholestatic process. Extra-hepatic biliary obstruction may result from peri-ductal adenopathy or from ductal infiltration. Cholangioscopy may prove beneficial in directing biopsies and/or brushings to rule out carcinoma. Biliary sarcoidosis appears to be exquisitely sensitive to biliary stent decompression and corticosteroids.


Fedele DePalma, MD*, Nirmala Sivaprakasapillai, MD, Jae Hong, MD, Adam Elfant, MD. Department of Gastroenterology, Department of Internal Medicine, Cooper University Hospital, Camden, NJ.

Purpose: Diaphragmatic hernia is a rare cause of biliary obstruction. We report a patient who presented with obstructive jaundice and was diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) to have compression of the common bile duct (CBD) by the rim of a diaphragmatic defect.

Methods: A 64 year old female with history of breast cancer presented with jaundice, acholic stools, and weight loss. She denied any trauma, alcohol or drug use, tattoos, or blood transfusions. In addition to jaundice, exam demonstrated right upper quadrant and epigastric tenderness, and hepatomegaly. Laboratory data showed AST of 218 U/L, ALT of 167 U/L, alkaline phosphatase of 433 U/L, total bilirubin of 9.8 mg/dl. CT scan of abdomen and pelvis revealed a large right-sided diaphragmatic hernia with a portion of stomach, duodenum, pancreatic head, multiple loops of small bowel and the transverse colon in the thoracic cavity. There was hepatomegaly, dilated intrahepatic and pancreatic ducts. An ERCP was performed. Papilla was identified to be in a tangential position. Selective cannulation revealed normal CBD with a smooth concentric narrowing at the level of the crura with proximal dilatation and a biliary stent was placed. She subsequently underwent exploratory laparotomy with repair of the hernia defect and resection of the hernia sac. Several weeks later another ERCP was performed for stent removal. Papilla was identified in the usual position and CBD injection revealed resolution of the obstruction.

Results: Review of the literature revealed reports of patients with diaphragmatic hernias presenting with obstructive jaundice due to compression of the biliary system by the rim of a diaphragmatic defect. The etiology of the obstruction in those cases were diagnosed with CT scan, percutaneous transhepatic cholangiogram, or intraoperatively. To our knowledge, this is the first report where diagnosis was made utilizing ERCP.

Conclusion: ERCP can be utilized to facilitate diagnosis as well as provide temporary relief of obstructive jaundice secondary to diaphragmatic hernia.


Andrew Cummins, MD, MS*, Linda Nguyen, MD. Gastroenterology, California Pacific Med. Center, San Francisco, CA.

Purpose: A 79 year old Fijian female, was admitted to an outside hospital for progressively worsening shortness of breath over the preceding 6 months, for which she had been treated intermittently with oral steroids without relief. She had an extensive work up including CT of the chest which was negative for pulmonary embolism but revealed cystic bronchiectasis. Subsequent brochoscopy showed only nonspecific inflammatory cells. She was thus treated with high dose IV steroids for cystic bronchiectasis and COPD exacerbation, with no history of tobacco use. Approximately 1 month into her hospitalization, she developed dysphagia, nausea, vomiting, diarrhea and weight loss. She had an upper endoscopy that showed an esophageal ulcer, and biopsies showed HSV and H. Pylori. She was treated for both with acyclovir and triple therapy respectively. However, despite treatment she still had complaints of dysphagia and weight loss. A gastric emptying study showed delayed gastric emptying. She was treated with NG decompression, Metaclopramide and Erythromycin without improvement. She eventually became TPN dependent. After 1 month without improvement in her GI symptoms, she was transferred to our institution for further management and evaluation for a gastric neuro-stimulator. At our institution, she had confirmed gastroparesis with a 4 hour gastric retention of 75%. EGD showed Candida esophagitis, antral punctuate hemorrhagic lesions and duodenal edema, congestion and erythema. Limited biopsies of the duodenum were done since the patient was on Plavix. Esophageal manometry showed diffuse esophageal spasm. The antroduodenal manometry showed a neuropathic pseudo-obstruction. However, biopsy results showed larva in the duodenal glands consistent with Stonglyloides Stercoralis infection. This diagnosis helped explained both her pulmonary and gastrointestinal symptoms, likely exacerbated by her chronic steroid use. She was slowly tapered off her steroids and treated with Ivermectin and Mebendazole. Within 1 week of therapy, her symptoms improved and she was able to start eating again without nausea and vomiting.

Methods: N/A

Results: S. Stercoralis can present with vague gastrointestinal symptoms such as nausea, vomiting, diffuse abdominal pain and malabsorption. In hyper infection syndrome there may be complete disruption of the mucosal wall, ulcerations, and paralytic ileus. The definitive diagnosis is often difficult to make but is usually made on the basis of detection of larvae in the stool. Treatment is often difficult as well, as S. Stercoralis requires complete eradication to remove the potential danger of hyper infection and death. Ivermectin is the best studied and currently recommended for treatment.

Conclusion: N/A


Nathan Landesman, DO*, Justin Miller, DO, Brent Himes, DO. Pathology, Gastroenterology, Genesys Regional Medical Center, Grand Blanc, MI.

Purpose: 24 y.o. female referred for 10-month history of emesis and abdominal pain underwent EGD revealing a white-yellow submucosal growth at 32 cm from the incisors measuring 1 cm in length and 0.5 cm in width. Pathology report read: "One fragment consists of pink-staining granular cells with small, rounded nuclei consistent with granular cell tumor (GCT). Cells are strongly positive for S-100 and vimentin. Features of malignancy are absent".

Methods: Abrikossoff first described "granular cell myoblastoma" in 1926. It was considered a myogenic tumor until Fisher and Wechsler's 1962 challenge. Using electron microscopy and Wallerian degeneration studies, they noted similarities between a myoblastoma cell and a degenerating Schwann cell. Today, most pathologists and oncologists acknowledge the neural origin of GCTs supported by positive IHC staining for CD68, Ki-67 (slightly), NKI/C3, NSE, nestin, p53 (slightly), S-100 protein, and vimentin. In addition, positive PAS stain with resistance to diastase digestion and nonreactivity to HHF35, desmin, and alpha-smooth muscle actin are characteristic.

Results: GCTs comprise only 0.03% of all tumors, and GI GCTs are even more rare with the distal 1/3 of esophagus cited most frequently. Mean age of diagnosis is 45 years with equal M:F ratio. Dysphagia is the most common symptom correlating to >1 cm size. Classic appearance is a small, non-tender, broad-based, submucosal growth resembling a "molar tooth" when central depression exists. A rubbery or firm consistency is characteristic with pink-tan, gray-white, or white-yellow coloration. EUS reveals a homogenous, hypo/isoechoic submucosal lesion. Approximately 200 cases have been documented.

Conclusion: GCTs are notoriously benign, but no management guidelines exist. Presently, an esophageal GCT > 2 cm size, symptomatology, interval growth, recurrence, tissue invasion, or advanced histologic/sonographic features prompt resection. Preoperative EGD re-evaluation with confirmatory biopsy followed by EUS to address muscularis and lymphatic invasion are recommended. EMR, Nd:YAG laser ablation, and APC are safe, effective alternatives to surgery in the absence of muscularis or lymphatic involvement. Esophageal GCTs are not radiosensitive, but recurrence is uncommon.


Bassel Ericsoussi, MD*, Robert Andina, MD, Melvin Wichter, MD, Charles Berkelhammer, MD, FACG. Internal Medicine, University of Illinois, Oak Lawn, IL.

Purpose: Introduction: Ischemic colitis, acalculous cholecystitis and transverse myelitis are known hypercoagulable and autoimmune manifestations of antiphospholipid syndrome (APS) and Sjogren's vasculitis (SV). We describe a patient who developed ischemic colitis, acalculous cholecystitis and catastrophic longitudinal transverse myelopathy (CLTM) secondary to APS and SV. Case: 52 year old previously well female presented with severe right upper quadrant (RUQ) pain associated with constipation. Physical examination was only notable for RUQ tenderness. Her ALT was 74 U/L (normal 10-40). Her AST, bilirubin and alkaline phosphatase were normal. Ultrasound of gallbladder was normal. Hepatobiliary scan showed ejection fraction of 4% (normal < 35%) consistent with gallbladder dyskinesia. Colonoscopy showed circular ulcerations in the left colon, raising the possibility of ischemic colitis from vasculitis. Colonic biopsies were consistent with ischemic colitis. Post-operatively she developed rapidly progressive paraplegia. MRI was consistent with CLTM. She also developed deep venous thrombosis. Cardiolipin antibodies were elevated: IgG 34 gpl (normal < 20), beta-2-glycoprotein IgM was 95 gpl (normal < 20) and IgG 57 gpl (normal < 20). These antibodies remained positive three months later. Lupus anticoagulant was negative. The Anti-Ro (SS-A) was elevated at 129 U/ml (normal < 25). She responded well to a course of steroids, azathioprine and anticoagulation. Discussion: Ischemic colitis, acalculous cholecystitis and transverse myelitis have been rarely associated with APS as well as SV. In previous reports these manifestations have occured separately in association with APS and SV, rather than as a cluster complex. We feel our patient likely had both APS and SV. She did satisfy the International Consensus criteria for probable catastrophic APS (CAPS) as well. Physicians should consider APS and SV as well as CAPS in patients with ischemic colitis, acalculous cholecystitis and transverse myelitis.


Iryna Hepburn, MD*, Subbaramia Sridhar, MBBS, Robert Schade, MD. Medicine, Medical College of Georgia, Augusta, GA.

Purpose: Eosinophilic ascites (EA) is a rare disorder of unknown etiology that is a part of the syndrome of eosinophilic gastroenteritis. Characterized by peripheral and tissue eosinophilia it can affect any area of the digestive system and all layers of the gut wall.

Methods: We report a case of EA that developed 10 weeks postpartum.

Results: The patient a 20 year old female had no past medical history. She experienced rapid onset of nausea, nonbloody vomiting and diarrhea for several weeks accompanied by abdominal pain and swelling. She noted weight gain of 20 Lbs and leg edema. Her pregnancy had been uneventful. There was no history of transfusions, recent travel, respiratory symptoms, rash, allergies, or ill contact. There was no history of illicit drug or alcohol use, she was taking no medications, and there was no history of thyroid or liver disease. Physical examination: Skin and mucosa clear, no jaundice. Cardiovascular exam and thyroid were normal. Abdomen was distended and tender to palpation diffusely with shifting dullness present. Bilateral leg edema was seen. Laboratory data: Hgb 11 g/dL, Hct34, PLT 278, WBC 12.8 k/ml, differential segmentonuclear 50%, lymphocytes 9%, monocytes 1%, eosinophils 38%. Serum electrolytes, coagulation studies, thyroid and liver tests were normal. HIV ELISA was negative. Parasitic infestation was excluded by stool and serological studies. US of the liver was normal with all vessels patent. Diagnostic paracentesis revealed hazy dark fluid with no cytological signs of malignancy, protein level 4.5 g/dL, albumin 2.4 g/dL, RBC 12 K/ml, WBC 1780/ml with significant eosinophilia 82%. Tuberculosis was ruled out by negative cultures. Bone marrow biopsy showed normal hemopoesis with 20-25% eosinophils and normal cytogenetics. EGD demonstrated mild mucosal erythema. Mucosal biopsies from the esophagous, stomach and duodenum contained no eosinophils. The patient was treated with prednisone with rapid resolution of her symptoms.

Conclusion: EA is classified according to the predominance of eosinophilic infiltration in the different layers of the intestinal wall. Clinical manifestations depend on the affected layers and range from barely perceptible symptoms to intestinal obstruction or ascites. The mucosal infiltration results in vomiting and diarrhea sometimes with hematochezia. Muscularis involvement results in gut wall thickening and may lead to obstruction. The serosal form is the most unusual and leads to eosinophilic ascites. Steroid therapy is effective, sometimes long term low dose maintenance steroid therapy is required to prevent reoccurrence of the EA. It is an important consideration in the differential evaluation of ascites.


Purna Kashyap, MBBS*, Fabiola Medeiros, MD, Michael Levy, MD, David Nagorney, MD, Mark Larson, MD. Surgery, Pathology, Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.

Purpose: Gastrointestinal endometriosis is uncommon, but when present usually involves the rectosigmoid and manifests as lower gastrointestinal bleeding, pelvic pain or constipation. Endometriosis involving the upper GI tract is very rare, but as this case illustrates, its presentation can be dramatic. Patient was a 35 year old G4P3 admitted at 19 weeks gestation with constant epigastric pain associated with nausea, vomiting and an episode of melena. She denied use of NSAIDs, smoking or alcohol use. Her past history was unremarkable. On examination her abdomen was benign and the stool was dark and positive for blood. Hemoglobin on admission was 7.9. EGD showed a 3 cm luminal based mass with 1 cm surface ulceration but no evidence of a visible vessel. A subsequent linear endoscopic ultrasound exam revealed a 7 x 7 cm, inhomogeneous mass with irregular outer borders located in the proximal gastric body and extending to the spleen, left hemidiaphragm and the pancreatic tail. Fine needle aspiration cytology was interpreted as suspicious for malignancy and she underwent an en bloc partial gastrectomy and splenectomy. Pathology showed endometriosis with extensive decidualization forming a mass infiltrating the gastric wall and spleen. She did well after surgery and delivered a healthy baby at term Conclusion: Endometriosis is rare outside the lower GI tract, but can present as a symptomatic, bleeding, gastric mass. Pregnancy appears to lead to rapid growth of extra-uterine endometriotic tissue. While EUS is helpful in evaluating subepithelial masses that may arise from many etiologies, FNA sampling may be unrevealing, and ultimately surgical resection is required.


Sarah Manitsas, MD*, Christopher South, MD, Purvi Panchal, MD, Martha Yearsley, MD. Department of Pathology, Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Medical Center, Columbus, OH.

Purpose: Inflammatory pseudotumors are a type of solid tumor that may be comprised of spindle cells, myofibroblasts, plasma cells, or histiocytes as a secondary reaction to an underlying inflammatory process. Infection in an immunocompromised host is a common etiology of inflammatory spindle cell pseudotumors. Many infectious agents have been reported to cause inflammatory spindle cell pseudotumors although non-tuberculous Mycobacterial species are the most commonly reported infectious etiology in patients with Human Immunodeficiency Virus infection. To our knowledge this is the first reported case of a Mycobacterial spindle cell pseudotumor of the colon.

Methods: A 30 year man with a diagnosis of AIDS presented for evaluation of progressive fatigue and weakness for 3 weeks. The patient also complained of abdominal pain and diarrhea for 1 week with one episode of melena. He underwent an EGD and colonoscopy. The colonoscopy showed a 4 millimeter polyp in the transverse colon which was resected with jumbo cold forceps. The pathology of the transverse colon polyp was consistent with a Mycobacterial spindle cell pseudotumor.

Results: The lesion described as the transverse colon polyp was examined using a routine hematoxylin-eosin (H & E) stain, AFB stain, GMS histochemical stains, and CMV immunohistochemical stain. The lesion was described as a polypoid spindle cell proliferation and non-caseating epithelioid granuloma with numerous acid fast bacilli consistent with Mycobacteria. These findings were consistent with a Mycobacterial spindle cell pseudotumor. Duodenal biopsies were evaluated with AFB stain, GMS stain, PAS stain, Trichrome stain, and immunostain for CMV. The biopsies showed acute and chronic inflammation and macrophages containing numerous acid fast bacteria consistent with Mycobacteria.

Conclusion: The patient was placed on clarithromycin 500 mg every 12 hours, which was ultimately changed to azithromycin 500 mg daily, and ethambutol 1200 mg daily for Mycobacterium avium complex. He continued darunavir, raltegravir, ritonavir, and emtricitabine-tenofovir for his HIV/AIDs. The patient was seen in a clinic follow up visit two months after the initial presentation to the hospital. He continued his antiretroviral medication and azithromycin and ethambutol. The patient's diarrhea and abdominal pain had resolved. He had a good appetite and was gaining weight. This case is an example of an inflammatory pseudopolyp caused by MAC found in the colon in a patient with AIDS. It highlights the importance of recognizing that inflammatory pseudopolyps may be a result of infection in an immunocompromized patient and the importance of providing the appropriate clinical treatment.


Bryan Sauer, MD, MS*, Vanessa Shami, MD, Michel Kahaleh, MD. Digestive Health, University of Virginia, Charlottesville, VA.

Purpose: To demonstrate the diagnosis and management of necrotizing esophagitis including esophageal stricture

Methods: A 50 year-old woman presented to the emergency room with abdominal pain, nausea, and coffee ground emesis. She was admitted to the hospital with systolic blood pressures greater than 200 mmHg and upper gastrointestinal bleeding. Her past medical history was significant for cocaine abuse, stroke, diabetes mellitus, poorly-controlled hypertension, and gastroesophageal reflux disease. An esophagogastroduodenoscopy (EGD) (Fig. 1-top left) showed a black esophagus and a diagnosis of necrotizing esophagitis was made. The patient was empirically started on broad-spectrum antibiotics and fluconazole, placed on strict NPO status, and started on total parenteral nutrition (TPN). Repeat upper endoscopy two weeks later showed healing necrotizing esophagitis and a severe distal esophageal stricture that was unable to be passed with the endoscope (Fig. 1-top right). Multiple endoscopic therapy sessions including dilation and temporary metal stent placement (Alimaxx Stent) were required (Fig. 1-bottom left). On long-term follow-up (13 months) the patient is asymptomatic and has no evidence of residual esophageal stricture.

Results: Acute necrotizing esophagitis is rare and severe form of acute esophagitis diagnosed endoscopically by the black appearance of the esophagus.(1-3) The incidence ranges from 0.01-0.28% of all upper endoscopies and the overall mortality is approximately 33%. The etiology appears to be multifactorial attributed to ischemic, traumatic, toxic, and infectious causes.(1) The most typical complication is esophageal stricture occurring in approximately 10% of cases.(3) Therapy is supportive including parenteral alimentation, intravenous proton pump inhibitors, and antibiotics if infectious etiologies are suspected.(1,3)

Conclusion: The patient's necrotizing esophagitis likely resulted from severe reflux with ischemia related to cocaine use and hypertension.

(clockwise): a) necrotizing esophagitis, b) healing necrotizing esophagitis with esophageal stricture c) barium swallow d) placement of fully-covered metal stent (Alimaxx, Alveolus Inc).


Jennifer Leigh, MD, MPH*, James Roa, DO, Mitchel Hoffman, MD, MPH. Gastroenterology, Bay Pines VA, St. Petersburg, FL, USF College of Medicine, Tampa, FL.

Purpose: Acute appendicitis following colonoscopy is exceptionally rare with less than a dozen documented in current literature. We describe two cases of this rare complication.

Methods: N/A

Results: Case 1: A 46 year old male underwent a follow-up colonoscopy for a family history of colon cancer and history of polyps with no remarkable findings other than internal hemorrhoids. The prep for the procedure was excellent and the entire colon was visualized without difficulty. The patient returned to the hospital approximately three hours post procedure complaining of nausea, vomiting and 9 out of 10 sharp pain in the upper mid to left abdominal area. On admission patient had a temperature of 100.9 F and a WBC of 17.9. A CT of the abdomen revealed a distended appendix and significant stranding in the surrounding mesentery consistent with appendicitis. The following morning a laparoscopic appendectomy was performed with findings of a necrotic appendix. Case 2: A 53 year old male underwent colonoscopy for the evaluation of chronic constipation and possible narrowing of the colon as seen on barium enema. The colonoscopy was to the terminal ileum and revealed skipped areas of ulceration and granularity in the terminal ileum, right colon and sigmoid colon. Multiple biopsies were taken within these areas. The colonoscopy and biopsies were consistent with Crohn's colitis. Three days later the patient began to experience abdominal pain but did not seek medical attention until eight days post procedure. Upon presenting to the emergency room patient had peritoneal signs with hypotension and leukocytosis. An abdominal x-ray revealed free air below the diaphragm. During emergent laparotomy there was no evidence of colonic perforation and there was a great amount of foul smelling pus in the area of the appendix and the tip of the appendix was perforated.

Conclusion: Diagnosis of appendicitis can be quite challenging following colonoscopy since the early symptoms may mimic other, more frequently encountered complications such as post-polypectomy syndrome and other non specific causes of abdominal pain. While rare, appendicitis is an important complication to keep in mind when treating patients with post colonoscopy abdominal pain.


Corrine Glynn, MD*, William Harford, MD, Ali Siddiqui, MD. Internal Medicine, Dallas Veterans Affairs Medical Center, Dallas, TX.

Purpose: Benign lipomas of the esophagus are extremely rare and account for only 0.4% of the tumors arising from the digestive tract. These tumors arise from the proximal esophagus near the cricopharyngeal muscle. We report a case of an asymptomatic patient with a giant intramural lipoma of the upper thoracic esophagus found incidentally on a CT scan. A 75-year-old asymptomatic white male undergoing a preoperative chest x-ray prior to hand surgery was found to have a mass in the superior mediastinum. Computed tomography (CT) of the chest revealed a polypoid submucosal mass with fat density that arose from the cervical esophagus and extended 12 cm caudally (Fig. 1). Upper gastrointestinal endoscopy showed a submucosal space-occupying mass with normal overlying mucosa. Based upon the above findings, the patient was referred for surgical resection. A vertical esophagotomy was made and the mass was resected along with the pedicle. The pedicle was cauterised. The esophageal incision was then sutured. Pathology of the polyp showed a lipoma comprising of mature adipose tissue collection. The postoperative course was uneventful, and the patient was discharged 3 days after the operation. Giant esophageal lipomas are extremely rare and fewer than 20 surgical cases have been reported in the literature. These are benign slow-growing, pedunculated tumors that usually arise from the upper third of the esophagus. Most cases are asymptomatic and are found incidentally. Symptoms include dysphagia, regurgitation, and epigastric pains. Our case was unique because of the patient was asymptomatic despite the large polyp size. In most cases, the diagnosis is made by endoscopy or barium esophagogram. Diagnosis can also made in a rapid, noninvasive fashion by CT scan which shows low-density tissue absorption related to fatty tissue having (-50 to -150) Hounsfield Units. The size and location often determines the method of resection. Small polyps can safely be removed endoscopically while large masses should be resected surgically because of the risk of bleeding.


Nayan Patel, Second Year resident, MD*, Immanuel Ho, Division of Gastroenterology & Hepatology, MD, FACP, FACG., Kim Olthoff, Liver Transplant Program, MD, FACS. Gastroenterology, Internal Medicine, Crozer Chester Medical Center, Upland, PA, Liver Transplant Center, Hospital of University of Pennsylvania, Philadelphia, PA.

Purpose: Hepatic Adenomatosis was first described in 1985 by Flejou et al as more than 10 adenomas, lack of association with steroid use, oral contraceptives or glycogen storage disease. It affects both sexes, and is associated with abnormal liver enzymes. This is the first case report of an African American female with Hepatic Adenomatosis.

Methods: Our patient is 43 year old African-American female who presented to her primary physician with RUQ abdominal pain since August 2007. The pain was constant, throbbing in nature. It occurred 3/7 days a week, was non-radiating and not associated with nausea, vomiting or changes in bowel habits. An abdominal ultrasound report showed multiple liver masses. She had no significant past medical or surgical history. Her only medications were Advil and MVI, and did not include any recent oral contraceptives. Physical exam was positive for moderate tenderness over the right upper quadrant without palpable masses or bruits. Laboratory data revealed Hgb of 12.7 mg/dL, AST 17 U/L, ALT 18 U/L, Alkaline Phosphatase 66 U/L, Albumin 3.8 g/dL, INR 1.2, and AFP 1.0 ng/mL. A follow-up abdominal MRI on Dec, 07 showed multiple T1 arterial enhanced lesions. The largest mass measured 7.5 x 9.6 x 7.7 cm in the left hepatic lobe. Another lesion on the right hepatic lobe measured 5 x 3.6 x 4 cm. There were also additional smaller lesions in the right lobe of the liver near the hepatic dome and near the porto-venous bifurcation. The patient was referred for hepatic artery embolization and hepatic resection.

Results: N/A

Conclusion:* Hepatic adenomatosis is a rare entity and may present in African-Americans. * Management of Hepatic adenomatosis is a challenge and must be individualized.


Ira Shafran, MD*, P. Burgunder, ARNP. Shafran Gastroenterology Center, Winter Park, FL.

Purpose: The pathophysiology of Crohn's disease (CD) most likely involves abnormal immune responses to enteric bacteria. Clinical data suggest the nonabsorbed antibiotic rifaximin may be effective for treating mild-to-moderate CD. However, information on the efficacy of rifaximin in treatment-naive patients with CD is lacking.

Methods: This case series evaluated the long-term efficacy of rifaximin monotherapy on clinical and endoscopic outcomes in 2 patients with newly diagnosed CD.

Results: Case 1 was a 26-yr-old female who presented with a 4-mo history of chronic abdominal pain, diarrhea, and weight loss. Biopsy during colonoscopy and small bowel capsule endoscopy (SBCE) suggested CD diagnosis. Colonic biopsy showed noncaseating granuloma with erosion and active ileitis; SBCE identified multiple aphthous ulcerations, cobblestoning, and denudation of the mucosa. The patient's baseline Crohn's disease activity index (CDAI) score was 260. Approximately 5 wk after initiating treatment with rifaximin 800 mg/d, the patient had complete relief of gastrointestinal symptoms and SBCE revealed >75% healing of the small bowel mucosa. After 13 mo of continued treatment with rifaximin 800 mg/d, SBCE revealed 90% healing of the small bowel mucosa and the patient's CDAI score of 122 was within normal range. The patient has not required any additional CD therapy during rifaximin treatment. Case 2 was a 42-yr-old male who presented with painful bowel movements and a history of painful, nonhealing anal fissures. Biopsy during colonoscopy, SBCE, computed tomographic enterography, and serologic panel results indicated CD diagnosis. Ileal biopsy showed follicular lymphoid hyperplasia, and SBCE revealed nodular hyperplasia, fissuring, edema, erythema, and aphthous ulcerations. Baseline CDAI score was 175 and serum CRP level was 5.4 mg/L. After receiving rifaximin 800 mg/d for 7 wk, the patient's CDAI score had improved to 91 and SBCE revealed substantial small bowel musocal healing. The total area of active disease decreased, with active disease confined to the distal ileum at the 7-wk follow-up. After 1 yr of continued rifaximin treatment (800 mg/d), SBCE revealed complete healing of small bowel mucosa and the patient had complete resolution of anal fissures; his CDAI score was 14, and his serum CRP level was 0.78 mg/L. The patient has not required any additional CD therapy during rifaximin treatment.

Conclusion: In conclusion, patients with newly diagnosed CD who received rifaximin monotherapy had substantial and sustained improvement of clinical and small bowel endoscopic measures of disease activity. These findings suggest that rifaximin may provide therapeutic benefits when administered as first-line therapy for CD, warranting further investigation.


Jonathan Fenkel, MD*, Maya Spodik, MD, Bheema Singu, MD, David Loren, MD. Division of Gastroenterology and Hepatology, Thomas Jefferson University Hospital, Philadelphia, PA.

Purpose: A 43 year-old male presented complaining of left upper quadrant pain for one week, and fevers for 3 days. He had no localizing symptoms for other sources of fever. His only medical history was a positive PPD 7 years ago treated with 1 year of INH, and infectious colitis 9 months earlier treated with metronidazole. During treatment he developed acute pancreatitis attributed to the metronidazole. At current presentation, he was febrile to 104[degrees]F and diaphoretic, although appeared comfortable. His chest was clear. His pulse was regular at 120 bpm without murmur. There were active bowel sounds and no abdominal distention. There was moderate left-upper quadrant tenderness without peritoneal signs. There was no skin rash. Serum laboratories: sodium 132 mmol/L, hemoglobin 10.2 g/dL; WBC count, platelets, amylase, lipase, liver tests, and creatinine were normal. Abdominal CT scan demonstrated a 3.6 x 3.0 cm, thick-walled, cystic mass without septation at the pancreatic neck, without acute or chronic pancreatitis. This lesion was new compared to imaging during his episode of pancreatitis. Chest x-ray was normal. Blood and urine cultures were negative. The patient was transferred to our facility for further evaluation.

Methods: Endoscopy revealed esophageal candidiasis. EUS identified a 3.2 x 2.8 cm thick-walled cyst with heterogeneous hyperechoic reflectors. Fine needle aspiration was performed with a 19G needle yielding 6 mL of purulent fluid. The cyst was then accessed with a needleknife and cystduodenostomy was established using a 10 mm x 40 mm balloon dilator and two 6 Fr double-pigtail stents. A 5 Fr nasocystic catheter was placed into the cyst for irrigation over the next three days.

Results: The initial stain of the aspirate revealed numerous acid-fast bacilli. A four-drug regimen for M. tuberculosis was initiated along with clarithromycin for MAI. Cultures grew M. tuberculosis after 7 days. The patient's fever and pain resolved 6 days after endoscopic drainage. A follow-up CT scan 7 days later showed a decrease in the abscess size to 1.5 cm. HIV testing was positive with an absolute CD-4 count of 18/mcl.

Conclusion: This is an unusual presentation of M. tuberculosis as fever and a pancreatic cystic lesion, diagnosed as isolated tubercular abscess by EUS-guided aspiration. The presence of esophageal candidiasis suggested unrecognized immunosuppression and served as a clue to the diagnosis. Endoscopic ultrasound is often used in the evaluation of pancreatic cystic lesions but infrequently for the diagnosis of pancreatic tuberculosis. We believe this is the first reported case of an endoscopic cystduodenostomy for therapy of a tubercular pancreatic abscess. Endoscopic management of tubercular pancreatic abscesses is feasible and effective.


Rada Shakov, MD*, Joseph DePasquale, MD. St. Michael's Medical Center, Newark, NJ.

Purpose: HCV, a major cause of chronic liver disease, can lead to chronic active hepatitis, cirrhosis, & liver failure. An array of extrahepatic manifestations, including mixed cryoglobulinemia, MPGN (most often type 1 & 3), & porphyria cutanea tarda, are seen in association with HCV. Patients with glomerulonephritis may have no clinical evidence for systemic or liver involvement, and LFTs may be normal.

Methods: We illustrate a case of a young female presenting with edema, found to have MPGN, HCV, & hypothyroidism.

Results: 38 year old female without PMHx presents with 1 week of progressive headaches & edema. Pt. incurred a 20 lb weight gain over 4 months. She admitted to prior IVDU & nasal cocaine use. There was a history of thyroid disease in the patient's mother, but no history of liver or renal disease. On exam the patient was afebrile, with a BP 154/100 and pulse of 80. The patient had severe periorbital edema, abdominal wall edema & 3+ lower extremity edema. Labs on admission: Hgb 8.8, platelets 385, INR 1.1, Cr 0.83, T. Protein 3.1, Alb 1.3, AST 25, ALT 21, TSH 9.63 with normal T3 and T4. HIV test was negative. Further lab tests revealed: HepC Ab + (genotype 3a), 24 hour urine protein 4788 mg, ESR 71, negative cryoglobulins & autoimmune markers. Renal biopsy was performed and revealed MPGN with mild to moderate arterio- & arteriolosclerosis. The patient was started on diuretics, as well as valsartan, and synthroid. The patient was started on treatment for HCV using pegylated interferon & ribavirin. Due to severe neutropenia and anemia, growth factors had to be administered. After 4 weeks of treatment, the HCV viral load was undetectable. The patient decided to terminate therapy after 21 weeks due intolerance of side effects. Significant proteinuria is still persistant.

Conclusion: MPGN, with or without cryoglobulinemia, & membranous glomerulonephritis are the best characterized glomerulonephropathies associated with HCV. The pathogenesis of HCV-associated MPGN is probably a result of glomerular deposition of circulating HCV & anti-HCV antibodies. Our patient was discovered to be hypothyroid, but it is not yet well established if HCV plays a role in development of thyroid dysfunction & autoimmune thyroiditis. Interferon-alpha has been shown to improve proteinuria, suppress viremia, & stabilize renal function. Combination with ribavirin has led to improved suppression of HCV RNA levels. Patients often relapse after therapy is stopped. Immunosuppressive treatment has been used to treat mixed cryogbobulinemia & MPGN in the past, but effects of this treatment on HCV viremia & antibody response, & on the liver and renal disease needs to be evaluated further.


Cynthia Lau, MD*, Stanley Cohen, MD, Joseph Ahn, MD, Edie Chan, MD, Shriram Jakate, MD, Nikunj Shah, MD. Pathology, General Surgery, Gastroenterology and Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Acute fatty liver of pregnancy (AFLP) is a rare serious disorder that typically occurs in the third trimester. Complications include fulminant hepatic failure (FHF) and encephalopathy, renal failure, and acute pancreatitis (AP). The association of AFLP and AP has infrequently been reported in the literature and is associated with a high maternal and fetal mortality rate. Treatment is prompt delivery and supportive care, however, orthotopic liver transplantation (OLT) may be necessary in some cases. We describe a case of AFLP complicated by AP that had a favorable maternal and fetal outcome after OLT.

Methods: A previously healthy 39 year-old multigravida, at 34 weeks' gestation, was admitted to an outside hospital in preterm labor. A male infant was delivered by emergency cesarean section because of fetal distress. On Day 2 following delivery, the patient developed nausea, vomiting, abdominal pain, and poor urine output. Laboratory findings included hyperbilirubinemia, raised serum transaminases, prolongation of serum prothrombin time, hypoglycemia, and increased creatinine, amylase 455 U/L, and lipase 5,855 U/L levels. On Day 3, imaging studies suggested possible pancreatitis and no evidence of gallstones. Her mental status deteriorated and she was transferred to our center for further evaluation. The patient subsequently required intubation due to encephalopathy and respiratory distress, a continuous intravenous dextrose infusion to correct for persistent hypoglycemia, and intracranial pressure monitoring. A liver biopsy was performed and confirmed the diagnosis of AFLP. The decision to proceed with OLT was made on the basis of progressive clinical deterioration despite aggressive support.

Results: During OLT, severe pancreatitis was found. Histopathological examination of the native liver revealed microvesicular steatosis with characteristic changes consistent with AFLP. The patient recovered completely five weeks later, and was discharged home. Her baby boy was healthy and testing for LCHAD (3-hydroxyacyl-CoA dehydrogenase) deficiency is pending.

Conclusion: AFLP is an uncommon disorder that is associated with significant fetal and maternal mortality. Complications of AFLP may require aggressive intensive care management after delivery, especially if pancreatitis occurs. We present a unique case of AFLP, complicated by pancreatitis, which after OLT resulted in survival of mother and baby.


Scott DiGiacomo, MD*, Rada Shakov, MD, Shivangi Khara, MD, Medhat Ismail, MD, Hossam Elfarra, MD, Walid Baddoura, MD. Gastroenterology, St. Joseph's Regional MEdical Center, Paterson, NJ.

Purpose: In acute pancreatitis (AP), serum amylase rises within 6-12 hours of onset & remains elevated for 3-5 days in uncomplicated attacks. Amylase is excreted by the reticuloendothelial system (75%) & kidneys (25%). Serum lipase peaks at 24 hours, has a half-life between 7-14 hours & may stay elevated for 8-14 days; it is secreted by the biliary ductal system & kidneys. The sensitivity of serum amylase & lipase for the diagnosis of acute pancreatitis ranges from 85-100% in various reports. Furthermore, the negative predictive value of lipase is between 94-100%.

Methods: A 66 year old male with PMHx of IDDM, HTN & CAD presented to the ER with 2 days of generalized malaise, ill-defined abdominal discomfort & associated nausea & vomiting. He denied alcohol use & was not taking new medications. Exam was significant for fever & non-specific abdominal tenderness.

Results: Diagnostic work-up revealed diabetic ketoacidosis & an acute myocardial infarction. Additional lab values revealed: WBC 13, ALT 44, AST 52, blood sugar 1320, serum bicarbonate 11, BUN 149, creatinine 5.5, amylase 115 & lipase 48. Serum calcium & lipid panel were normal. Five days into his admission, the patient was still experiencing vague abdominal pain, persistent fevers and leukocytosis. Repeat amylase and lipase were 86 and 15, respectively; they continued to be persistantly normal throughout hospitalization. CT of the abdomen was performed and revealed marked inflammatory changes surrounding the region of the pancreas consistent with acute pancreatitis. An abdominal ultrasound was unremarkable for gallstones or common bile duct dilation. Interval CT scans revealed the development of extensive pancreatic necrosis; serum amylase and lipase remained normal. The patient had a prolonged hospital course complicated by CAD, sepsis and multi organ system failure. He expired 2 months following admission. Autopsy revealed diffuse fatty necrosis of the pancreas with extension into the mesentery.

Conclusion: The setting of acute pancreatitis associated with a normal serum amylase is rare, but well described. Multiple factors may contribute to the absence of hyperamylasemia on admission, including a return to normal enzyme levels before hospitalization, inability of the inflamed pancreas to produce amylase, or suppressed levels due to hypertriglyceridemia. However, elevated levels of serum lipase are invariably present. Despite a thorough literature review, we were unable to find a case report of acute necrotizing pancreatitis with a normal serum lipase.


Rodney Eddi, MD*, Scott DiGiacomo, MD, Rada Shakov, MD, Amabelle Pinzon, MD, Walid Baddoura, MD. Gastroenterology, Internal Medicine, St. Joseph's Regional Medical Center, Paterson, NJ.

Purpose: Gastrointestinal Stromal Tumors (GIST) originate from mesenchymal stem cells and have a mutation in c-kit tyrosin kinase proto-oncogene. The majority of GIST's (60% to 70%) arise in the stomach, while 20% to 30% originate in the small intestine and less than 10% in the esophagus, colon, and rectum. GIST's can rarely occur in extraintestinal sites in the abdomen or pelvis such as the omentum, mesentery, or retroperitoneum.

Methods: A 39 year-old Macedonian male, without significant past medical history, presented to our institution with complaints of increased abdominal girth for 2 months. The patient denied alcohol abuse. Physical examination was unremarkable except for large ascites without stigmata of cirrhosis.

Results: CT scan of abdomen revealed ascites without any other abnormalities. Abdominal paracentesis was performed. Ascitic fluid was grossly hemorrhagic. Analysis of fluid revealed: RBC = 94250, WBC = 1680 with 5% PMNs, 49% Lymphocytes, 39% Monocytes, Glucose = 68, Protein = 4.4, Albumin = 2.8. SAAG was calculated to be 0.5. Liver function tests as well as hepatitis profile were within normal limits. A PPD test was positive, but CXR did not show any evidence of TB. Abdominal ultrasound, doppler studies of hepatic and portal veins, EGD and colonoscopy were all inconclusive. Imaging of the small bowel is pending. At laparoscopy extensive "caking" of omental surfaces was seen; biopsies were suggestive of an epithelioid malignancy. Immunostaining was positive for CD34 and CD117 consistent with GIST. Patient was started on Imatinib Mesylate (Gleevac.sup.[R]).

Conclusion: This case illustrates a rare presentation of GIST. Extensive work up to date did not reveal any primary tumor in the gastrointestinal tract. The prognosis of this type of presentation remains to be determined. The tyrosine kinase inhibitor Imatinib Mesylate (Gleevac.sup.[R]) has shown promising results in treating metastatic disease. Based on current evidence, lifelong treatment with this agent is required.


Nadia Hafeez, MD*, Tanyanan Tanawuttiwat, MD, Charles Berkelhammer, MD. Internal Medicine, UIC, Oak lawn, IL.

Purpose: Introduction: Psoas muscle abscess can occur as a purulent complication of Crohn's Ileitis. We present a case of a sterile seroma of the psoas muscle occurring after surgical drainage of a chronic purulent psoas muscle abscess in Crohn's disease. Case: A 32 years old female underwent Ileal resection for Crohn's Ileitis and drainage of a chronic right psoas muscle abscess. Her psoas muscle abscess had been present for 3 years. She had previously refused surgical resection and drainage of her abscess and was therefore treated with prolonged course of antibiotics. She did not require immunosuppressant, immunomodulators, steroids or biologics postoperatively. 3 years after the resection she presented with right lower quadrant pain and a positive psoas sign. She was afebrile and had a normal white cell count. CT scan showed a 15 cm x 6 cm fluid collection in right psoas muscle at the site of her previous psoas muscle abscess. Colonoscopy with Ileoscopy showed no recurrence of Crohn's disease. Small bowel barium x-ray was negative for ileo-psoas fistula. CT guided aspiration showed a sterile fluid collection, with no organisms and sparse white cells. Multiple cultures were negative. She was treated with a prolonged course of percutaneous drainage and ultimately tetracycline injection to sclerose the remaining sinus tract. There has been no recurrence of her sterile seroma in 3 years. Discussion: Psoas muscle abscess is a known purulent complication of Crohn's ileitis. We describe a sterile seroma of the psoas muscle occurring 3 years after surgical drainage of a chronic purulent psoas muscle abscess. We speculate that the seroma developed in the dead space remaining in the psoas muscle after drainage of the chronic walled off abscess. Her sterile seroma was initially concerning for a recurrent purulent psoas muscle abscess. Gastroenterologists should be aware of the possible development of sterile seromas in such cases.


Raman Battish, MD*, Hiral Shah, MD, Averell Sherker, MD, FRCP(C). Gastroenterology, Washington Hospital Center, Washington, DC.

Purpose: Sarcoidosis is an idiopathic granulomatous disease commonly affecting the lung. Extrapulmonary involvement occurs in 50% of cases and can be the major manifestation of the disease.

Methods: Case report.

Results: A 40-year-old black man presented with malaise, abdominal pain, jaundice, dark urine, and pruritis of 3 weeks duration. The patient lost 25 lbs and reported intermittent melena. Abdominal exam revealed hepatosplenomegaly. Laboratory values displayed anemia and a predominantly cholestatic pattern of liver associated tests: AP 1789 IU/L, AST 202 IU/L, ALT 113 IU/L, TB 11.2 mg/dl, DB 4.7 mg/dl, Albumin 2.9 and INR 1.2. Hepatitis serologies, AMA, ANA, ASMA, and AFB cultures were negative. ACE was elevated. US displayed hepatosplenomegaly with liver heterogeneity and normal common bile duct. CT further revealed ill-defined masses throughout the liver concerning for diffuse metastatic disease. Endoscopy revealed a 4 mm pre-pyloric gastric ulcer with no bleeding. Biopsy of the ulcer displayed a granuloma. Liver biopsy revealed multiple confluent non-caseating granulomas in the portal and periportal zones consistent with sarcoidosis.

Conclusion: Hepatic sarcoidosis covers a broad spectrum from asymptomatic hepatic granuloma formation and slightly deranged liver associated tests to chronic cholestasis, cirrhosis and portal hypertension. Hepatosplenomegaly (15-40%) and abdominal pain (5-15%) are the commonest clinical findings. Constitutional symptoms are rare (5%). Increased serum AP, bilirubin (usually <5 mg/dL) and slightly elevated transaminase levels may be seen. Increased AP can be found in up to 90% of patients with signs of hepatic disease. Hepatomegaly is found on imaging in up to 50% of cases, and may be accompanied by splenomegaly and abdominal lymphadenopathy. Hepatic granulomas are rarely visualized on CT (<5% of patients) and when confluent must be differentiated from neoplastic conditions. Glucocorticoid treatment is first-line therapy for hepatic sarcoidosis, improving symptoms and abnormal laboratory values but generally having no effect on progression of disease. Subclinical GI tract sarcoidosis is rare, seen in 5-10% of patients with systemic sarcoidosis. Symptomatic GI involvement is less frequent. The stomach is most often involved in GI tract sarcoidosis and is typically asymptomatic. Ulcerative gastric sarcoidosis occurs with mucosal infiltration by granulomatous inflammation. This typically occurs in the antrum, pylorus and lesser curvature. Epigastric pain is the most common symptom of gastric sarcoidosis occurring in 75% of cases and 25% of patients with GI tract sarcoidosis have signs of upper GI bleeding. Our case highlights rare but important manifestations of sarcoidosis.


Muslim Atiq, MD*, Syed Ali, MD, Shyam Dang, MD, Elias Anaissee, MD, Kevin Olden, MD, Farshad Aduli, MD. Myeloma Institute of Research and Therapy, Gastroenterology, University of Arkansas for Medical Sciences, Little Rock, AR.

Purpose: 1. To describe a rare presentation of plasmacytoma involving pancreas 2. To describe complications arising from pancretic plasmacytoma

Methods: Review of clinical history, imaging stides and endoscopic records

Results: Extramedullary plasmacytomas are neoplastic plasma cell proliferation outside the bone marrow. We describe a case of pancreatic plasmacytoma presenting as gastric variceal hemorrhage secondary to splenic vein thromois. Case A 49 years old Caucasian female with history of diabetes type II, hypertension and congestive heart failure underwent work up for recurrent episodes of acute pancreatitis and was found to have a pancreatic mass. Fine needle aspiration of the lesion was consistent with monoclonal plasma cell dyscrasia. Bone marrow biopsy confirmed the diagnosis of multiple myeloma. Chemotherapy was being contemplated when she started to have acute onset of hematemesis with drop in hemoglobin requiring multiple transfusions of packed red blood cells. After hemodynamic resuscitation an EGD was performed. It showed presence of prominent gastric varices with active bleeding. Endscopic sclerotherapy was performed with control of bleeding. CT scan of abdomen revealed a 3.9 cm mass in the body of the pancreas. The tumor resulted in the invasion and occlusion of the splenic artery and vein. Multiple collateral vessels were visible near the splenic hilum and along the lesser and greater curvatures of the stomach. Patient responded well to the endoscopic sclerotherapy. No further intervention was needed. Systemic chemotherapy was started resulting in a decrease tumor size; and after 2 months of follow up, patient has remained free of any recurrent variceal hemorrhage. Repeat EGD at 2 months showed almost complete obliteration of gastric varices.

Conclusion: Pancreatic Plasmacytoma is a rare entity. To our knowledge, this is the first case of pancreatic plasmacytoma presenting as gastric variceal hemorrhage.


Taraneh Soleymani, MD*, Rada Shakov, MD, Chintan Mody, MD, N. Parikh, MD, Robert Spira, MD, Joseph DePasquale, MD. Internal Medicine, St. Michael's Medical Center, Newark, NJ, Seton Hall University, South Orange, NJ, Pathology, Gastroenterology, St. Michael's Medical Center, Newark, NJ.

Purpose: Meckel's diverticulum, a true congenital diverticulum, is found in 2% of the population, is located about 2 feet from the ileocecal valve, and often is no more than 2 inches in length. Fifty percent of these cases contain ectopic tissue most commonly gastric and pancreatic. Two percent of patients are symptomatic, most often presenting by the age of 2 years. Males are twice as likely to experience symptoms.

Methods: This case illustrates a rare presentation of Meckel's diverticulum in a adult female with the diverticulum infected by actinomycosis.

Results: A 37 year-old female with history significant for diabetes, presented with 3 day complaints of peri-umbilical abdominal pain. The pain was constant, nine out of ten in severity, dull in nature, non-radiating and associated with nausea and vomiting. Fever, diarrhea, constipation, urinary symptoms, and vaginal bleeding were denied. On admission, the patient's vitals were stable. On exam, there was epigastric and right upper quadrant tenderness with a positive Murphy's sign. Lab results: WBC 21.7, Hbg 12.4, T. Billi 0.9, Alk. Phos 84, AST 19, ALT 13, Amylase 41, and Lipase 19. Patient was kept NPO and started on ciprofloxacin and metronidazole. CT of abdomen revealed a small non-contrast filled loop of bowel in the right mid abdomen suspicious for a Meckel's diverticulum, this was confrimed at exploratory laparotomy and was resected. It measured 7.5 cm in length and 2-3 cm in diameter; the lumen was distended with a thick, whitish, cloudy fluid consistent with an abscess, which grew actinomycosis, sensitive to ciprofloxacin. On post-op day two, the patient was discharged home. She remained symptom free on follow up.

Conclusion: Meckel's diverticulum, the most prevalent congenital anomaly of the gastrointestinal tract, is due to failure of the vitelline duct to obliterate during the fifth week of fetal development. Symptomatic adult patients most commonly present with acute bleeding, diverticulitis or obstruction. In symptomatic patients, surgical resection is the standard treatment. Other complications of Meckel's diverticulum include abscess formation, enteroliths, hemorrhage, obstruction, intussusception, volvulus, perforation, and malignancy (sarcomas). To our knowledge, there has only been one previously reported case of Actinomycosis associated with Meckel's diverticulitis.


Jeremy Davis, MD, MPH*, Muslim Atiq, MD, Laura Lamps, MD, Kevin Olden, MD, James Rose, MD. Pathology, Gastroenterology, University of Arkansas for Medical Sciences, Little Rock, AR.

Purpose: To present two cases of amiodarone induced liver cirrhosis To elicit amiodarone induced cirrhosis may occur at low doses To describe histopathological features of amiodarone induced liver cirrhosis

Methods: Case Review and review of literature regarding amiodarone induced liver cirrhosis

Results: A 72 y/o gentleman was admitted with generalized fatigue and worsening ascites. Pertinent medications included amiodarone at 200 mg per day, simvastatin and glipizide. Initial labs were as follows: bilirubin of 1.9 mg/dL, AST 106 IU/L, ALT 75 IU/L, Alk Phos 147 IU/L, prothrombin time of 20 seconds. Liver ultrasound showed a cirrhotic liver, splenomegaly and ascites. Serologic studies were negative for viral hepatitis. There was no evidence of autoimmune hepatitis, Wilson's disease, or hemochromatosis. A liver biopsy showed steatohepatitis with a striking amount of Mallory hyaline within the hepatocytes, and a neutrophilic infiltrate, consistent with amiodarone toxicity (Fig. 1). The patient died during his hospitalization secondary to complications from his liver disease. Case 2: This patient was a 67 yo woman with a history of coronary artery disease who was admitted with increasing confusion. There was no history of alcohol use. She was on low dose amiodarone. Her initial work up revealed AST 377 IU/L, ALT 277 IU/L, Alk Phos 551 IU/L, PT of 12.7 seconds. Serologic studies were negative for viral hepatitis, and there was no evidence for auto-immune hepatitis, Wilson's disease, or hemochromatosis. Ultrasound of the liver showed homogenous liver parenchyma with ascites. Liver biopsy showed a neutrophilic infiltrate with associated degenerating hepatocytes and a remarkable amount of Mallory hyaline with well developed pericellular fibrosis and at least bridging fibrosis, consistent with amiodarone toxicity (Fig. 2).

Conclusion: Drugs such as amiodarone may inhibit the mitochondrial [beta]-oxidation of fatty acids resulting in mitochondrial dysfunction, thus activating a cascade leading to fibrosis. To date, a total 8 cases of amiodarone induced cirrhosis have been reported in the literature. These cases illustrate the importance of checking baseline liver associated enzymes in patients who are being considered for amiodarone therapy, as well as monitoring them closely during therapy even with low dose amiodarone.


Raman Battish, MD*, Hiral Shah, MD, Averell Sherker, MD, FRCP(C), James McFadden, MD. Radiology, Gastroenterology, Washington Hospital Center, Washington, DC.

Purpose: Meckel's diverticulum (MD), occurring in 2% of the population, is the most common congenital abnormality of the GI tract. Small bowel MRI (SBMRI) is an emerging imaging modality that allows for transmural evaluation without ionizing radiation. We present a case of MD diagnosed by SBMRI.

Methods: Case.

Results: 17 year old man admitted with lower abdominal pain and maroon stools for the past evening. The patient reported a history of anemia but denied any previous bleeding. Physical examination revealed orthostatic hypotension, benign abdomen and red blood in rectal vault without hemorrhoids or fissures. Hemoglobin was 5.1 Gm/dl with iron deficiency, MCV-62fL and ferritin <15 nG/ml. Following volume resuscitation and blood transfusion- Tc-99m pertechnetate and bleeding scans were negative. EGD was normal. Colonoscopy displayed apthous ulcers in the ascending colon and terminal ileum with sparing of the cecum. Biopsy demonstrated changes consistent with Crohn's disease (CD). SBMRI, performed to evaluate extent of CD involvement, revealed a 6.7 cm diverticulum arising from the anti-mesenteric border of the distal small bowel (Figure).

Conclusion: MD, a remnant of the omphalomesenteric duct, is typically diagnosed before age ten due to complicatons. Hemorrhage is the most common presentation of MD in children. Adults typically present with obstruction or diverticulitis. The lifetime risk of developing complications from MD is cited as 6%, and controversy exists whether this risk decreases with advancing age. Giant MD are greater than 6 cm in diameter. MD are composed of all layers of the ileal wall and heterotopic tissue is present in half of resected specimens. Gastric mucosa (GM) is found in 50% and panctreatic tissue (PT) in 5-16% of resected specimens. Acidic secretions from heterotopic GM and alkaline secretions from heterotopic PT result in mucosal ulceration. Tc-99m pertechnetate scan with a sensitivity of 75% is the best imaging modality for diagnosis. SBMRI has been advocated for evaluation of submucosal and serosal-mesenteric involvement of CD. Interestingly, a higher prevealence of MD in CD patients has been shown. SBMRI is a valuable addition in the diagnostic armamentarium for MD.


Nelson Lim, MD*, Donald Rankin, MD, Michael Lim, BS, Hin Wah Lee, MD. Department of Pathology, Department of Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA.

Purpose: To report a rare case of a high grade neuroendocrine tumor of the extra-hepatic biliary tract.

Methods: A 62 year old male presented with obstructive jaundice. CT scan showed dilated intrahepatic ducts with no evidence of a pancreatic mass. ERCP revealed a mid-common bile duct (cbd) stricture and a stent was placed for drainage. Brushings were negative for malignancy. He was referred to our institution for endoscopic ultrasound (EUS). A 1.4 x 1.2 cm hypoechoic lesion was seen at the mid-CBD at the cystic duct take off, resulting in dilation of common hepatic duct (chd), cystic duct and gallbladder. There was a 1.8 x 1.1 cm lymph node at the porta hepatis. FNA was obtained from both the CBD lesion and porta hepatis lymph node. Histologic review from both samples showed clusters of atypical and hyperchromatic cells consistent with a high grade neuroendocrine tumor (NET). Upon immunohistochemical analysis, the cells stained positive for synaptophysin but negative for chromogranin. The patient is scheduled to start chemotherapy.

Results: Malignancies of the extrahepatic bile ducts are predominantly cholangiocarcinomas (80%). Neuroendocrine tumors (NETs) of the bile duct are the most rare and occur in less than 2% of cases.1 NETs arise from embryonal neural crest cells (Argentaffin or Kulchitsky cells) that migrate to the respiratory and gastrointestinal tracts during development. The paucity of these cells in the biliary tract account for its rarity.2 There have been approximately 52 cases described in the literature since 1959.2 Most patients present with symptoms of biliary obstruction, biliary-colic pain and pruritis.3 It occurs more frequently in women than in men (1.9:1).3 The mean age is 2-3 decades below that of patients with neoplasm in the same anatomic site.3 The incidence of false negatives with brush cytology is high due to its submucosal location.3 The location of the tumor and the extent of the disease usually dictate the type of intervention. Synaptophysin-positive cases showed a worse prognosis (median survival, 27 months) vs. synaptophysin-negative (median survival, 38 months) groups (P < 0.5).4 Prior to endoscopic ultrasound with fine needle aspiration, most cases of NETs have been found accidentally (i.e. incidentalomas) during biliary tract operations. 3

Conclusion: NETs of the extrahepatic bile duct are a rare cause of biliary tract malignancy. However, it should be considered in the differential diagnosis in patients presenting with obstructive jaundice. EUS with FNA should be the main diagnostic modality. The presence of synaptophysin in tissue indicates poorer prognosis.


Stephen Rashbaum, MD*, Luke Lee, Brian Hudes, MD. Advanced Gastroenterology Associates, Suwanee, GA.

Purpose: Tropical sprue is a malabsorptive small bowel disorder especially characterized by deficiencies of folate and vitamin B12. We present a case where capsule endoscopy in conjunction with appropriate travel history identifies this disease. The case also helps to elucidate the appearance of tropical sprue at M2A capsule endoscopy which has rarely if ever been described in the literature.

Methods: Case: A 56-year old male with recently discovered B12 and folate deficiencies presented with alternating bowel habit and bloating. EGD showed bulbar duodenitis with biopsies revealing mild to moderate chronic inflammation, focal gastric metaplasia, and associated focal villous blunting. The distal duodenum and proximal jejunum were described as normal with biopsies showing mild chronic nonspecific mucosal inflammation. All small bowel biopsies were without viral inclusions, giardia, helicobacter or other organism. Other testing included a normal Endomysial AB IgA, t-Transglutaminase IgA, and serum IgA levels. Patient was sent for small bowel capsule endoscopy with M2A Capsule which demonstrated mucosal changes of villous atrophy throughout the jejunum and ileum. Mild jejunal lymphangiectasia was also noted. Upon further patient questioning, he noted recent travel to St. Lucia two months prior to his diagnosed B12 and folate deficiencies consistent with a diagnosis of tropical sprue.

Results: Discussion: Celiac sprue is characterized by villous atrophy occurring in the proximal small bowel with lesser changes if any in the ileum. However, atrophy may be apparently more widespread in tropical sprue, as described by capsule endoscopy in the presented case. This case also evidences that persistent diarrhea may not be present.

Conclusion: 1) Diagnosis of tropical sprue should be entertained in all patient's with vitamin B12 and folate deficiency. Special care should be made to obtain a travel history in such individuals. 2) Persistent diarrhea may not always be present in tropical sprue 3) Capsule endoscopy of the small bowel may be useful in the diagnosis of tropical sprue by demonstrating extensive changes of villous atrophy throughout the small bowel including the ileum.


Anne Thai, MD*, Kanat Ransibrahmanakul, MD, Danny Yen, MD, Lynne Do, MD, Valentina Medici, MD, Christopher Bowlus, MD. Internal Medicine-Gastroenterology and Hepatology, Internal Medicine, University of California, Davis Medical Center, Sacramento, CA.

Purpose: Cryptococcus neoformans is an encapsulated yeast, most commonly affecting the immunocompromised including patients with HIV/AIDS, hematological malignancies, prolonged steroid use, or organ transplantation. The typical forms of Cryptococcal infection consist of meningoencephalitis, pulmonary infiltration, skin lesions, and osteomyelitis. Cryptococcal infection of ascites is a rare and fatal infection that is often unrecognized due to vague presenting symptoms that resemble spontaneous bacterial peritonitis (SBP). Here, we present a case of Cryptococcal peritonitis in a patient with hepatitis C (HCV) related cirrhosis.

Methods: A 63 y/o HIV-negative Latino male with decompensated cirrhosis due to HCV, undergoing evaluation for liver transplantation, presented to the ED with a 10 day history of increasing confusion. On admission, he was obtunded and unable to communicate clearly. His wife reported a decrease in frequency of his bowel movements. She denied any fevers, chills, nausea, vomiting, abdominal pain, melena, or hematechezia. She reported that the patient was compliant with his Ciprofloxacin prescribed for SBP prophylaxis. Physical exam revealed a somnolent, thin male with bitemporal wasting, scleral icterus, spider angiomas, diffuse abdominal tenderness, and clonus.

Results: Lab results included a normal WBC (6.8), elevated INR (2.8), reduced complement level, venous ammonia level of 52, hypoalbuminemia (1.6), alkaline phosphatase of 87, total bilirubin of 11.3, AST 111, and ALT 46. Urine drug screen was negative. A CT abdomen illustrated cirrhosis and massive ascites. Ascites fluid contained only 67 WBC/mm3 with only 2% neutrophils. On hospital day 4, blood cultures and ascites fluid grew yeast that was later identified as Cryptococcus neoformans. Treatment with IV Fluconazole was initiated and changed to Liposomal Amphotericin B and 5-fluorocytosine once the organism was identified. On hospital day 8 he became acutely hypoxic and hypotensive. In light of the patient's wishes, the family declined mechanical ventilation, and comfort care was initiated.

Conclusion: Cryptococcal peritonitis is a rare but usually fatal infection of ascites. It is often acquired through hematogenous dissemination from subclinical pulmonary infection. Patients with cirrhosis have impaired opsonization, phagocytic dysfunction, and complement deficiency, making them more susceptible to Cryptococcal infection. The mortality rate for Cryptococcal peritonitis with antifungal therapy has been reported to be 73%. Although a rapid antigen test is available, on average, it takes six days for the detection of Cryptococcus in ascites by culture. A low ascites white cell count and fungemia should lead to a heightened suspicion of Cryptococcal peritonitis.


Kumaravel Perumalsamy, MD*, Jack Tin, MD, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD, MPH. Division of Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Biliary Papillomatosis is a rare pre-malignant condition which is being increasingly recognized as imaging of the common bile duct improves. Early identification remains important in preventing morbidity and mortality from subsequent cholangicarcinoma. We report the first case of using Spy-Scope (choledochoscopy) in establishing the diagnosis of intraductal biliary papillomatosis.

Methods: A 64 year old Asian gentleman presented with RUQ abdominal pain and weight loss of few months duration. There was no fever, chills, nausea or vomiting. Recently, several friends had told him he looked "yellow". Physical examination revealed an icteric male with right upper quadrant tenderness. Laboratory analysis demonstrated an elevated bilirubin to 3.5 mg/dl, direct 2.5 mg/dl. The AST was elevated to 180 U/L, ALT 220 U/L, alkaline phosphatase 280 U/L and a normal albumin of 3.8 mg/dl. MRI of the abdomen, including MRCP, revealed dilatation of the right hepatic duct and mild intra-hepatic ductal dilation. Cholangiogram showed amorphous filling defects in the right main duct and filling defects in the right intra hepatics. Sphincterotomy was performed. Balloon sweep retrieved friable non-specific debris. To further characterize the filling defects in the biliary tree, a choledochoscope was introduced (Spy Glass, Boston Scientific). On direct visualization, multiple, soft, fleshy, mobile, polypoid growths with fine villous projections on the surface were seen in the intra hepatic ducts. Targeted biopsies were taken from the polypoid tissue using small forceps. Biopsy showed exophytic papillary adenoma and fibro-vascular stroma consistent with Biliary Papillomatosis.

Results: Biliary papillomatosis is a rare but increasingly recognized neoplastic disorder of the biliary tree. Common clinical presentations include repeated episodes of abdominal pain, jaundice, acute cholangitis, hemobilia and mucobilia. The disorder typically affects middle aged adults, male to female ratio of 2:1. There is a high malignant potential which progresses via the adenoma-carcinoma sequence. Due to a degree of malignant transformation, surgical resection is necessary.

Conclusion: Given the importance of early identification and treatment of this disorder, this novel method as described with endoscopic visualization of the biliary tree (Spy-Scope) should be considered in select patients suspected of having biliary papillomatosis.


Cynthia Lau, MD*, Stanley Cohen, MD, Joseph Ahn, MD, Shriram Jakate, MD, Mariano Dy-Liacco, MD, Nikunj Shah, MD. General Surgery, Pathology, Gastroenterology and Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Cholangiocarcinoma (CCA), a rare malignancy of the biliary duct system, arises from epithelial cells of the intrahepatic or extrahepatic bile ducts. Clinical presentation varies depending on location of tumor, but includes jaundice, pruritus, abdominal pain, weight loss, and fever. Primary sclerosing cholangitis, choledochal cysts, and infection with parasitic liver flukes are risk factors strongly associated with CCA. Hepatitis B virus infection (HBV) is associated with hepatocellular carcinoma, but very rarely with CCA. We present an unusual case of CCA in a patient with chronic HBV infection.

Methods: A 38 year old Asian male with chronic untreated HBV infection presented to an outside hospital with fever, fatigue, and right upper quadrant abdominal pain for one week. Imaging studies revealed a right hepatic lobe mass and portal vein thrombosis. Liver biopsy was performed and the patient was referred to our hospital for further management. Physical exam revealed jaundice and hepatomegaly. Hemoglobin was 12.8 g/dl, platelet count 236 x 10.sup.3/mcL, albumin 3.1 g/dl, bilirubin 0.7 mg/dL, alkaline phosphatase 147 IU/L, aspartate aminotransferase 57 IU/L, alanine aminotransferase 39 IU/L, INR 1.5, alpha-fetoprotein level 114 ng/ml, CA 19-9 of 45 U/ml, and HBV DNA 27,567 IU/ml. Repeat imaging demonstrated a 9.9 x 6.8 cm infiltrating mass extending from the dome inferiorly and invading the gallbladder, as well as portal vein thrombosis. A chest computed tomography (CT) and bone scan were negative for metastatic disease. Liver biopsy of the mass showed moderately differentiated adenocarcinoma and dysplasia of bile ducts. Immunostaining was compatible with CCA. A liver biopsy obtained from the left unaffected lobe revealed HBV hepatitis with early cirrhosis. The patient was not a candidate for liver transplantation.

Results: Subsequently, an exploratory laparotomy revealed no obvious peritoneal seeding, thus a right hepatectomy and cholecystectomy were performed. Pathology was consistent with CCA and an abundance of hepatocytes positive for hepatitis B surface antigen. The patient had an uncomplicated postoperative course and was discharged on antiviral HBV medications and follow up with oncology and radiation oncology.

Conclusion: We demonstrate a unique, rare case of CCA associated with chronic HBV. It has been proposed that HBV may infect biliary epithelium resulting in an immunologic attack causing inflammation and degenerative changes. More research is needed to evaluate the potential role of HBV in the pathogenesis of CCA, so that we can prevent and control this devastating disease.


Maqsood Khan, MD*, Srinadh Komanduri, MD, FACG, Michael Brown, MD, FACP, FACG. Internal Medicine, West Suburban Medical Center, Oak Park, IL, Gastroenterology, Rush University Medical Center, Chicago, IL.

Purpose: Introduction: Non-Hodgkins lymphoma (NHL) is the 6th leading cause of cancer death in USA. Plasmablastic lymphoma (PBL) is a rare AIDS related NHL (ARL) arising in the oral cavity. Herein, a patient is presented with plasmoblastoma of colon as the initial presentation of AIDS. Case report: A 40 year old female came to the ER complaining of a brown vaginal discharge for about 2 weeks and intermittent rectal bleeding. Physical exam and CT scan of abdomen and pelvis revealed a 10 x 9.8 cm mass extending into the vaginal introitus, as well as a mass on the rectal exam. On day 2 of hospital stay she developed rectal bleeding. Subsequent sigmoidoscopy showed a large circumferential exophytic mass (Fig. 1). Jumbo biopsy demonstrated a plasmablastic lymphoma. The cells were strongly positive for MUM1, CD138 and ebstein barr encoded RNA (EBER). Subsequent testing demonstrated the patient to be HIV positive with a HIV RNA of 427976 & CD4 count of 60. The patient was started on R-EPOCH therapy for plasmablastic lymphoma and HAART for her HIV. Her vaginal discharge improved and she was discharged in a stable condition Discussion: Patients with HIV/AIDS are at a significantly increased risk of developing NHL. PBL is rare types of ARL. Based on recent series of ARL, PBL accounts for approximately 2-4% of all ARL. Initially described as tumors which developed primarily in the oral cavity, HIV associated PBL can rarely present in other extranodal sites such as the bones, soft tissue, and gastrointestinal tract. Much like other NHLs, combination chemotherapy forms the backbone of therapy for PBL, and CHOP-like regimens are considered first-line therapy. Although extension to other sites can occur, in most patients, the neoplasm is limited to the oral cavity at initial presentation. Our case is a unique presentation of PBL with rectal bleeding, vaginal discharge, and initial manifestation of AIDS. Occurrence of PBL in sites other than the oral cavity expands our knowledge of AIDS-related lymphoproliferative disorders and increases our insights about this rare entity.

Sigmoidoscopy showing bleeding large exophytic mass.


Maqsood Khan, MD*, Srinadh Komanduri, MD, FACG, Michael Brown, MD, FACG, FACP. Internal Medicine, West Suburban Medical Center, Oak Park, IL, Gastroenterology, Rush University Medical Center, Chicago, IL.

Purpose: Introduction:Primary intestinal natural killer (NK)-cell lymphomas are exceedingly rare. We present a case of NK- cell lymphoma in the stomach and colon Case Report: 45 year old female with history of peptic ulcer perforation who was undergoing surveillance upper endoscopies every two years showed erosive gastritis (Fig. 1A). The gastric biopsy showed active ulceration of fundic gastric mucosa with glandular atypia and abundant lymphocytes which were positive for CD3, CD56, and CD43 by immunohistochemistry. PET scan demonstrated high radioactivity on the left side of the pelvis. A subsequent colonoscopy revealed numerous moderate sized exudative ulcers located throughout the colon (Fig. 1B). The colon biopsy was also positive for NK/T cell lymphoma. The tumor responded well to 6 cycles of CHOP regimen and subsequent EGD and colonoscopy with biopsys were negative for lymphoma which indicates the disease to be in complete remission Discussion: Primary NK cell lymphoma also known as angiocentric lymphomas or CD56 lymphomas have marked propensity to occur in the nose and paranasal sinuses. They are more common in men. This lymphoma produces usually ulcerative, destructive lesion in the nasal/nasopharyngeal region. Other organs include the skin, gastrointestinal tract, testis, soft tissue, brain, liver, spleen, and bone marrow. The identifying trait is found by immunohistochemistry which shows strong immunopositivity for CD56, a marker for natural killer (NK) cell differentiation. EBER and TCR gene rearrangement are useful in distinguishing NK cell lymphoma from NK-like T-cell lymphoma. The disease is closely associated with Epstein-Barr virus (EBV) infection. Natural killer cells comprise 10-15% of the normal circulating lymphocytes in the peripheral blood and play an important role in the immune system by lysing tumor cells without prior sensitization. In our patient as CD 30 was negative, this was not the usual aggressive NK/T cell lymphoma of nasal type. Treatment of NK/T-cell lymphomas is by standard CHOP regimen. Other treatment options, like peripheral blood stem cell transplant combined with chemotherapy for more resistant lymphomas do exist.


Muhammad Siddiqui, MD*, Charles Berkelhammer, MD, FACG. Internal Medicine, University of Illinois, Oak Lawn, IL.

Purpose: Introduction: Lymphoma of esophagus is rare. We present a case of superficially ulcerating lymphoma of distal esophagus mimicking ulcerative reflux esophagitis. Case: A 72 year old female with history of Hepatitis C cirrhosis, presented to an outside hospital with profound iron deficiency anemia and hemoccult positive stools. Her hemoglobin was 5.4 with an MCV of 56. Iron indices were consistent with iron deficiency anemia. Endoscopic evaluation revealed erosive reflux esophagitis and diverticulosis of colon. Her anemia responded to iron therapy, but she remained continually strongly hemoccult positive. On referral to our institution, she refused repeat endoscopic evaluation of persistently hemoccult positive stool until she developed odynophagia 11 months later. Endoscopy revealed superficial ulceration of the distal 5 cm of her esophagus. The margins of the ulceration were raised and there was no luminal compromise. Biopsy showed diffuse large B-cell lymphoma. Gastric biopsies were negative for Heliobacter pylori. CT scan showed a mass in the distal mediastinum in continuity with the distal esophagus. She was treated with dexamethasone and rituximab. She ultimately succumbed to an exsanguinating upper gastrointestinal bleed. Conclusion: Distal esophageal lymphoma can rarely mimic erosive reflux esophagitis. A high index of suspicion with biopsies of abnormal areas is required for early diagnosis.


Dushyant Singh, MD*, Wendell Clarkston, MD. Internal Medicine, University of Missouri Kansas City, Kansas City, MO.

Purpose: Pancreatic and peripancreatic tuberculosis is extremely rare even in countries with high endemism. Fewer than 40 cases of pancreatic tuberculosis have been reported worldwide. There is a recent increase in such cases, but the infrequency with which it is encountered makes it a formidable diagnostic challenge.

Methods: We report a 47 year old Ethiopian immigrant male with HIV presented with fever, abdominal pain and weight loss. He appeared weak and diaphoretic but was awake and oriented. His vital signs were stable, except for temperature of 103.0F. His physical exam was unremarkable, except for mild abdominal tenderness and splenomegaly.

Results: CT scan abdomen showed a complex cystic mass in the pancreatic head with internal septations, associated with extensive retroperitoneal adenopathy. Necrotic pancreatitis and pseudocyst were considered much less likely given the apparent septations and associated adenopathy. A CT guided biopsy of multiple periaortic lymph nodes was positive for mycobacterium tuberculosis complex by smear and culture. He was started on 4 drug antitubercular therapy, resulting in resolution of the pancreatic mass after 9 months (see images).

Conclusion: Although rare, pancreatic and peripancreatic tuberculosis should be considered in the differential diagnosis of cystic lesions of the pancreas. On review of literature, the key to diagnosis of pancreatic tuberculosis is CT guided needle biopsy of the involved tissue and these masses respond well to antitubercular therapy.


Nan Sandar, MD*, Sharique Nazir, MD, Philip Xiao, MD, Mohammed Aladdin, MD, Alan Go, MD, FACS, Sury Anand, MD. Interventional Radiology, Pathology, Surgery, Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY.

Purpose: Angiodysplasia (AD) is the second leading cause of lower gastrointestinal (GI) bleeding especially in the elderly. We report a case of a young patient with significant lower GI bleeding from AD requiring emergency surgery.

Methods: A healthy 23 year old male presented to the emergency room after passing 9 episodes of black stool associated with crampy abdominal pain and dizziness. There was no nausea, vomiting or hematemesis. He was orthostatic and tachycardic but afebrile. He denied drinking alcohol or taking any medication. Nasogastric lavage was negative. Rectal exam revealed melanotic stool. His lab values showed hemoglobin of 7.8 G/dl with normal coagulation profile. He was immediately resuscitated with intravenous fluid and 3 units of packed red blood cells without much improvement. Esophagogastroduodenoscopy was normal. Colonoscopy was attempted but it was terminated because of poor visualization due to a large amount of blood in the colon. The bleeding source was identified near the hepatic flexure in the bleeding scan. Angiography revealed early venous filling and active extravasation in the proximal ascending colon. Coil embolization of the feeding vessel was attempted with achievement of hemostasis for 5 hours. After that, the patient deteriorated again with a significant hemoglobin drop. Exploratory laparotomy with right hemicolectomy and primary anastomosis was performed. Pathology revealed an irregular 3 cm dark blue discoloration under the mucosa of the ascending colon. Histology demonstrated dilated and distorted vessels lined by endothelium with scanty smooth muscle in the submucosa consistent with AD. The patient received multiple units of blood transfusion for his massive lower GI bleeding. His postop period was complicated by anastamotic leak and he became septic for which he had to undergo reconstruction of ileocolic anastomosis and diverting loop ileostomy. He was also given Xigris for the severe sepsis. He then developed bleeding from ileostomy site. Xigris was discontinued and the bleeding was resolved. Ileoscopy revealed punctuate hemorrhages but no fresh or old blood was noted. Capsule endoscopy was essentially normal.

Results: The patient had no more bleeding episode and feeling well at his 2 month follow up visit.

Conclusion: Massive bleeding from AD in the young is very rarely described. Our patient not only had significant bleeding from AD requiring multiple units of blood, but he also presented with melena rather than hematochezia. We hope this case report will remind us that those presenting with melena, though usually implying upper GI bleeding, can also indicate bleeding from the lower GI tract. Lastly, bleeding from AD should be in the differential diagnosis of lower GI bleeding even in the young.


Adeel Seyal, MD*, Christopher Marino, MD. Internal Medicine, University of Tennessee, Memphis, TN, Internal Medicine, Veterans Affairs Medical Center, Memphis, TN.

Purpose: INTRODUCTION Hemolysis induced pancreatitis has been rarely reported in literature. We describe a dialysis patient who developed severe hemolysis due to dialysis tube kinking resulting in release of free heme causing acute pancreatitis

Methods: N/A

Results: Case Report:- 53 years old African American male with past medical history of hypertension and end stage renal disease on hemodialysis developed chest tightness and shortness of breath during routine hemodialysis. A kink was noticed in the dialysis tubing after the patient was symptomatic. Examination showed temperature 98.9 F, pulse of 88, and blood pressure of 228/114 mm of Hg. Other than mild icterus rest of the examination was unremarkable. Hemoglobin dropped from 15.2 g/dL to 8.2 g/dL with a Hematocrit of 15.2%. Total Bilirubin was 17.9 mg/dl and unconjugated Bilirubin was 15 mg/dl. Aspartate aminotransferase and alanine aminotransferase were 723 U/L and 34 U/L respectively, lactate dehydrogenase of 16,231 U/L, and serum Haptoglobin was low indicating intravascular hemolysis. Next day he started experiencing escalating epigastric pain. Serum amylase was 960 U/L and serum lipase was 3600 U/L consistent with acute pancreatitis. CT scan did not show gallstones or changes consistent with chronic pancreatitis. Serum calcium level was 7.4 mg/dL and triglycerides were 265 mg/dL. Patient was not on any medication known to cause pancreatitis. Diagnosis of hemolysis induced pancreatitis was made. He was kept nothing per oral and given intravenous fluids, blood transfusions and proton pump inhibitors with resolution of symptoms.

Conclusion: Acute pancreatitis is an acute inflammatory condition of the pancreas. Etiologies include alcoholism, gallstones, hypertriglyceridemia, hypercalcemia, drugs, and trauma. Although mechanism of hemolysis induced pancreatitis is not well understood, massive intravascular hemolysis leads to release of large amounts of free heme exceeding the binding capacity of hemopexin and overwhelming heme oxygenase system. Free heme causes increase in vascular permeability, formation of reactive oxygen radicals, adhesion molecule expression and leukocyte recruitment. Massive hemolysis also leads to activation of coagulation cascade forming microthrombi and damaging vascular integrity of pancreatic microvasculature. Some or all of these mechanisms can potentially cause pancreatitis. Management is largely conservative for acute pancreatitis.


Rachana Potru, MD*, Joseph Ahn, MD, Henry Fung, MD, Stanley Cohen, MD. Hepatology, Hematology, Rush University Medical Center, Chicago, IL.

Purpose: There is a known increased incidence of myelodysplastic syndrome (MDS) after heart and lung transplant. There is, however, only one reported case of MDS in a liver transplant (LT) patient. This abstract presents the second known case of MDS in a LT patient and discusses the role of immunosuppression in development of MDS after LT.

Methods: PubMed search using keywords "myelodysplastic syndrome" and "liver transplant" was done to identify any previous reported case of MDS in LT. Patient data was gathered from the patient and the medical record.

Results: A 54-year-old white man underwent LT in 2003 for hepatitis C (HCV) related cirrhosis and hepatocellular carcinoma and in 2004 for recurrence of his HCV. He developed pancytopenia in 2006 which was attributed to his pegylated interferon treatment for HCV. The peg-interferon dose was intitally decreased, later stopped entirely and erythropoietin was initiated. In January 2007, the patient presented to his hepatologist complaining of weakness, malaise, and shortness of breath. WBC was 3.47 x 1000/[mu]l, hemoglobin 10.6 gm/dL, Hct 33.8%, platelets 21 x 1000/[mu]l, and neutrophils were 1.61 x 1000/[mu]l. A liver biopsy revealed bridging fibrosis and recurrent hepatitis C. A bone marrow biopsy revealed myelodysplastic syndrome, type refractory anemia with excess blasts (RAEB)-1. He underwent 4 cycles of azacitidine from February to May 2007 with no improvement on repeat bone marrow biopsy in May 2007. Prograf dose was lowered and the patient underwent 3 cycles of decitabine. His last bone marrow biopsy done in November 2007 continued to show MDS, RAEB-1 with hypocellular marrow. The patient underwent 1 more cycle of decitabine without significant improvement in his laboratory testing.

Conclusion: This is only the second reported case of MDS occurring in a post-LT patient. Our patient developed MDS almost 2 years after his second LT, as compared to the previous report in which the patient developed MDS 3 months after LT with subsequent progression to acute myelogenous leukemia within 2 months of the MDS diagnosis. Our patient's MDS type carries a very poor prognosis and high likelihood of conversion to acute myelogenous leukemia. He was treated with chemotherapy and reduction in immunosuppression without a clinical response. Given the rarity of MDS after LT, further study is needed to optimize the medical management of these patients. Although rare, MDS should be considered in the evaluation of pancytopenia after LT.


Nan Sandar, MD*, Mahesh Krishnaiah, MD. Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Gastroenterology, Lutheran Medical Center, Brooklyn, NY.

Purpose: For prolonged enteral feeding, gastrostomy tubes (GT) are prefered over nasogastric tubes. Most of GT complications are minor but some can lead to significant morbidity and even mortality if not recognized early. We report a case of pancreatitis and cholecystitis secondary to migrated GT.

Methods: A 77 year old hispanic male with history of cerebrovascular accident had a GT inserted about 4 years ago. His GT was replaced with a balloon GT endoscopically about 8 months ago due to leakage around the tube. His GT was attended by a visiting nurse. He was admitted to our hospital with complaint of moderate to severe non-radiating epigastric pain associated with vomiting and leaking around the GT. Nasogastric tube was inserted and about 300 cc of greenish colored fluid was obtained. His vital signs were stable and he was afebrile. Physical exam revealed marked tenderness in the epigastrium and the GT was found to be migrated more than 10 cm into the stomach. His abnormal laboratory results were white blood cell count 17.3 x 10.sup.6/L, amylase 3249 IU/L, lipase 3007 IU/L, aspartate transaminase 214 IU/L, alanine transaminase 140 IU/L, and alkaline phosphatase 165 IU/L. He had normal triglyceride and bilirubin levels. Ultrasound of the abdomen revealed distended gall bladder with thickened wall and edema consistent with acalculus cholecystitis. Computed tomography of the abdomen confirmed the ultrasound findings. It also revealed peripancreatic inflammatory changes extending into anterior pararenal spaces and paracolic gutters. GT was seen in the second portion of the duodenum with its balloon significantly distended with air and fluid. The gastric antrum, pylorus and third and fourth portion of the duodenal wall were noted to be edematous and thickened. The GT balloon was deflated and the tube was repositioned. The patient's symptoms and laboratory values significantly improved the next day and became normal over the course of 3 days. There was no more leakage around GT.

Results: The patient tolerated his feeding and was discharged uneventfully.

Conclusion: Endoscopic enteral access for enteral nutrition in patients who are unable to maintain oral intake is an important tool in the armamentarium of the gastroenterologist. Even though GT is relatively safe, sometimes it can lead to severe life threatening complications such as pancreatitis and cholecystitis if GT is not handled well. Proper care of GT by trained persons is extremely important in order to prevent GT related severe complications. This reported case clearly proved that fact.


Neil Nagaria, MD*, Ankit Kansagra, MBBS, Sushil Ahlawat, MD. Gastroenterology, UMDNJ-NJMS, Newark, NJ.

Purpose: INTRODUCTION:Gastrointestinal involvement in schistosomiasis is well known; however, colon polyps associated with schistosoma are reported occasionally. To the best of our knowledge, colon adenoma associated with S. mansoni has not been reported.

Methods: CASE:A 64-year-old female was referred for colorectal cancer screening. She was asymptomatic and had a normal physical exam. However, her last laboratory test nearly 3 years ago had shown Hb level of 14.0 g/dl, and white blood cell count of 7300/mm.sup.3 with 8% eosinophils, which was not worked up. On colonoscopy, an 8 mm pedunculated polyp with a long stalk was seen in the ascending colon, along with a 1 cm sessile polyp in the sigmoid colon. Both polyps were removed by electrosurgical snare polypectomy technique. Histopathological examination revealed a tubular adenoma in which two discrete ova with chronic inflammation could be seen in the lamina propria. High power demonstrated the ova were oval in shape, one showing the characteristic lateral spine of Schistosoma mansoni, and both contained viable miracidia. Further history revealed the patient had lived in Liberia for most of her life where she had bathed and drank water from a lake. She was treated with praziquantel [20 mg/kg]. She continues to remain symptom free and her immigrated family members were recommended surveillance.

Results: DISCUSSION:Majority of Schistosoma mansoni remains an endemic in parts of Brazil, Venezuela, and Caribbean. During their life cycle, the larvae penetrate the skin, migrate to the lungs through venous circulation and mature into adult worms in the liver. They migrate to the mesenteric vessels of bowel or bladder where the female worms lay eggs. Eggs retained in the intestinal wall cause an inflammatory response leading to hyperplasia, ulceration, microabscess, and granuloma formation. Clinically they may present as colicky abdominal pain, change in bowel habits, or occult gastrointestinal bleeding. Only one report of colorectal polyposis associated with S. mansoni was found in the literature. The relationship between colorectal cancer and schistosomiasis is controversial. Some studies suggest an increased risk of colorectal cancer in patients with schistosoma egg induced polyps particularly those with atypical hyperplasia. The data on long-term outcome with and without praziquental treatment doesn't exist. We treated our patient in an effort to destroy any viable eggs.

Conclusion: This patient demonstrates how uncommon diseases are being seen frequently with an increase in migration. A keen vigilance should be kept on history, and labs which may suggest parasitic infection in an asymptomatic individual that comes for routine screening.


John Sotiriadis, MD, PhD*, Ankit Kansagra, MD, Kunal Grover, MD, Zamir Brelvi, MD, PhD. Division of Gastroenterology, Department of Medicine, University of Medicine and Dentistry of New Jersey - The University Hospital, Newark, NJ.

Purpose: Dieulafoy's lesion is an uncommon, but well recognized cause of life threatening bleeding in the gastrointestinal (GI) tract. Typically, Dieulafoy's lesions occur in the upper GI tract. However, due to increased awareness of this entity, Dieulafoy's lesions have gained the reputation as an unusual, but important cause of lower gastrointestinal bleeding.

Methods: We describe a case of a patient that developed a lower GI bleed due to a Dieulafoy's lesion of the cecum.

Results: A 41 year old female with HIV/AIDS was admitted with Pneumocystis jiroveci pneumonia. On the day of planned hospital discharge, the patient developed blood clots per rectum and an acute drop in hemoglobin, requiring transfer to the intensive care unit. On colonoscopy, despite bowel prep, there were numerous blood clots throughout the colon. In the cecal caput, there was a healed ulcer as well as a protuberant, visibly bleeding vessel that was likely the source of bleeding. A single hemoclip was deployed on the bleeding vessel and achieved good hemostasis. There was no further bleeding and the patient was subsequently discharged 10 days later.

Conclusion: Endoscopic diagnosis of extragastric Dieulafoy's lesions is difficult because of their rarity and small size. Early endoscopic evaluation during acute bleeding episodes is crucial. Hemoclipping has emerged as an effective treatment option at extragastric sites.


Neil Nagaria, MD*, Ankit Kansagra, MBBS, Sushil Ahlawat, MD. Gastroenterology, UMDNJ-NJMS, Newark, NJ.

Purpose: Bezoars are accumulations of food and fiber in the alimentary tract. We present a case of a patient with recurrent trichobezoar in which endoscopic removal was tedious, time consuming, and ultimately unsuccessful.

Methods: CASE:A 37-year-old female with medical history of hypertension and depression was admitted with nausea, vomiting and constipation for four days. It started 1 month ago with bloating, early satiety and weight loss of 40 pounds. Her medical history was significant for trichotillomania, and trichobezoar 18 months ago, which was removed successfully endoscopically over 2 days. On physical exam, she was of moderate built, malnourished, with a HR of 103 and BP of 156/91 mmHg. Scalp examination revealed sparse hair and red colored extensions that were missing in some areas. Abdominal exam was significant for mild epigastric fullness and tenderness on palpation. Labs were significant for a Hb of 10.4 g/dL. An abdominal radiograph showed a dilated loop of duodenum measuring 4.6 cm with mottled lucencies in the left upper quadrant. A CT confirmed a gastric bezoar within the stomach and small bezoars in the distal duodenum. She underwent upper endoscopy which showed a black hair bezoar. After spending 2 hours with multiple passes, less than 25% was removed and was referred for surgery. Two masses of hair 17 x 5 x 5 cm and 12 x 10 x 6 cm were removed via gastrotomy and a 6.5 x 3 x 3 cm was removed via ileal enterotomy.

Results: DISSCUSSION:The term "bezoar" comes from the Arabic "badzhar" or the Persian "pahnzahr", both meaning counterpoison or antidote. They are indigestible foreign body masses in the GI tract. They are classified into five types: phytobezoar, trichobezoar, pharmacobezoar, lactobezoar, and foreign body bezoars. Trichobezoar is seen in females less than 30 years of age. Ingestion of hair, (trichophagia), carpet, and clothing fiber are commonly implicated. They become trapped in the gastric folds forming a mass with symptoms of early satiety, weight loss, abdominal pain, and leading to obstructive symptoms. Plain radiographs and CT may be diagnostic, but endoscopy still remains the gold standard. Many approaches have been described such as enzymatic dissolution, to endoscopic removal with advanced instrumentation. Surgical removal via gastrotomy allows it to be removed in its entirety.

Conclusion: CONCLUSION:Our case suggests that although endoscopic advances have been made, and success has been accomplished by some, their superiority to conventional techniques is still lacking. Gastrotomy should be considered over the tedious and time consuming endoscopic attempts. More ever, the patient should have psychiatric follow up to prevent recurrence, which our patient did not have, after her first episode.


Ihab El Hajj, MD, MPH*, Jawad Ahmad, MD, MRCP (UK), Adam Slivka, MD, PhD. Internal Medicine-Division of Gastroenterology, Hepatology and Nutrition, Internal Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA.

Purpose: Introduction: Primary sclerosing cholangitis is characterized by inflammation of the bilary tree typically diagnosed at ERCP. A similar cholangiogram can be seen in patients with a rapidly progressive form of sclerosing cholangitis in the setting of pancreatic pseudotumor. We present a case of a 54-year-old man presenting with obstructive jaundice that illustrates the diagnostic challenge and opportunity for immunosuppressive treatment of this entity. Case: A 54-year-old man presented with painless jaundice and weight loss. CT scan revealed a 7 cm mass in the head of the pancreas. ERCP demonstrated a distal bile duct and pancreatic duct stricture. Percutaneous biopsy of the mass showed inflammatory changes but there was concern for pancreatic cancer. At surgery a large inflammatory mass of the pancreatic head was found and a cholecystojejunostomy was performed. Follow-up CT scan two months later showed complete resolution of the mass suggesting that it was due to focal pancreatitis. Several months later, he developed recurrent jaundice. ERCP showed diffuse biliary strictures with a dominant hilar stricture and biliary stents were placed. CT scan revealed portal adenopathy. Endoscopic ultrasound with needle aspiration of the lymph nodes and pancreatic head showed only atypical cells. Liver biopsy showed acute and chronic cholangitis and marked hepatocanalicular cholestasis. Ultrasound showed normal liver morphology and vasculature. Autoimmune serology and colonoscopy were normal. A diagnosis of secondary sclerosing cholangitis was considered. Because of the rapid progression and the presence of significant inflammation, a short course of steroids tapered over several months and methotrexate 15 mg weekly were initiated. Repeat cholangiogram several months later showed complete normalization of the biliary tree. Over the next five years, the patient was maintained on azathioprine 100 mg daily with normal liver enzymes. Upon tapering his azathioprine down to 50 mg daily he developed acute cholangitis. Repeat ERCP revealed sclerosing cholangitis. A short prednisone taper and azathioprine 75 mg daily resulted in a markedly improved stricture. The patient is currently doing well with normal liver enzymes, maintained on azathioprine 75 mg daily. Discussion: This case illustrates the potential for sclerosing cholangitis to develop after biliary bypass surgery in patients with pancreatic pseudotumor. The rapid development of biliary strictures and prompt response to immunosuppression suggest an immune-mediated etiology to this entity. This diagnosis should be entertained in patients with sclerosing cholangitis on cholangiogram in the setting of inflammatory conditions of the pancreas.


Ihab El Hajj, MD, MPH*, Shahid Malik, MD, Hany El-Wakeel, MD, Obaid Shaikh, MD, Eizaburo Sasatomi, MD, Hossam Kandil, MD, PhD. Pathology-Division of Transplantation Pathology, Internal Medicine-Division of Gastroenterology, Hepatology, and Nutrition, Internal Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA.

Purpose: Introduction: Selective COX-2 inhibitors are widely used because of their efficacy and good safety profile. Recent reports described varying degrees of liver injuries secondary to the use of COX-2 inhibitors. We present a unique case of Celecoxib-induced liver injury, which rapidly progressed to liver failure requiring liver transplantation. Case: A 52-year-old woman developed generalized aches one day after performing yard work. Over the next 48 hours, she took eight 200 mg tablets of Celecoxib. One week later, she presented to the ED with fatigue, loss of appetite, pruritus, 'coke' colored urine, and 10 pound weight loss. No history of alcohol intake, smoking, use of herbals, medications, or drugs. On PE, she was afebrile and jaundiced with mild RUQ tenderness. Lab studies revealed an absolute eosinophilic count of 760 with abnormal LFTs (Table 1). Repeat testing 2 weeks later revealed worsening LFTs (Table 1). Serologies for hepatitis were negative. Iron studies, autoimmune panel, and ceruloplasmin were normal. CT scan showed normal liver morphology and vasculature. Liver biopsy showed ductopenia and cholestasis with mild periportal fibrosis. The patient was started on ursodiol, and steroids for presumed drug induced liver injury (DILI). Two weeks later, the patient was admitted to the MICU because of somnolence and worsening symptoms. Repeated LFTs are summarized in Table 1. INR increased to 3.4 and bilirubin reached 51 mg/dL. She underwent orthotopic liver transplantion (OLTx), exactly 54 days after the initial ingestion of celecoxib. The postoperative course was uneventful. On follow-up visits at one and six months, the patient has remained well with normal LFTs (Table 1). Discussion: Celecoxib is a widely used COX-2 inhibitor. Six cases of celecoxib-induced liver injury have been reported in the literature: 5 cases of cholestatic hepatitis, and one case of mixed hepatocellular and cholestatic injury. Our patient developed cholestatic liver injury which rapidly progressed to liver failure. Given our patient's clinical presentation and evolution of the disease, a DILI caused by celecoxib is "probable" as confirmed by the RUCAM/CIOMS scoring system. The underlying mechanism of COX-2 inhibitors-induced liver injury is not clear. The main treatment of DILI is to discontinue the offending agent. The decision to take our patient for OLTx was based on the rapidly progressive deterioration of her clinical condition, worsening coagulopathy and hyper-bilirubinemia despite medical therapy, and the histological evidence of severe ductopenia.

Conclusion: Physicians should be aware that despite its better safety profile compared to conventional NSAIDs, celecoxib may be associated with severe fatal hepatotoxicity.

Laboratory values


Amjad Mreyoud, MD*, Shahid Mehboob, MD. Internal Medicine/Gastroenterology, VAMC/University at Buffalo, Buffalo, NY.

Purpose: A 57 year-old Caucasian male with previous history of cholecystectomy presented with two weeks history of generalized pruritus, jaundice, dark-colored urine and acholic stool associated with right upper quadrant abdominal discomfort, and anorexia. His clinical data showed a total bilirubin level of 25.4 mg/dL (0.1 to 1.0 mg/dL), alkaline phosphates level of 455 U/L (50 to 136 U/L), an Aspartate Aminotransferase (AST) level of 109 U/L (12 to 34 U/L) and Alanine Aminotransferase (ALT) level of 278 U/L (10 to 55 U/L). Abdominal CT scan demonstrated a low density lesion in the pancreatic head with dilated intra-hepatic and common hepatic ducts. ERCP revealed high grade distal CBD stricture with upstream dilation of common hepatic duct. A biliary stent was placed successfully through the stricture with drainage of colorless-transparent fluid "White bile". Brushings from the biliary stricture showed atypical cytology suspicious for malignancy. CA 19-9 was elevated 420 Units/mL (0-35 U/mL). PET scan demonstrated hyper metabolic lesion in the head of the pancreas with no evidence of metastases. Patient underwent surgical exploration with intent for Whipple's procedure but was found to have pancreatic head carcinoma with metastatic lesion to the surface of the liver. Therefore, surgery was aborted. He underwent Hospice care and expired three months later.

Results: White bile (WB) is a misnomer, referring to the translucent, colorless bilirubin - free fluid occasionally found in occluded bile ducts. The cause for the absence of the bile pigments, salts, or cholesterol in this "White bile" are not completely understood. WB was experimentally developed in a dog model when the common bile and the cystic ducts were ligated. In contrast "black" bile occurred when only the common bile duct was ligated leaving the gallbladder in communication with obstructed duct. Flow in the extrahepatic duct was assessed by the aid of radioiodinated human serum albumin. When "Black bile" was present, the direction of flow was from the extrahepatic ducts into the gallbladder. Whenever "white bile" developed, a reverse flow from the extrahepatic into the liver was observed. The pressure in extrahepatic ducts that contain white bile was higher than those filled with black bile. In the absence of the gallbladder and its water absorption activity, the colorless mucus secretion of the bile ducts seems to "back wash" into the liver and replaces the bile present in the ducts at the time of obstruction. The presence of "white bile" in patients with malignant obstructive jaundice underwent endoscopic biliary drainage is associated with more cholangitis after drainage and significantly less bilirubin, total bile acid and median survival.


Mukund Venu, MD*, Samer Gawrieh, MD, Kia Saeian, MD. Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI.

Purpose: To present an unusual case of acute hepatotoxicity caused by toluene.

Methods: A 21 year old male presented with a 3 week history of jaundice and worsening itching. He noticed dark urine and increased fatigue. He had no history of drug or alcohol abuse. On exam, the patient had scleral icterus, but no hepatomegaly, ascites, abdominal tenderness or stigmata of cirrhosis. Blood chemistries were abnormal: ALT (1496 U/L), AST (878 U/L), total bilirubin (8.8 mg/dl), alkaline phosphotase (132 U/L). CBC, PT/INR, albumin, and ammonia levels were within normal limits. Serologies for Hepatitis A, B, and C were negative. ANA, ASMA and anti-LKM were also negative. Serum ceruloplasmin was normal. 24 hour urine copper was slightly elevated (84 mcg/24 hour). Testing for ATP7B mutation for Wilson's disease was negative. Abdominal ultrasound was normal. The patient's liver enzymes and bilirubin continued to rise.

Results: Liver biopsy was performed and revealed necrotic hepatocytes and inflammation consistent with drug toxicity. The biopsy was negative for fibrosis as well as iron and copper staining. Additional history revealed that the patient had recently moved to his sister's basement and was applying weather-proofing caulk containing toluene on the windows without using mask or gloves. In the absence of other potential etiologies, it was felt that toluene toxicity was the likely cause of his hepatitis. Cholestyramine was prescribed for itching and the patient was advised to move out of the basement. At his one month follow-up, the jaundice had resolved and liver tests showed continued improvement.

Conclusion: We believe this to be an unusual presentation of acute toluene exposure resulting in hepatotoxicity. Our patient exposed himself to the weather-proofing caulk containing toluene without proper protection during application, and inhaled the solvent while living in the basement. Industrial use of toluene is on the rise. Intentional inhalation of glues, paints, and solvents makes toluene one of the most abused hydrocarbon compounds. The primary route of toluene exposure is via inhalation, and peak concentration in the blood occurs 15 to 30 minutes after inhalation. Nearly 80% of absorbed toluene is oxidized in the liver. Aromatic hydrocarbons are converted by microsomal enzymes in the liver to alkylating agents which produce hepatic necrosis by bonding with tissue macromolecules. Aside from liver injury, they can cause CNS depression, bronchospasms, and cardiac dysrhythmias. The management consists of preventing exposure to aromatic compounds and supportive measures.


Ihab El Hajj, MD, MPH*, Mohamad Hawchar, MD, Assaad Soweid, MD, Karim Maasri, MD, Ayman Tawil, MD, Kassem Barada, MD. Internal Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, Pathology & Laboratory Medicine, Internal Medicine-Division of Gastroenterology, Hepatology, and Nutrition, American University of Beirut Medical Center, Beirut, Lebanon.

Purpose: Introduction: Fundic gland polyps (FGPS) are the most common gastric polyps. They are usually small in size, sporadic and asymptomatic. We present a unique case of "giant" fundic gland polyp. Our case is particular because of the clinical presentation, the endoscopic and endosonographic documented features. Case: A previously healthy 63-year-old man was referred for evaluation of borderline microcytic anemia (Hb 12.9 g/dl, MCV 79 fl, serum iron 34 [mu]g/dl) and positive stool occult blood test. Physical exam was unremarkable. Colonoscopy was normal. EGD showed a sessile, broad-based, smooth-surfaced polyp, similar in color to the surrounding mucosa and extending around 8 cm (with a width of 2 cm) from the cardia along the lesser curvature with two small satellite polyps (Fig. 1). Multiple biopsies confirmed the diagnosis of fundic gland polyp. Heliobacter pylori (HP) was negative. EUS revealed a wide-based, large, predominantly hypoechoic polyp that involved the mucosa without reaching the submucosa or muscularis propria (Fig. 2). Small intestinal series test was normal. Treatment was conservative and the patient was started on iron supplementation. He was re-evaluated at 3 and 8 months. He remained asymptomatic. Repeat laboratory studies showed normal CBC and iron studies, but stool occult blood was positive on 3 occasions. A repeat EGD and EUS confirmed the previous findings. Biopsies from the polyp were unchanged, and biopsies of the surrounding mucosa revealed mild chronic active gastritis with rare HP-like organisms for which the patient received eradication therapy. Discussion: FGPs account for about 47% of all gastric polyps. They are usually asymptomatic. They have distinct endoscopic features, and usually measure less than 5 mm in size. Six cases of giant gastric polyps have been reported in the literature, one of them only was a FGP. The diagnosis of FGPs is usually established by pathology and inflammatory changes in the surrounding mucosa are usually absent. EUS helps to describe the endosonographic features and confirm the superficial nature of the polyp. The natural history of FGPs is still unclear and there are no guidelines for surveillance and treatment. In our patient, the polyp is most likely the cause of positive stool occult blood. The question whether to remove such a giant polyp by endoscopic mucosectomy or surgical resection or to observe remains debatable, although keeping it imposes negligible harm.


Parminder Sidhu, MD*, Leelavathi Kasturi, MD, Deepak Mahajan, MD, Adam Moskowitz, MD, Henry Safier, MD, FACP. Internal Medicine, Mount Sinai School of Medicine at Queens Hospital Center, Jamaica, NY.

Purpose: Amyloidosis is common in multiple myeloma; however, extensive gastrointestinal tract involvement without involvement of other organ systems is extremely rare. We are describing a case of gastroparesis and gastrointestinal bleeding associated with kappa light chain multiple myeloma. A 55 year old female with kappa light chain multiple myeloma and a fourteen month history of chemotherapy, was admitted with complaints of nausea, vomiting, and rectal bleeding of five days duration. Five months prior to admission, patient had a gastrointestinal work-up because of recurrent vomiting and guaiac positive stool, which revealed gastritis and internal hemorrhoids. The patient had type II diabetes mellitus, without diabetic triopathy and hemoglobin A1c was less than 6. Patient did not have a history of renal failure or thyroid disease. Echocardiography was negative for any signs of cardiac amyloidosis. On physical examination, she was lethargic and appeared cachectic. She had bibasilar crackles and diminished breath sounds in right lower lobe. The patient had 2 + pitting edema in the lower extremities. Laboratory data were within normal range except for hemoglobin of 7.8, with a drop from 8.8 one week prior to admission. Gastroparesis was confirmed on gastric scintigraphy (nuclear gastric emptying study). Friable gastric mucosa with active oozing of blood was noted on upper endoscopy. Bleeding was controlled with injection of submucosal epinephrine and gold probe therapy. Due to persistent nausea and vomiting, a second upper endoscopy was done and revealed edematous mucosa of pylorus and several regions of submucosal bleeding. There was no evidence of gastric outlet obstruction. Antral and pyloric biopsies revealed active gastritis with submucosal pink material and special stains for amyloid were positive. Patient was treated with metoclopramide and intravenous erythromycin and was discharged home on regular diet.

Conclusion: Amyloid is a fibrous protein with local extracellular deposition that can involve any organ system and present with or without clinical manifestations. Our patient's chronic anemia is multifactorial including components of multiple myeloma and chronic gastrointestinal bleeding secondary to amyloidosis. Gastroparesis is common in familial amyloidotic polyneuropathy but infrequent in patients with kappa light chain multiple myeloma.


Ritu Saha, MD*, Robert Bonasera, MD, Kavita Kongara, MD. Gastroenterology, Hepatology, and Nutrition, Winthrop University Hospital, Mineola, NY.

Purpose: Rumination Syndrome is a highly under-diagnosed entity in the adult population which can be attributed to lack of awareness of the condition.

Methods: A 41 year-old man presented with complaints of vomiting 10-30 minutes after meals for three years. Past history included SLE and sleep apnea. The patient had had an extensive workup consisting of CT scans (head and abdomen), upper endoscopy, push enteroscopy, colonoscopy and a gastric emptying scan; none of which explained his symptoms. He had also undergone a "celiac release" procedure one year prior without sustained relief. Systemic steroids for SLE enteritis did not alleiviate the symptoms. Physical exam and laboratory data were unremarkable. A detailed history revealed that our patient suffered from vomiting without antecedent nausea, retching, weight loss, abdominal pain, or altered bowel habits for three years. He would often re-chew and re-swallow the vomitus.

Results: Given the clinical scenario and lack of findings on multiple radiological and invasive tests, rumination syndrome was diagnosed. This syndrome, also termed mercyism is defined as regurgitation of partially digested food particles, followed by expulsion or reswallowing with or without rechewing. Typical clinical features are adequate for diagnosis without extensive testing. Features include repetitive, effortless regurgitation of gastric contents within minutes of every meal. Regurgitation is not preceded by nausea. Mild weight loss and postprandial gastroesophageal reflux may be witnessed. Though the mechanism is unclear, it is accepted in pediatric and adult literature that no abnormalities in the structure or motility of the GI tract exist. Many have suggested that regurgitation is triggered by the Mueller Manuever which is a forced inspiration against a closed glottis. Manometric studies in ruminators have revealed spike waves corresponding to increased intra-abdominal pressure and relaxation of the lower esophageal sphincter but is not necessary to make the diagnosis. Psychological factors have also been suggested. Despite the benign nature of rumination syndrome, significant functional disability occurs secondary to frequent visits to physicians and hospitalizations in search for a diagnosis. Though there is no efficacious medical treatment yet, realizing its higher than recorded prevalence is the first step towards finding a cure. The best approach thus far has been patient education and behavioral modification, neither of which can occur without the diagnosis.

Conclusion: Patients with Rumination Syndrome usually present to multiple internists, gastroenterologists, and hospitals in search of their diagnosis. This report highlights the importance of a thorough history in an often-overlooked diagnosis.


Hui Hing Jack Tin, MD*, Kadirawel Iswara, MD, FACG, Jianjun Li, MD, FACG, Scott Tenner, MD, MPH, FACG. Internal Medicine - Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Plummer-Vinson syndrome is a rare disease characterized by iron deficiency anemia and esophageal "webs". The disorder is little understood and treated with esophageal web dilatations and iron supplementation. Celiac disease is characterized by gluten sensitivity resulting in atrophy and flattened villi in the small intestine, resulting in iron deficiency anemia, and malabsorption. Although previously shown to be associated diseases, the underlying nature of the relationship is unknown. We present a patient with both disorders who had a resolution of both disorders when avoiding a gluten free diet.

Methods: A 53 yo female with history of dysphagia and iron deficiency anemia presented for evaluation. She reported to occasional feelings of having food stuck in her throat when eating meat for the last year. She denied any diarrhea, weight lost, nausea or vomiting. There were no prior hospitalizations or surgeries. There were no medications. Physical examination was unremarkable. Laboratory analysis was remarkable for hematocrit: 30.5%, MCV: 73, serum iron: 25, iron saturation: 8%, TIBC 328, Anti-TTG >1:640. Upper endoscopy was performed, revealing a mid-esophageal web and atrophic appearing duodenum. Duodenal biopsies revealed subtotal to total villous flattening.

Results: The patient was placed on a celiac-free diet, iron supplements and repeat blood test three months later showed resolution of the anemia, hematocrit of 38%. A repeat endoscopy 1 year later demonstrated complete resolution of the esophageal web.

Conclusion: We suggest that patients with Plummer-Vinson syndrome without severe dysphagia and celiac disease be managed conservatively with direct treatment of the underlying Gluten enteropathy. This case suggests that Plummer-Vinson Syndrome may be a manifestation of Celiac disease.


Hui Hing Jack Tin, MD*, Anita Torok, MD, Yarnel Lafortune, PA, Scott Tenner, MD, MPH, Pratap Gadangi, MD. Surgery, Coney Island Hospital, Brooklyn, NY, Internal Medicine - Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Anorectal Tuberculosis is a rare clinical variant of mycobacterium tuberculosis infection, once known as tuberculosis cutis orificialis. Patients often respond to anti-tuberculin therapy. Though uncommon, anal squamous cell carcinomas are often diagnosed by gross inspection of the anal canal, followed by biopsy confirmation and radiation therapy. Though treatment is markedly divergent, the clinical appearance of the two disorders is similar.

Methods: a 54 yo Pakistani gentlemen who presented initially to the primary care physician with complaints of an anal-rectal ulcer with pus and bleeding noted on defecation for 2-3 months. The patient denied any fever, chills, hemoptysis, diarrhea, constipation, abdominal pain, or weight lost. He denied any prior pulmonary disease, and had never undergone a screening colonoscopy. The patient had been in the United States for more than 20 years but visited Pakistan often. His last PPD was 2 years prior and negative. There were no prior hospitalizations or surgeries, no medications. There was no alcohol, tobacco or illicit drug use. Physical examination was significant for a fleshy linear ulceration at right posterior region of the anus.

Results: Colonoscopy and small bowel series to rule out Crohn's disease and other colorectal involvement was normal. Multiple biopsies were taken of the ulcerated site which was limited to the anal canal. Biopsy revealed granulomas and acid fast bacilli identified as mycobacterium tuberculosis. Subsequently patient was sent to pulmonary clinic where a PPD was read as 20 mm induration and chest x-ray showed RLL infiltration. The patient was started on four drug tuberculosis regimen. Within 4 weeks, cutaneous and pulmonary findings resolved.

Conclusion: Although tuberculous anorectal ulcer is rare, especially in the United States, this case shows the importance of considering the diagnosis in persons presenting with these findings, especially immigrants from endemic areas.


Ritu Saha, MD*, Timothy Wong, MD. Gastroenterology, Hepatology, and Nutrition, Winthrop Univ Hospital, Mineola, NY.

Purpose: Pylephlebitis is a rare complication of certain inflammatory processes in the gastrointestinal tract and often pose many challenges for gastroenterologists.

Methods: A 54 year-old man presented with a 1 week history of epigastric pain, fevers, and decreased appetite. He had a history of diabetes mellitus, hypertension, hyperlipidemia, peripheral vascular disease and moderate alcohol use in the past. Admission vitals were BP 114/71 mmHg, pulse of 133/min and temperature of 101F. Exam revealed jaundice, distended and diffuse abdominal tenderness with a positive Murphy's sign. Labs included wbc 17.6 K/uL, albumin 4.2 gm/dL, INR 1.35, total/direct bilirubin 5.7/4.3 mg/dL, alkaline phosphatase 154 IU/L, with normal transaminases. HIDA scan showed decreased hepatic uptake consistent with hepatic dysfunction without cystic duct obstruction. Abdominal CT scan showed sigmoid diverticulitis with a pericolic collection and thrombosis of the left portal vein. No thrombosis was seen in the mesenteric veins. The diverticulitis was treated with meropenem. The total bilirubin increased to a peak of 9.7 mg/dL and INR at 1.57 over the next 3 days. Anticoagulation therapy was initiated on day 3. Leukocytosis and fevers resolved by day 4 and oral feeding was started on day 5.

Results: Based on clinical symptoms and radiologic findings of sigmoid diverticulitis and portal vein thrombosis (PVT), pylephlebitis was diagnosed. Pylephlebitis, also known as infective suppurative thrombosis of the portal system, is a rare complication of intra-abdominal processes such as diverticulitis, appendicitis or inflammatory bowel disease. Significant controversy surrounds the benefit of anticoagulating these patients. Literature suggests that only patients with a malignancy, clotting factor deficiencies, or mesenteric vein involvement should be anticoagulated. We initiated heparin because of worsening hyperbilirubinemia and witnessed gradual hepatic function normalization. Another challenge was the timing of initiating oral nutrition since enteral nutrition may stimulate portal vein flow, further exacerbating the PVT. Oral feedings were started on day 5 without any complications. To the best of our knowledge, there is no previously published data on the issue of feeding in patients with pylephlebitis. Our patient's favorable course and prompt recovery provides anectodal evidence that enteral feeding is not contraindicated in this condition.

Conclusion: We present a rare case of pylephlebitis in which diverticulitis caused significant hepatic dysfunction due to a left portal vein thrombus. The issues of anticoagulation and enteral feeding are addressed. We believe that given the right clinical setting, enteral feeding can be started early with favorable results.


Truptesh Kothari, MD, MS*, Mark Korsten, MD, Shivangi Kothari, MD, Thomas Schiano, MD. Internal Medicine, J.J. Peters VA Medical Center, Bronx, NY, Liver Transplant, Mount Sinai School of Medicine, New York, NY, Gastroenterology, St. Joseph's Regional Medical Center, Paterson, NJ.

Purpose: Liver transplantation (LT) has been the curative therapy for patients with Caroli's disease (CD) having recurring episodes of cholangitis, sepsis and biliary stone formation. There have been no reported cases on the recurrence of intrahepatic bile duct complications in patients with CD who underwent LT. We report a patient with CD who developed a recurrence of intrahepatic biliary dilatation and stricture formation 12 years post - LT.

Methods: A 49 year old female was diagnosed with CD in 1992. She had right upper quadrant pain, cholestatic liver disease and was found to have intrahepatic ductal dilatation without portal fibrosis but associated with bilateral multiple renal cysts. She underwent LT with Roux-en- Y anastomosis in 1995 after having recuurent cholangitis with septicemia. In 1999, patient presented with elevated alkaline phosphatase and CT abdomen revealed moderately dilated intrahepatic ducts, patent hepatic-portal veins and a normal common bile duct- CBD. In 2007, she presented with cholangitis and cholangiogram showed a stone in the left bile duct with progressive intrahepatic biliary dilatation. The patient underwent PTC with stent placement followed by stone removal. Since then, the patient has had 2 episodes of right upper quadrant pain with elevated alkaline phosphatase, the last being in 03/2008. On both occasions, the patient underwent PTC with stent exchange and the symptoms improved. Recent abdominal MRI is suggestive of worsening of intrahepatic biliary dilatation with no evidence of biliary mass. CA 19-9 always remained normal. The worsening progression of intrahepatic biliary dilatation leading to recurrent hospitalizations for cholangitis has led to the consideration of retransplantation.


Conclusion: Caroli's disease (CD) is a nonobstructive segmental dilatation of the intrahepatic bile ducts. Most common variant, Caroli's syndrome involves bile duct dilatation with hepatic fibrosis. Women are predominantly affected; the average age at diagnosis is 22 years. The diagnosis is established by USG, ERCP and MRCP that demonstrate intrahepatic biliary dilatation with a normal CBD. Medical treatment includes antibiotics for bacterial cholangitis and ursodiol for prevention of bile stone formation. LT is successful with high survival rate for 5 year of 90% and 10 year survival rate of 78%. Patients with Caroli's syndrome due to portal fibrosis develop portal hypertension requiring the need for LT. Most patients with Ischemic-related injury present with complaints within the first 6 months of LT. Another possibility could have been the PKHD1 gene mutation causing the recurrent biliary complications. The etiology for recurrent bile duct complications post LT in our patient after 12 years is unclear.


Richard Blatt, MD*, Nikrad Shahnavaz, MD, Tanvi Dhere, MD, Marney Goldstein, MD. Emory University, Atlanta, GA.

Purpose: A 37-year-old impoverished African-American male with a history of hemophilia A presented with complaints of two months of right upper quadrant abdominal pain, nausea, night sweats, and low grade fevers. Abdominal exam revealed a tender right upper quadrant. Labs were unremarkable. A right upper quadrant ultrasound revealed a thickened gallbladder wall and gallstones consistent with cholecystitis, which led to a cholecystectomy. There was no evidence for peritoneal tuberculosis intraoperatively. However, the pathology report of the gallbladder revealed caseating granulomas containing acid fast bacilli (AFB) consistent with a diagnosis of tuberculosis. The patient's PPD, HIV test, chest X-ray and sputum AFB were all negative. Post-operatively the patient showed an improvement in symptoms and was discharged two days later and referred for tuberculosis treatment. Tuberculosis (TB) has changed its face recently due to increasing numbers of HIV infections, poverty, and migration. Very few cases of gallbladder tuberculosis (GT) have been reported. A correct preoperative diagnosis of GT is rare, and it can mimic other gallbladder diseases. GT often occurs in women over 30 years of age and can present with cystic duct obstruction and gallstones. The route of infection may be peritoneal, hematogenous or lymphatic. GT may present with symptoms such as abdominal pain, weight loss, fever, nausea, vomiting or a palpable abdominal mass. Anemia, elevated ESR, and positive tuberculin tests are usually found during laboratory examination. In most reported cases the chest X-rays were normal. The abdominal ultrasound and computed tomography scan findings may also show a gallbladder mass, dilated gallbladder, thickened gallbladder wall, ascites, biloma or abdominal lymphadenopathy. However, these finding are not specific for GT. The correct diagnosis of gallbladder tuberculosis is usually made after a cholecystectomy. However, with a high index of suspicion, aspiration cytology of tuberculomas or percutaneous drainage of bile with culture could confirm the diagnosis of GT in some patients without surgery. This case demonstrates the need to consider GT in patients with known TB or high risk patients with symptoms consistent with gallbladder disease.


Nison Badalov, MD*, Ian Wall, DO, Jack Braha, DO, Konstantin Vaizman, MD, Jianjun Li, MD, FACG, Kadirawel Iswara, MD, FACG, Scott Tenner, MD, MPH, FACG. Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Although iatrogenic colon perforation is uncommon, it is a feared and possibly life threatening complication of colonoscopy. Traditionally, colon perforations have been managed by surgery. We report a case of an iatrogenic colon perforation managed endoscopically by closing the defect with endo-clips.

Methods: A 51-year-old gentleman underwent a screening colonoscopy. The colon was well prepped without any residual stool, and 4 right sided colon polyps (less then 1 cm each) were removed by snare polypectomy. During withdrawal, a 2 cm laceration of the sigmoid colon with visualization of mesentery and small bowel was noted. The defect was immediately closed with three Resolution Endoclips (Boston Scientific).

Results: Following the procedure, the patient denied abdominal pain nor developed peritoneal signs or fever. Urgent abdominal X-ray revealed free air under the diaphragm. A surgical consultation was obtained. The patient was made NPO and started on intravenous fluids and antibiotics. As the patient remained asymptomatic, clear liquid diet was initiated 48 hours after the procedure. The presence of increased amounts of peritoneal air on a follow-up abdominal x-ray on day 3 prompted a computed tomographic (CT) scan with oral contrast to rule out a colonic leak at the site of the perforation. No leak was appreciated on CT scan. The patient's diet was advanced. He was discharged on the day 4 of the hospital stay and remains well.

Conclusion: Although iatrogenic colon perforations have been managed by surgery, this approach is costly, invasive, and carries a risk for a wide range of complications. This case llustrates that the immediate use of endoscopic clips during colonoscopy may be a safe and effective, less invasive approach to treating iatrogenic perforations.


Nison Badalov, MD*, Ava Anklesaria, MD, Anita Torok, MD, Ian Wall, DO, Jack Braha, DO, Jianjun Li, MD, FACG, Kadirawel Iswara, MD, FACG, Scott Tenner, MD, MPH, FACG. Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Although gallstones and alcohol are the most common causes of acute pancreatitis (AP) world-wide, parasites such as ascariasis have been shown to be an important cause in other parts of the world.

Methods: We present a case of a patient recently emigrating from Asia found to have a rare parasitic infection causing biliary sepsis in a patient with AP.

Results: A 33 year old gentleman presented with a 2 day history of nausea, vomiting, fever, and epigastric pain-which was described as burning and radiating to the RUQ. The patient denied any medical or surgical history, or history of alcohol use. The patient was born and raised in Uzbekistan (former USSR), and moved to the U.S. 2 months prior. Vital signs at admission were significant for a fever of 38 C, and heart rate of 115 beats per minute. Significant findings on physical exam were scleral icterus, and RUQ tenderness. Laboratory findings on admission included a WBC of 16,000/mm3 with a differential including eosinophilia of 11%. Liver enzymes (LFT) were elevated with AST of 282 u/l (range 1-37), ALT of 319 u/l (range 1-40), total bili of 5.4 mg/dl (range 0-1.0), direct bili of 3.8 mg/dl (range 0-0.3) and alk phosphatase of 319 u/l (range 39-120). Serum amylase and lipase were elevated at 636 u/l (range 0-131) and 155 u/l (range 1-52), respectively. Serum calcium and triglyceride levels were normal. Ultrasound findings included thickened gallbladder wall, normal common bile duct (CBD) and no gallstones or sludge was appreciated. As the patient remained febrile with persistently abnormal LFT's, ERCP was performed. ERCP revealed mild intra and extra hepatic biliary dilatation with filling defects in the mid CBD. Sphincterotomy was performed followed by balloon sweep of the CBD. A motile, flat, brown, leaf like parasite was retrieved and sent for pathology. Fasciola hepatica was identified. Triclabendazole was initiated, and the patient rapidly improved and remains well.

Conclusion: Manifestations of human fascioliasis depends upon the stage and intensity of the infection. Fasciola hepatica has rarely been shown to cause AP. This case demonstrates the classic presentation of biliary sepsis complicating AP. Clinicians must consider fasciola in the differential diagnosis of AP in patients emigrating from endemic countries, especially Central Asia.


Subhra Banerjee, MD*, Aaron Walfish, MD, Vivek Gumaste, MD, Maria Angelova, MD. Gastroenterology, Mount Sinai Services at Elmhurst Hospital Center, Elmhurst, NY, Pediatrics, Winthrop University Hospital, Mineola, NY.

Purpose: Lymphomas may appear in the colon as primary malignancy or as a part of systemic disease. The incidence of this tumor is increasing, and its presentations are varied. Knowledge of the forms of presentation is therefore important in order to suspect the disease and reach an early diagnosis. Additionally, colonic lymphoma often requires a multidisciplinary treatment approach. We present a case that illustrates these points.

Methods: A 59 years old male was admitted with a chief complaint of left sided dull, non-radiating abdominal pain associated with 20 lbs of weight loss over the last 2 months. On physical examination, his abdomen was soft with normal bowel sounds and mild tenderness in the left lower quadrant without any rebound. A firm mass with an irregular margin, about 10 x 12 cm in size was palpable in left lower quadrant of the abdomen. Rectal exam was positive for fecal occult blood. All laboratory tests including CBC were normal. He had had an unremarkable screening colonoscopy about 18 months prior to this visit. CT scan of abdomen showed an 8 x 17 cm lobulated irregular soft tissue mass in left lower quadrant arising from the descending colon. A colonoscopy showed a 15 cm long circumferential, ulcerated, friable, nearly obstructing lesion in the descending colon 60 cm from the anal verge. The biopsy findings, negative for cytokeratin and CD 117 and equivocal for CD45, were suspicious for lymphoma, although not conclusive. The patient underwent surgical resection of the tumor.

Results: Histopathological examination of surgical specimen confirmed the diagnosis of large B cell lymphoma. Margins of the resected colon and adjacent lymph nodes were tumor free. The patient was started on adjuvant chemotherapy with R-CHOP regimen. At six months the patient has not shown any evidence of recurrence of his disease.

Conclusion: Primary colonic lymphoma is a rare entity. We found our case unique because of the large size of tumor, the rapidity of growth and the lack of traditionally described risk factors for the development of lymphoma. Our case illustrates that treatment involving a multi-disciplinary approach including surgery and chemotherapy is considered ideal.


Nayantara Coelho-Prabhu, MD*, Patrick Kamath, MD. Gastroenterology, Mayo Clinic Rochester, Rochester, MN.

Purpose: Granulomatous diseases including sarcoidosis are an unusual cause of pre-sinusoidal portal hypertension. We present a case of a patient with both Hepatitis C and sarcoidosis who had significant improvement in portal hypertension following steroid therapy.

Methods: A 51 year old Caucasian woman was diagnosed in 2001 with chronic Hepatitis C during a workup for elevated liver enzymes. She was offered treatment with interferon and Ribavirin but she refused. In 2002, she developed peripheral edema, severe anemia, grade 2 esophageal varices and significant splenomegaly. A liver biopsy showed grade 2 hepatitis with stage 3 fibrosis. In 2004, she developed jaundice for the first time and had worsened splenomegaly with secondary pancytopenia. She had gastric varices and grade 3 esophageal varices which required banding. She had never developed encephalopathy. She was offered a TIPS procedure and splenectomy but she came to our institution in 2005 for a second opinion. Laboratory studies showed pancytopenia, mildly elevated liver enzymes, normal albumin and INR. Contrasted CT scan showed extensive abnormal lymphadenopathy in the abdomen, massive splenomegaly, extensive portosystemic varices, mild ascites, normal appearing liver and a spontaneous spleno-renal shunt. Her previous biopsy was reviewed at our institution and showed multiple large granulomas consistent with sarcoidosis along with stage 3 fibrosis. Transjugular liver biopsy was repeated and confirmed the findings. Hepatic venogram showed a hepatic venous pressure gradient (HVPG) of 19 mmHg. Serum angiotensin converting enzyme level was normal. Bone marrow biopsy showed hypercellularity with no evidence of lymphoma. A diagnosis of portal hypertension secondary to sarcoidosis of the liver was made because the fibrosis in the liver was not considered advanced enough to explain the severity of portal hypertension.

Results: Prednisone 60 mg a day was started to treat the sarcoidosis and was slowly tapered. Six months later, a repeat hepatic hemodynamic study showed HVPG of 7 mmHg, while still on Prednisone 20 mg a day. CT showed resolution of ascites and repeat endoscopy showed no esophageal or gastric varices. In one year, HVPG decreased further to 5 mmHg. Currently, she is on Prednisone 2.5 mg a day without any further worsening of her portal hypertension.

Conclusion: This is a patient with non cirrhotic stage Hepatitis C who had portal hypertension out of proportion to her chronic viral liver disease. She was found to have extensive sarcoidosis in the liver which ultimately was treated with steroids and the portal hypertension resolved. This report supports the use of steroid therapy in patients with sarcoidosis who have portal hypertension.


Erika Madrigal, MD*, Matthew Tsushima, MD, Wichit Srikureja, MD, Ronald Griffin, MD, Christian Jackson, MD. Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA, Gastroenterology, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA.

Purpose: Most cases of multiple cancers with esophageal adenocarcinoma are associated with head and neck cancers or gastric cancers. We report a rare case of synchronous esophageal and pancreatic adenocarcinoma.

Methods: A 59-year-old Caucasian male with a history of alcohol abuse and a 40-pack year smoking history presented with a chief complaint of severe epigastric abdominal pain, anorexia, and a 25-pound weight loss over 6 months. On admission, he was afebrile and in mild distress. Physical examination revealed tenderness to palpation in the mid-epigastric region. Laboratory examination revealed a total bilirubin 3.4 mg/dL [0.2-1.2 mg/dL], direct bilirubin 2.1 mg/dL [0.0-0.3 mg/dL], alkaline phosphatase 708 IU/L [50-136 IU/L]. Abdominal CT scan showed intrahepatic biliary dilatation, common bile duct 1.5 cm in diameter, and mild pancreatic duct dilatation, with no obvious abnormal density or enhancing lesion in the pancreas. Bilateral adrenal gland masses, 3.5 cm on the left, 2.6 cm on the right, were also noted. EGD showed a circumferential mass in the distal esophagus, extending from 35 to 40 cm from the incisors. Biopsies revealed poorly differentiated adenocarcinoma. A subsequent EUS showed that the esophageal mass extended through the muscularis propria. In addition, a 9.1 x 6 mm hypoechoic left lobe liver nodule, a 2.5 x 1.6 cm left adrenal mass involving the body and tail of the pancreas with upstream ductal dilatation, and a 2.3 x 1.9 cm mass in the head of the pancreas were observed. FNA of the pancreatic body mass and celiac node showed malignant cells consistent with adenocarcinoma. Ascitic fluid obtained during the EUS showed reactive mesothelial cells.

Results: ERCP revealed a stricture in the head of the pancreas and a 2 cm distal common bile duct stricture with marked dilation of the proximal bile duct. A 10 x 40 mm metal biliary stent was successfully placed across the stricture. An EGD followed with successful placement of a covered 10 cm esophageal stent. The patient was referred for palliative chemoradiation followed by systemic chemotherapy. However, the patient and his family opted for hospice care. He died two months later.

Conclusion: In order to be considered synchronous secondary to a dual primary source, each cancer must appear malignant and distinct. In addition, the probability of one being a metastatic lesion of the other must be excluded. Although a distinction may be based on histology, as CA 19-9 stain is very specific for pancreatic cancer, up to 55% of esophageal adenocarcinomas will stain for CA 19-9 as well. This patient was considered to have two primaries due to the location of the mass in the head of the pancreas, which is the usual presentation for a primary pancreatic tumor.


Martin Moehlen, MD, MPH*, John Hutchings, MD, Kenneth Paris, MD, Stephen Abshire, MD, FACG. Internal Medicine, Section of Gastroenterology, Internal Medicine, Tulane University School of Medicine, New Orleans, LA, Department of Internal Medicine, Division of Allergy/Immunology, LSU Health Sciences Center and Jeffrey Modell Foundation, New Orleans, LA.

Purpose: Introduction: We report a newly diagnosed thymoma in a patient with recurrent candidal esophagitis.

Methods: Case Presentation: A 60 year-old white woman presented to her gastroenterologist for evaluation of dysphagia to solid foods. There was no personal history of diabetes mellitus, HIV, scleroderma, achalasia, recent use of glucocorticoids or antibiotic use. Physical exam was unremarkable. EGD examination revealed Candidal esophagitis. A CBC was noted for lymphopenia prompting a detailed immune evaluation. This evaluation revealed normal numbers and percentages of CD4 and CD8 T cells, serum chemistries, thyroid function, quantitative immunoglublins, CRP and ESR. ANA was weakly positive. TTG and Gliadin antibody were normal. HIV testing was negative. Delayed hypersensitivity testing showed anergy to Candida species. Chest CT showed an anterior mediastinal mass suspicious for thymoma. A stage II thymoma was subsequently removed. Her post-operative course has been complicated with recurrent candidal esophagitis and new onset myasthenia gravis.

Results: Discussion: Esophageal candidiasis may present with substernal pain, dysphagia, odynaphagia or often, without any symptoms at all. The finding of esophageal candidiasis should warrant an investigation for an underlying etiology (Table). A thorough history and physical should be sought. Routine laboratory tests should be ordered to rule out common predisposing diseases for candidal esophagitis, such as diabetes and HIV. In our patient the history did not reveal any past infections. A review of her medication list was noted only for a previous course of acid suppression therapy for her peptic ulcer disease. Her physical exam did not reveal any stigmata of mucocutaneous candidiasis. EGD revealed normal structure. Routine laboratories ruled out HIV, diabetes, and endocrinopathies; however, CBC showed lymphopenia. The immunologic evaluation suggests an underlying T cell defect, as the patient had normal numbers of T cells and quantitative immunoglobulins, yet an anergic response to delayed hypersensitivity testing to Candida. Part of the work up in evaluating a patient with obvious thymocyte defect is a chest CT to rule out thymoma, as confirmed in this case.

Conclusion: In summary esophageal candidiasis is normally related to a predisposing condition. The clinician generally should identify first whether one is immunocompetent or immunodeficient. In the immunocompetent individual, medications should be considered and structural abnormalities of the esophagus should be ruled out. Classifying a patient as immunodeficient may not be as obvious as expected, as such in this case, one can have a seemingly normal immunologic evaluation.


Priyanka Kanth, MBBS*, Jaykumar Thumar, MD, Guada Respicio, MD, Eytan Rubinstien, MD, Zaldonis Anthony, MD. Internal Medicine, University of Connecticut Health Center, Farmington, CT, Gastroenterology, Infectious disease, St. Francis Hospital and Medical Center, Hartford, CT.

Purpose: Cytomegalovirus colitis is an uncommon condition seen in immune-competent patient. We describe a case of CMV colitis in an immune-competent patient. Also discussed is literature review of endoscopy findings of CMV colitis in immunocompetent patient.

Methods: A relatively healthy 60 yr old lady presented with one week h/o bloody diarrhea. She was seen in community and was tested c-diff stool toxin positive. She was started on metronidazole followed by vancomycin after no improvement in symptoms were noticed. She continued to remain ill and colonoscopy was performed. Colonoscopy biopsy and Antigen test detected CMV infection. She was started on treatment with gancilcovir with dramatic clinical response. During her hospital stay she also developed pulmonary embolism. She recovered from above complications and was discharged with uneventful follow up.

Results: Colitis is most prevalent presentation of CMV infection in immune-competent patients. Comprehensive data of endoscopy findings of CMV colitis in such pts is not well documented in literature. We reviewed endoscopic findings of all individual documented cases of CMV colitis in immunocompetent patients in English literature. Patients with Inflammatory bowel disease were excluded. As per our review of 50 patients (Table), 40% underwent colonoscopy. Recto-sigmoid region was the most predominant location involved. 40% of pts undergoing colonoscopy had right colon involvement. Approx 50% patients had either isolated or multiple ulcerations. The ulcerations described were largely superficial in nature. Some cases described linear ulceration. Inflammation, edema and erythema of colonic mucosa were other prominent features. Few cases described 'pseudomembrane' formation. One case of large mass like lesion masquerading colon cancer have been reported. The predominant pathology apart from ulcerations were acute and chronic inflammation including inflammatory cells in lamina propria and sub-mucosa. Few cases of cryptitis and crypt abscess have also been reported.

Conclusion: Cytomegalovirus colitis, although predominantly seen in immunosuppressed state, can also occur in previously healthy patient. It is important to recognize the infection earlier in course of disease process to prevent worse outcome.


William Gallahan, MD*, Joseph Jorizzo, MD, Richard Bloomfeld, MD. Dermatology, Gastroenterology, Wake Forest University Baptist Medical Center, Winston Salem, NC.

Purpose: Case: A 29 year old man with a history of Crohn's disease presented with an ulcerating skin lesion on his right flank. He required an ileocecal resection two years ago. He had a post-operative recurrence and was then in clinical remission on Azathioprine monotherapy. The patient initially developed a subcutaneous nodule on his right flank. This progressively enlarged, became erythematous, and finally ulcerated (see Figure A). Magnetic Resonance Enterography revealed a minimally thickened ileum and a subcutaneous soft tissue lesion over the right flank with no associated fistula. Skin biopsy revealed granulomatous dermatitis, consistent with metastatic Crohn's disease (see Figure B). The patient was treated with adalimumab with resolution of this lesion. Discussion: Metastatic Crohn's disease is a rare cutaneous manifestation of the disorder which involves granulomatous inflammation which is not contiguous with the gastrointestinal tract. The hallmark histologic findings are sterile granulomas, mimicking the classic intestinal findings of Crohn's disease. Other conditions which must be excluded include pyoderma gangrenosum, cutaneous sarcoidosis, and mycobacterial infection. The presence of these lesions typically parallels active intestinal inflammation. Metastatic Crohn's disease often arises in skin creases, including submammary, inguinal, and perineal folds. However, lesions have been reported to occur on the limbs, trunk, vulva, penis, and face. The treatment of metastatic Crohn's disease includes standard Crohn's disease therapies, such as systemic steroids, antibiotics, azathioprine, and 6-mercaptopurine. Successful treatment with infliximab has been reported. We believe that this is the first case report of metastatic Crohn's disease successfully treated with adalimumab.


Nayantara Coelho-Prabhu, MD*, Suresh Chari, MD. Gastroenterology, Mayo Clinic Rochester, Rochester, MN.

Purpose: Pancreatic neuro-endocrine tumors (PNET) are rare malignancies which present with either symptoms from excess hormone production or are detected incidentally. Autoimmune pancreatitis (AIP) is associated with markedly elevated serum IgG4 levels.

Methods: N/A

Results: A 64 year old woman presented with a 1 year history of steatorrhea, a 50 pound weight loss and diabetes. This was preceded by 4 attacks of pancreatitis over 3 years. Steatorrhea was confirmed by a 24 hour stool study showing 84 grams of excreted fat/day. Contrasted CT scan showed evidence of chronic pancreatitis with atrophy of the body and tail, non dilated pancreatic duct and mildly dilated common bile duct to the level of the pancreas. She had been started on pancreatic enzyme replacement and noted an improvement in diarrhea with slow weight gain. At our institution, baseline labs showed mildly elevated transaminases, normal amylase and lipase and highly elevated serum IgG4 464 mg/dl (normal 8-140). Endoscopic ultrasound (EUS) showed changes consistent with AIP with diffusely hypoechoic gland interspersed with marked lobularity and hyperechoic bands, and a thickened bile duct wall; no masses were seen. Yet, Tru-cut biopsies of the gland were suggestive of NET with mildly positive staining for synaptophysin. IgG4 stains were negative. Repeat pancreas protocol CT did not show a focal mass and an Octreotide scan did not show any evidence of NET. With surgical consultation, we decided to reassess her after treatment with 4 weeks of oral prednisone for presumed AIP. On follow-up, her serum IgG4 had decreased to 314 mg/dl. Repeat pancreas protocol CT was unchanged, and EUS showed features consistent with chronic AIP, though an infiltrating carcinoma could not be ruled out. Tru-cut biopsies again showed stage 2 of 3 neuro-endocrine tumor. She then underwent a total pancreatectomy, splenectomy and hepatico-jejunostomy. The specimen showed a 14 x 2.2 x 1.5 cm multinodular well differentiated NET involving the entire pancreas with changes of chronic pancreatitis, including complete acinar loss, dense fibrosis and chronic inflammation in the adjacent tissue.

Conclusion: We report a sporadic case of multifocal non-functioning neuro-endocrine tumors with many unusual features. Imaging studies failed to show any evidence of PNET and her presentation was highly suggestive of chronic pancreatitis with some features of AIP. This unusual presentation led to treatment with steroids which caused a serologic response but not a radiologic response. The possibility that AIP predisposed to multifocal PNET was not confirmed on pancreatic histology. Differentiating AIP from other pancreatic disease can be difficult. Elevated serum IgG4 and serologic "response" to steroids are not diagnostic of AIP.


Paul Feuerstadt, MD*, Arthur Harris, MD. Gastroenterology, North Bronx Health Network/AECOM, Bronx, NY, Gastroenterology, Montefiore Medical Center/AECOM, Bronx, NY.

Purpose: Large transdiaphragmatic hernias more often are seen as a consequence of trauma (penetrating, blunt or post-surgical) than of progressive enlargment of hiatal hernias. Given widespread availability of EGD, diaphragmatic hernias of various sizes are frequently identified. We present a patient with a massive left-sided diaphragmatic hernia who experienced unique complications related to performance of EGD.

Methods: A 62 year old woman presented in 2006 with UGI bleeding. An EGD utilizing IV conscious sedation was completed uneventfully and without complications; findings included a gastric ulcer and a large hiatal hernia, despite the patient having undergone a fundoplication in 1977. Review of her medical records revealed a CT scan done from 2004 that revealed a large left-sided diaphragmatic hernia containing stomach, spleen, mesenteric fat and a portion of the transverse colon. She had been previously referred to a thoracic surgeon but told she was "too high risk" for surgical repair of the diaphragmatic hernia. She was lost to follow-up until 2008 when a repeat CT scan showed the pancreatic tail and portions of the jejunum, descending and transverse colon in the hernia, as well as the stomach and spleen. Also described was compressive atelectasis of the left lung secondary to the herniated abdominal viscera. The patient was again referred for surgical evaluation and repeat EGD was recommended as part of her pre-operative workup. Immediately prior to EGD while the patient was in the left lateral decubitus position, it was noted on pulse oximetry that her 02 saturation fluctuated between 60-90%. These readings were considered spurious, since she was completely awake and alert. EGD was subsequently performed utilizing IV conscious sedation; pulse oximetry values ranged between 60-80% during the less than 10 minute procedure. Afterward, the patient remained hypoxemic and lethargic. She then began complaining of dyspnea and appeared confused and disoriented, so IV naloxone and flumazemil were administered. Over the next 15-20 minutes her disorientation and dyspnea slowly abated, with improvement in her O2 saturation to 80-90%.

Results: The patient's respiratory decompensation after EGD was attributed to respiratory depression secondary to IV conscious sedation superimposed on the marked loss of left lung function resulting from the compressive effects of abdominal organs and exacerbated by both the left lateral decubitus position and air insufflation of the stomach.

Conclusion: Routine EGD, and probably colonoscopy as well, should be performed with caution in patients with giant diaphragmatic hernias (especially those containing abdominal viscera besides the stomach) because of the significant risk of respiratory complications.


Stuart Akerman, MD*, Andrew Pellecchia, MD, Samer Khader, MD, Sammy Ho, MD. Pathology, Gastroenterology, Medicine, Montefiore Medical Center, Bronx, NY.

Purpose: Introduction: Primary B cell lymphomas may be found in a host of tissues outside of the lymphatic system, including the stomach, heart, thyroid, oral cavity, mediastinum, and liver. One organ that in general appears to be spared is the pancreas, although this case report demonstrates that this is not always the case.

Methods: None

Results: Case Report: A 64 year old man with hypertension, diabetes mellitus type II, and interstitial lung disease secondary to asbestos exposure was seen for hematuria and complaints of increasing abdominal pain. The patient had known history of bilateral renal cysts seen on CT imaging in the past. He was sent for repeat imaging of his abdomen and a 5.0 x 3.4 cm homogenous solid mass in the body of the pancreas was found (Fig. 1). Three weeks later the patient was admitted for abdominal pain. Endoscopic exam was within normal limits, without evidence of external compression of the stomach. On the endoscopic ultrasound examination, a 3.5 cm round, hypoechoic mass was seen in the body of the pancreas, and fine needle aspiration was performed. The cytological specimen collected contained small cells with irregular nuclear contours (Fig. 2), suggestive of a lymphoproliferative disorder, of which B and T cell lymphoma, and neuroendocrine tumor were included in the differential. Immunostaining showed the cells to be positive for CD20 and negative for CD3 and neuroendocrine markers and chromogranin, making the findings support the diagnosis of B-cell lymphoma

Conclusion: Summary: Although the pancreas is an atypical primary site for B Cell lymphoma, it should be included in the differential diagnosis when a mass is discovered in the pancreas.


Stuart Akerman, MD*, Andrew Pellecchia, MD, Samer Khader, MD, Sammy Ho, MD. Pathology, Gastroenterology, Medicine, Montefiore Medical Center, Bronx, NY.

Purpose: Introduction: Malignant Fibrous Histiocytoma (MFH) is a common soft tissue sarcoma, most often found in the extremities; it is usually found to be amenable to surgical excision therapy when found in its early stages of development.

Methods: none

Results: Case Report: An 87 year-old woman with hypertension, hypercholesterolemia, a history of a retinal bleed, and a recent temporo-parietal infarction was sent from her long-term care facility to our hospital for increasing dementia. It was also known from her history that she had a right thigh tumor removed 5 years ago, and the surgical pathology confirmed a diagnosis of malignant fibrous histiocytoma. While being evaluated by her physicians a Chest X-Ray was performed, and sub-carinal fullness was observed. To better evaluate the lesion, a Chest CT was performed, and a sub-carinal mass measuring 5.1 x 5 x 3.3 cm was seen in both the contrast and non-contrast windows (Fig. 1). It was felt that the best approach to obtain a biopsy of the mass would be via endoscopic ultrasound (EUS) with fine needle aspiration (FNA). On preliminary endoscopy, no lesions were seen in the esophagus. On EUS a 4 cm hypoechoic mass was seen, and in it were found multiple small cystic spaces. FNA was performed; Cytologic examination of the aspirate revealed numerous malignant sarcomatoid cells, compatible with malignant fibrous histiocytoma (Fig. 2).

Conclusion: Discussion: Comparison with prior pathology suggests that this lesion is in fact a metastasis from the patient's prior tumor from 5 years ago. This case demonstrated the use of EUS-FNA to diagnose a relatively uncommon disorder.


Sophie Balzora, MD*, Vinita Jacob, MD, Ellen Scherl, MD, Brian Bosworth, MD. Roberts IBD Center, Division of Gastroenterology and Hepatology, Weill Medical College of Cornell University, New York, NY, Medicine, New York Presbyterian Hospital: Columbia Presbyterian Center, New York, NY.

Purpose: Introduction: Establishing a successful treatment regimen for severe ulcerative colitis (UC) during pregnancy, while minimizing risk to the developing fetus, is a complicated endeavor. Whether to treat steroid-refractory UC with cyclosporine (CSA) or infliximab, an anti-TNF-[alpha] monoclonal antibody, is controversial, and the debate is even less clear when the goal is to induce rapid remission and avoid colectomy during pregnancy. We present the first case of steroid-refractory UC in which CSA was initiated during the first-trimester. Case Description: A 30 year-old woman was diagnosed with left-sided UC at age 27, and was initially induced into remission with mesalamine enemas. Her two additional flares were treated with oral and rectal mesalamine. When the patient discovered she was pregnant at 6 weeks gestation, she stopped all her UC treatment. Two weeks later, she developed severe bloody diarrhea and a 5-pound weight loss. She restarted both oral and rectal mesalamine without response. When she presented at 9 weeks gestation, she was placed on prednisone 60 mg daily with no response. Flexible sigmoidoscopy showed severe colitis and she was admitted for IV hydrocortisone. After several days of no response, IV CSA 2 mg/kg was initiated. She demonstrated a rapid, dramatic improvement in symptoms over 7 days and her Mayo score decreased from 11 to 2. She was discharged on a rapid prednisone taper and oral CSA. Subsequently 6-MP 1.5 mg/kg was initiated, and a taper of the CSA was begun after 8 weeks. The CSA taper led to recurrence of bleeding and her CSA dose was increased back to prior levels - maintaining her remission for the duration of her pregnancy (delivery at 38 weeks). Two months post-partum, her CSA was discontinued and she remained in remission. Discussion: The success of CSA for acute, severe UC refractory to steroids has been well-established in the literature; studies show its efficacy in inducing rapid remission, thereby staving off colectomy in the short-term. There is more limited data supporting infliximab as salvage therapy and when considering time to remission, little data exist. Infliximab induces remission generally in 2 weeks, but outcomes in this severe population are limited. However, numerous studies on CSA report mean response time from 5-10 days. Although infliximab is a pregnancy Category B and CSA a Category C, the short term risks to the patient and the fetus may be minimized with a faster induction of remission. Thus, given the rapid response rate to CSA, and its ability to allow pregnant UC patients to avoid surgery, CSA may be a more beneficial option for severe, steroid-refractory UC flares during pregnancy.


Sheila Kumar, MD*, Ellen Scherl, MD, Vinita Jacob, MD, Brian Bosworth, MD. Gastroenterology and Hepatology, Roberts IBD Center, Weill Medical College of Cornell University, New York, NY, Medicine, New York Presbyterian Hospital: Columbia Presbyterian Medical Center, New York, NY.

Purpose: Introduction: The 5-aminosalicylates are first-line therapy for treating ulcerative colitis (UC), and are generally well-tolerated and safe. However, despite their minimal systemic absorption, adverse effects include pancreatitis, pneumonitis, and interstitial nephritis. This is the first case of eosinophilic organizing pneumonia as a result of 5-ASA treatment. Case Description: A 28 year old man was in good health until the age of 26, when he presented with bloody diarrhea and was diagnosed with left sided UC with no evidence of Crohn's disease. He was initially treated with 6.75 g of balsalazide, however his symptoms persisted and he was later started on prednisone and an additional 2.4 g of mesalamine (Lialda, Shire Pharmaceuticals Inc., Wayne, PA) for a total molar equivalent of 4.8 g of mesalamine. He was steroid refractory and 6-MP 1.5 mg/kg was added. Symptoms persisted and he was admitted for IV cyclosporine (CSA). He was induced into remission on 4 mg/kg of CSA and placed on PCP prophylaxis. He was discharged on a rapid prednisone taper, oral CSA for 4 months, and continued on his 6-MP, Lialda and balsalazide. Several months later, he developed a non-productive cough and dyspnea. Chest CT revealed lobar consolidation and nodular infiltrates. Bronchoscopic biopsies demonstrated organizing eosinophilic pneumonia, and chronic and non-necrotizing granulomatous inflammation. Initially, all medications were discontinued and he was treated with clarithromycin. His cough resolved, but his bloody diarrhea returned. He was reinduced with CSA and 6-MP, and presently remains in remission 8 months later on 6-MP monotherapy with symptomatic and radiographic resolution of the pneumonia. Discussion: Inflammatory bowel disease itself can cause pulmonary infiltrates that may be associated with granulomas, and reports of inflammatory lung diseases related to 6-MP exist. However, in those circumstances, there is 6 months at the time of presentation. The eosinophilic inflammatory infiltrate is consistent with a medication reaction, but is not described in those patients with 6-MP exposure. Specifically as well, the presence of non-necrotizing granulomas associated with interstitial pneumonia appears to indicate mesalamine-induced injury. It is unclear whether the balsalazide, with a colonic azo-bonded release, or the Lialda, with an ileal a pH dependent release (allowing for increased potential for systemic absorption), is the culprit offensive agent. While 6MP and IBD can cause inflammatory lung disease, 5-ASA induced interstitial pneumonia is best recognized by its eosinophilic infiltrates and non-necrotzing granulomas.


Sharmeel Wasan, MD*, Ansu Mammen Noronha, MD, Carl O'Hara, MD, Francis Farraye, MD, MSc. Pathology, Gastroenterology, Boston Medical Center, Boston, MA.

Purpose: Inflammatory bowel disease is associated with various extraintestinal manifestations, with primary lung involvement being rare.

Methods: A 75-year-old female smoker with an eight year history of Crohn's disease (CD) presents for evaluation of shortness of breath. The patient underwent an ileocolectomy 16 months earlier and her CD was being treated with infliximab. Three months after surgery, she developed pneumonia that was treated with antibiotics but she continued to complain of mild shortness of breath and cough without fevers.

Results: Physical exam and laboratory data were unremarkable. A CT scan demonstrated a persistent right middle lobe infiltrate. Her infliximab was held. She underwent an extensive work up with negative sputum cultures, negative PPD, normal ACE level, a CT PA that ruled out the presence of an embolus, negative rheumatologic studies, and a non-diagnostic bronchoscopy. She ultimately underwent a right middle lobe resection given the concern for malignancy. Pathology demonstrated architectural distortion with fibrosis and coalescent non-caseating granulomas, thought to be consistent with pulmonary CD. An infectious etiology was not demonstrated by special stains and PCR. The patient was discharged to home post-resection with resolution of her shortness of breath. She was restarted on her infliximab and is currently doing well.

Conclusion: Pulmonary manifestations associated with inflammatory bowel disease include bronchitis, bronchiolitis obliterans with organizing pneumonia (BOOP), interstitial pneumonitis, necrobiotic nodules, pulmonary eosinophilia, thromboembolic disease and vasculitis. There are a few case reports in the literature of pulmonary "metastasis" of CD. Metastatic CD is characterized by the presence of extraintestinal granulomatous lesions that are often independent of intestinal inflammation. They primarily present as cutaneous lesions that are resistant to standard oral and topical therapies. Histology is important to exclude other granulomatous disorders. Most of these patients undergo resection of the involved segment of the lung. Given the significant rate of recurrence of pulmonary lesions, high dose steroids have been used with some success. Some patients have a rapid response to infliximab with sustained remission of respiratory symptoms. However, there are rare reports of interstitial lung disease thought to be an adverse effect of infliximab. Pulmonary manifestations of CD may be more common that previously appreciated and need to be considered in the differential diagnosis of CD patients presenting with respiratory complaints.


Yaron Langman, MD*, Ira Tepler, MD, Albert Kramer, MD, Amnon Gotian, MD, Lawrence Brandt, MD. Gastroenterology, Montefiore Medical Center, Bronx, NY.

Purpose: A case vignette providing insight in an usual GI manifestation of a rare disease.

Methods: Case report.

Results: JC is a 79 year old woman with systemic mastocytosis who presented with one month of fevers, nausea, vomiting and diarrhea. 1 month prior to admission, she was diagnosed with Clostridium difficile colitis. The diarrhea improved after a course of metronidazole, however, it worsened a few weeks prior to admission. The patient was first diagnosed with systemic mastocytosis 3 years prior to admission, and had received chemotherapy including Gleevec, dasatinib and steroids. Her disease course was notable for cutaneous manifestations, diffuse adenopathy and cirrhosis with ascites, thought secondary to hepatic infiltration of mastocytes. On exam, bitemporal wasting was noted. She had an erythemetous rash on her lower extremities, but no urticaria pigmentosa. Abdominal exam was significant for ascites and a palpable spleen tip and liver edge. On admission, her white blood cell count was 14,000 but a C. difficile toxin antigen was negative twice. She was empirically treated with metronidazole and cholestyramine without improvement. A colonoscopy was then performed. Endoscopically, the mucosa appeared erythematous with rare pseudomembranes. Biopsies were taken throughout the colon. On histologic examination, no pseudomembranes were seen but increased mast cells were found in the lamina propria throughout the colon. CKIT (CD117 and CD68) mutation markers were positive. Systemic mastocytosis is a rare disease likely related to mutations within KIT, a tyrosine kinase receptor for stem cell factor (involved in maturation of mast cells). The disease can have varied clinical manifestations most often including urticaria pigmentosa. Gastrointestinal manifestations have been well described and incidence ranges in different case series from 14% to 85% and include nausea and vomiting, peptic ulcer disease, gastrointestinal bleeding, hepatomegaly, splenomegaly and diarrhea. However, other than a few case reports, few studies have examined colonic involvement in mastocytosis. Because of the rarity of this disease most studies and case series have been small with heterogeneous patients.

Conclusion: Our patient was found to have many mast cells in the lamina propria and mutations in C KIT consistent with mastocytosis. Her diarrhea was possibly secondary to infiltration in the lamina propria by mast cells within the colon. Treatment includes histamine H2-receptor antagonists, mast cell stabilizers (such as cromolyn sodium) or interferon-alpha based treatment.


Muhammad Siddiqui, MD*, Charles Berkelhammer, MD, FACG. Internal Medicine, University of Illinois, Oak Lawn, IL.

Purpose: Introduction: Sodium phosphate bowel preparation can occasionally cause a mild decrease in serum calcium secondary to transient hyperphosphatemia. This is rarely of clinical significance except in renal insufficiency. We describe a patient with normal renal function who developed symptomatic hypocalcemia after sodium phosphate colonoscopy bowel preparation. Further evaluation of hypocalcemia revealed her underlying diagnosis of celiac disease. Case: A 66 year old female complained of numbness and tingling of her face, arms and legs when she presented for a screening colonoscopy after taking sodium phosphate bowel preparation. She had a history of osteoporosis and was on alendronate. Baseline calcium, 25-hydroxy vitamin D, parathyroid hormone, magnesium and creatinine were normal. She had taken the standard doses consisting of 45 mls of sodium phosphate the evening before and the morning of her colonoscopy. On presentation for colonoscopy her calcium was 7.5 mg/dl, albumin 3.8 gm/dl and phosphorus 7.8 mg/dl. To further evaluate her hypocalcemia an upper endoscopy was performed which revealed classic features of celiac disease (mosaic pattern of the duodenum and notching of duodenal folds). Small bowel biopsies confirmed marked villous atrophy. Tissue transglutaminase antibody (IgA) was markedly elevated at 200 units (negative <20 units). Discussion: Celiac disease can itself predispose to hypocalcemia. The sodium phosphate load during colonoscopy preparation can precipitate hypocalcemia in susceptible individuals. Decreased mobilization of calcium from bone by alendronate may also have been contributory. Conclusion: Celiac disease should be considered in patients with normal renal function who present with hypocalcaemia after sodium phosphate colonoscopy preparation.


Uzma Abbasi, MD*, Rishi Pawa, MD, Vishal Gupta, MD, PhD, Jay Cowan, MD. Gastroenterology, Columbia University College of Physicians and Surgeons, Harlem Hospital Center, New York, NY.

Purpose: The incidence of pancreatic tuberculosis has increased recently, probably because of increase in travel to countries where tuberculosis is endemic and in patients who are infected with HIV or otherwise immunocompromised. The manifestation of the disease is usually that of a pancreatic mass mimicking carcinoma, but can also present as obstructive jaundice, pancreatic abscess, acute or chronic pancreatitis.

Methods: Chart review and review of available literature using Medline and relevant bibliographies of published articles.

Results: A 32-year-old gentleman from Dominican Republic with no previous history of tuberculosis presented with abdominal pain, vomiting and a 15 lb weight loss over two months duration. Ultrasonography (US), computer tomography (CT) scan and magnetic resonance imaging (MRI) were suggestive of a multicystic irregular pancreatic head mass which appeared inseparable posteriorly form the IVC and extended along the portal vein and proper hepatic artery to the porta hepatis, without any associated biliary or pancreatic duct dilatation. Also noted were enlarged mesenteric lymph nodes and features suggestive of small bowel obstruction. Tumor markers, CEA and CA 19-9 were within normal limits. The initial impression was malignant pancreatic neoplasm with mesenteric spread and small bowel obstruction and the patient was scheduled for an exploratory laprotomy. At operation, 10 x 8 cm cystic mass was seen in mesentery, containing thick creamy material. The mesenteric cystic mass was dissected out and the small bowel involved with this area of mesentery was transected and resected en bloc with the mass. A fine needle aspiration of the pancreatic head mass was done with a 25 G needle and the same material as in the mesenteric cyst was obtained. Histological examination of the mesenteric lymph node and fine needle aspiration cytology from the head of the pancreas confirmed the diagnosis of tuberculosis. Patient recovered following the administration of antituberculosis chemotherapy.

Conclusion: Pancreatic tuberculosis should be considered in the differential diagnosis of pancreatic masses, particularly if the patient is young, not jaundiced and from an area of high TB prevalence.


Eric Choi, MD*, Walter Coyle, MD. Gastroenterology and Hepatology, The Scripps Clinic, La Jolla, CA.

Purpose: Vasculitides are an uncommon cause of bloody diarrhea and abdominal pain. Henoch-Schonlein Purpura (HSP) is a leukocytoclastic vasculitis of small vessels, and although HSP represents the most common vasculitis in children, it is infrequently described in the geriatric population. We describe a case of HSP with an initial presentation of abdominal pain and bloody diarrhea in a geriatric patient.

Methods: Case Report.

Results: A 65-year-old Asian female was admitted with bloody diarrhea and diffuse abdominal pain. She had no significant past medical history except for a recent upper respiratory tract infection, which was treated with a course of antibiotics. Eight days after starting antibiotics, the patient developed bloody diarrhea and diffuse abdominal pain. Three days into her hospitalization, she developed symptoms of diffuse arthralgias and petechiae in her lower extremities. Her only abnormalities on laboratory analysis were a WBC count of 12.0 K/cumm (normal 4.5-11), a hemoglobin of 11.0 g/dL (normal 12-15) and an ESR of 52 mm/hr (normal 0-20). The patient's urinalysis and renal function remained normal throughout her hospitalization. Colonoscopy demonstrated multiple areas of mucosal petechiae (Fig. A). A biopsy of the petechial skin lesions was performed, which demonstrated IgA deposition in the walls of the blood vessels in the dermis (arrow, Figure B). This confirmed the diagnosis of HSP and the patient was treated with a course of oral prednisone, resulting in complete resolution of her symptoms in 2 weeks and no recurrence on 6 month follow-up.

Conclusion: HSP typically manifests as a tetrad of clinical symptoms: purpuric skin lesions, arthralgias, abdominal pain, and nephropathy. The diagnosis of HSP can be very difficult because the constellation of symptoms may not be synchronous but appear in succession. The clinical diagnosis is most facilitated by the presence of cutaneous lesions, however when gastrointestinal symptoms precede the skin lesions, which occur in 14% of patients, the diagnosis can often be missed (1). Although most patients progress to complete recovery without therapy, early diagnosis is important because there is some evidence that corticosteroids may enhance the rate of resolution in patients with arthritis and abdominal pain. 1. Chen MJ, et al. Endoscopic findings in a patient with Henoch-Schonlein purpura. World J Gastroenterol. 2005 Apr 21;11(15):2354-6.


Panagiotis Panagiotakis, MD*. Gastroenterology & Hepatology, ISJ-Mayo Health System, Mankato, MN.

Purpose: A 50-year-old asymptomatic man came for repeat colonoscopy. One year before, he underwent a screening colonoscopy during which a diminutive polyp was found in the cecum. The polyp was removed with moderate difficulty. The biopsy showed a mucosal fragment with focal erosion. His gastroenterologist recommended repeat colonoscopy in 1 year. During repeat endoscopy, a 4 mm yellowish sessile hard polyp was found in the cecum. The Jumbo forceps could not excise the polyp, so polypectomy with a hot snare was performed successfully. There were no complications. Histological examination revealed a completely excised granular cell tumor.

Methods: Granular cell tumor (GCT) is a relatively rare soft tissue neoplastic tumor of neural derivation, which commonly occurs in the oral cavity and subcutaneous tissue and is uncommon in the colon and rectum. The GI tract harbors approximately 5% of all GCTs. The most common site for GCT in the GI tract is the esophagus, followed by the duodenum, anus and stomach. Lesions can be incidental findings, or they may give rise to obstructive or pressure symptoms when large enough and in a critical location. Malignancy is rare and has been found to correlate with tumor size (more than 60% of metastatic GCTs were larger than 4 cm). Since colonic GCTs are usually benign, endoscopic removal is the most appropriate therapy.

Results: Diagnosis is based on histopathological findings: (1) small, uniform nuclei without mitotic figures; (2) histiocyte-like bland-looking neoplastic cells with abundant granular eosinophilic cytoplasm containing acidophilic, PAS-positive, diastase-resistant granules; (3) stain positively for S-100 protein, neuron-specific enolase, and NK1-C3 in almost all cases. The tumor cells are non-immunoreactive for epithelial, muscle, endothelial and glial cell markers. This is useful for differentiating a granular cell tumor from other diagnostic possibilities. The found lesion had the typical characteristics of GCT. Since the patient was asymptomatic we did not pursue further work-up. He will have a repeat colonoscopy in 1 year.

Conclusion: In conclusion, GCTs of the colon can be found incidentally during colonoscopy and endoscopic removal of the tumor is a safe and feasible treatment. Endoscopists should consider GCTs in the differential diagnosis of submucosal tumors of the colon.


Eric Choi, MD*, Williamson Strum, MD. Gastroenterology and Hepatology, The Scripps Clinic, La Jolla, CA.

Purpose: With the mounting number of gastric bypass surgeries for the treatment of morbid obesity, complications of nutritional deficiencies must be recognized. A rare nutritional deficiency after gastrojejunal bypass is hypocupremia, which is clinically indistinguishable from the neurologic deficits of vitamin B12 deficiency. In addition, hypocupremia has been implicated in hematologic abnormalities of anemia and neutropenia. We describe a case with the rare combination of neurologic and hematologic abnormalities secondary to gastric bypass-associated hypocupremia.

Methods: Case Report

Results: A 45 year old white female underwent a Roux-en-Y gastric bypass for morbid obesity six years prior to presentation and complained of 15 months of progressive symptoms of lower extremity paresthesias, dysesthesias, and weakness. She had no other significant past medical or surgical history. On neurologic examination, the patient demonstrated a wide-based gait and a decreased tandem walk. Examination of her lower extremities demonstrated a bilateral absence of vibratory perception, decreased pin-prick to her ankles, strength of +1 and spastic quadriceps muscle stretch reflexes. A serum copper of 24 ug/dL (normal 80-155) and ceruloplasmin of 9 mg/dL (normal 22-58) were demonstrated. Concurrent with her neurologic deficits, the patient had episodes of anemia and neutropenia, which, at their nadirs, were 9.2 g/dL (normal 12-15) and 4.1 K/cumm (normal 4.5-11), respectively. Homocysteine, vitamin B12, ferritin and methylmalonic acid levels were normal. Upper endoscopy identified no abnormalities and biopsies of the small intestine were negative for celiac sprue. A thoracic spine MRI demonstrated a minimally increased focus of T2 signal intensity in the central spinal canal from T4 through T7. The patient was treated with an oral preparation of elemental copper at 2 mg/day, which halted the progression of the patient's neurologic symptoms and resulted in the complete resolution of her anemia and neutropenia within 2 months. She remains stable after 9 months follow-up.

Conclusion: Copper is absorbed in the stomach and proximal small intestine; as a result, gastrojejunal bypass predisposes patients to copper deficiency. Since the recognition of hypocupremia after gastric bypass as a cause of myeloneuropathy, 15 cases have been reported in the literature with a further smaller proportion of patients demonstrating concomitant hematologic disturbances. The aim of this report is to raise the index of suspicion for hypocupremia in post-gastric bypass patients, who present with either neurologic or hematologic abnormalities related to copper deficiency.


Ricardo Borsatto, MD*, Neil Shernoff, MD. Gastroenterology, Carl T. Hayden Veteran Affairs Medical Center - Phoenix, AZ, Phoenix, AZ, Gastroenterology/Hepatology, University of Arizona, Tucson, AZ.

Purpose: Introduction: Esophageal Intramural Pseudodiverticulosis (EIP) are abnormal dilated ducts of submucosal glands often associated with conditions that cause chronic esophageal inflammation such as gastroesophageal reflux, chronic candidiasis, previous caustic ingestion and esophageal cancer. EIP is most commonly seen in the sixth or seventh decade of age.

Methods: Case: A 56-year-old caucasian woman diagnosed with EIP in 1990 and submitted to esophageal dilation every 2 years in average due to intermittent dysphagia presents with new onset of upper esophageal discomfort pointed at the level of the thyroid cartilage. Previous barium-contrast esophagogram showed a diffuse narrowed esophagus and multiple flask-shaped outpouchings in the esophageal wall.

Results: Endoscopy was performed and revealed two areas of circumferential stenosis at 20 cm and 37 cm from incisors associated with multiple small diverticula in the esophageal wall. Initially a white lamp examination was performed then NBI system was applied and a considerable enhancement of the diverticula images was observed with a better appreciation of the disease extension throughout the esophagus. We choose to approach the double stenosis with a guidewire Savary dilation using a 36 Fr probe. Patient's symptoms improved considerably 2 days after the procedure.

Conclusion: Discussion: EIP is a rare condition with only about 200 cases reported although autopsy studies showed its incidence being as high as 55%. The endoscopic appearance of EIP is characteristic but the diverticula openings are small and often missed. Our report shows that NBI might be a helpful tool in the endoscopic armamentarium for diagnosis of this condition.


Eric Choi, MD*, Kevin Antonio, MD, Williamson Strum, MD. Internal Medicine, Gastroenterology and Hepatology, The Scripps Clinic, La Jolla, CA.

Purpose: Copper is absorbed in the stomach and small intestine, and patients with gastric bypasses are at risk for hypocupremia. Zinc, which is critical in cell growth, wound healing and host immunity, induces an increase in the protein, metallothionein, which preferentially binds copper within the gastrointestinal tract and prevents copper absorption. Zinc supplementation is frequently provided to patients after gastric bypass to prevent zinc-deficiency. We report a rare case of zinc-induced hypocupremia in a Billroth II patient, resulting in anemia and leukopenia.

Methods: Case Report

Results: An 81 year old male with a remote history of severe upper gastrointestinal bleeding related to peptic ulcer disease, necessitating a Billroth II operation 20 years ago, presented with exercise intolerance. The patient had a history of hypertension-related chronic renal disease with a Hgb of 11 g/dL (normal 12-15) and a normal absolute neutrophil count (ANC) at baseline. However over the course of 6 months, the patient's Hgb and ANC declined to 7.7 g/dL and 0 K/cumm, respectively. Despite treatment with darbepoetin, the patient's anemia did not improve. A bone marrow biopsy was performed, which demonstrated vacuolated RBC and WBC precursors, characteristic of hypocupremia (Fig. 1). Further blood work demonstrated a copper level of 2 ug/dL (normal 80-155) and a ceruloplasmin of 4 mg/dL (normal 22-58). The patient was on zinc supplements since his Billroth II operation. Zinc level was 137 ug/dL (normal 60-120). The patient was diagnosed with zinc-induced hypocupremia as the cause of his anemia and neutropenia. His zinc supplements were stopped and an oral copper preparation was initiated. On two month follow-up, the patient's Hgb and WBC counts normalized.

Conclusion: Copper is absorbed in the proximal gastrointestinal tract. A Billroth II operation in conjunction with the antagonistic effects of zinc on copper absorption predisposed our patient to hypocupremia, resulting in anemia and neutropenia. Zinc-induced hypocupremia represents a rare condition. Only 25 cases have been described since its first report in 1977. The aim of this case report is to raise awareness of the possible deleterious effects of zinc supplementation in the post-gastric bypass patient.


Ricardo Borsatto, MD*, Neil Shernoff, MD. Gastroenterology, Carl T. Hayden Veteran Affairs Medical Center - Phoenix, AZ, Phoenix, AZ, Gastroenterology/Hepatology, University of Arizona, Tucson, AZ.

Purpose: Introduction: Transmural migration of surgical material is a rare situation with few cases reported. The most common cases were related to migration of gel material placed at the submucosal GE junction as an alternative of fundoplication. Esophageal foreign bodies occur more often associated with accidental ingestion especially in children and in adults with mental disorder, alcohol intoxication and reduced oral-palate sensation.

Methods: Case: A 46-year-old caucasian woman who underwent laparoscopic Nissen fundoplication 10 years prior presents with symptoms described as increasing difficulty swallowing and chest discomfort for 1 month. Initially it was thought that symptoms could be related to GER with possible hiatal hernia recurrence. Barium swallow showed distorted GE junction and large sliding hiatal hernia although increased dosage of PPI to 40 mg twice a day did not improve symptoms.

Results: Endoscopy was performed and a foreign body consisting of suture material and a metalic clip was identified at 34 cm from incisors within the esophageal lumen. The suture was cut and retrieved using a Olympus loop cutter. There was a local edema and narrowing of the lumen but no difficult progression to the stomach. During retroflexion in the fundus we observed an intact fundoplication. Patient's symptoms subsided one week after the procedure.

Conclusion: Discussion: Although rare, foreign body secondary to transmural migration of surgical material should be thought in patients who underwent fundoplication and have recurrent symptoms even many after the procedure. Radiologic examination is important but could be misinterpreted. Endoscopic evaluation is essential for diagnosis and possible treatment.


Yuriy Tsirlin, MD*, Andrew Seymour, MD, Gerold Fruchter, MD. Gastroenterology, SUNY Downstate Medical Center, Brooklyn, NY, Pathology, Gastroenterology, VA NY Harbor Healthcare System, Brooklyn Campus, Brooklyn, NY.

Purpose: We present a case of incidentally diagnosed appendiceal neuroma, which has long been considered a rare histological finding. Case Summary: This is a case of a 65 year old male undergoing chemotherapy for a recently diagnosed metastatic urethral cancer. GI service was consulted to evaluate occult blood in the stool in view of recently diagnosed DVT and need for anticoagulation therapy. Pt underwent EGD, which was essentially unremarkable and a colonoscopy that revealed a 1 cm transverse colon tubulovillous polyp and a small 4 mm nodule that was seen protruding from the appendiceal orifice (Fig. 1). This appendiceal nodule was probed with biopsy forceps and then removed with same. Histological examination of the appendiceal nodule revealed a spindle cell lesion compatible with a neuroma (Fig. 2). This was confirmed by immunopathological staining; lesion was positive for S-100 protein and negative for CD34, CD117 and smooth muscle actin. Discussion: Differential diagnosis of an appendiceal nodule is fairly broad and includes both benign and malignant lesions. Among more commonly reported findings are those of adenocarcinoma, either primary or metastatic, carcinoid, lipoma and lymphangioma. Less commonly reported findings include mucinous cystadenocarcinoma and pseudomyxoma peritonei. Appendiceal neuroma (AN) is a rare histological finding and considered to be a benign entity. It is usually asymptomatic, though isolated cases of appendicitis-like symptoms have been described. AN can arise from mucosa or submucosa with or without fibrous obliteration of appendiceal lumen. The presence of fibrous obliteration would more likely present with associated symptoms. Enterochromaffin cell proliferation and neural elements are responsible for development of AN; the simple presence of endocrine cells within an AN should not be mistaken for carcinoid tumor.

Conclusion: The incidental colonoscopic finding of an appendiceal nodule has a broad differential diagnosis that clinicians should be aware of; malignancy should always be excluded. Fortunately, many of these nodules are benign, including such rare findings as an appendiceal neuroma, presented here.


Ritu Saha, MD*, Jessica Widmer, DO, Eugene Sullivan, MD. Gastroenterology, Hepatology, and Nutrition, Winthrop University Hospital, Mineola, NY.

Purpose: Campylobacter fetus has been documented as a cause of bacteremia, and it is typically diagnosed in immunocompromised patients with a febrile illness or extra-intestinal involvement including vascular infections, abscesses, and cellulitis. Unlike its well-known counterpart, C. jejuni, it is rarely associated with gastrointestinal manifestations. We present an unusual case of C. fetus bacteremia presenting with abdominal pain and diarrhea. An 81-year old female with a history of COPD on chronic steroid therapy and pulmonary embolism presented with complaints of abdominal pain, nausea and loose stools for the past month. Physical exam was significant for RUQ tenderness with guarding. A small bowel series and RUQ sonogram were negative. CT of the abdomen revealed a RUQ inflammatory process, better defined as a duodenal hemorrhage vs. perforation without evidence of free air. An EGD revealed chronic inactive gastritis with normal duodenal anatomy. With conservative management, the patient's symptoms improved, and she was discharged home. Three days after discharge, 2/4 blood culture bottles grew C. fetus, and the patient returned to the hospital for further evaluation. At that time, she complained of intermittent periumbilical pain without diarrhea. She was afebrile and abdominal exam was benign. WBC count was 10. During her hospitalization, the patient suffered from a single temperature spike with recurrence of diarrhea. Repeat blood cultures, stool cultures, and Clostridium difficile toxin were negative. To reassess her symptoms, a repeat CT scan was performed which demonstrated no significant change. The infectious disease specialists' impression was that the Campylobacter bacteremia was likely secondary to a GI source and recommended treatment with Meropenem for 12 days. The patient recovered without further complications, and was discharged home.

Conclusion: A literature search on C. fetus yielded reports of appropriate antibiotics use, but limited information regarding clinical presentation and management. We aim to highlight an unusual presentation of Campylobacter fetus bacteremia with abdominal pain and diarrhea. This diagnosis requires a high degree of suspicion in immunocompromised hosts, and requires an adequate length of IV antibiotic therapy since it is rarely self-limited.


Eric Choi, MD*, Williamson Strum, MD. Gastroenterology and Hepatology, The Scripps Clinic, La Jolla, CA.

Purpose: Linitis plastica is the diffuse type of gastric adenocarcinoma in which the individual cells infiltrate the gastric wall without forming a discrete mass. It typically presents in younger patients and portends a poorer prognosis than the intestinal type of gastric adenocarcinoma. We present a case of metastatic linitis plastica, which was initially misdiagnosed as Crohn's disease.

Methods: Case report

Results: A 55 year old male presents with pain on defecation, tenesmus, intermittent hematochezia and epigastric abdominal pain. His symptoms began 7 months prior to presentation, during which time he lost 30 lbs. The patient underwent an upper endoscopy and colonoscopy, demonstrating gastric mucosal erythema as well as a stricture and area of erythema in the distal sigmoid. Biopsies of the gastric and colonic mucosa demonstrated "inflammatory changes". The patient was diagnosed with Crohn's disease and started on a course of steroids and mesalamine. Despite two months on this regimen, the patient's condition did not improve and the patient was referred to a tertiary care center. A repeat endoscopy demonstrated a poorly distensible stomach (Fig. A) and a loss of rugal folds in the body of the stomach (Fig. B). Colonoscopy again demonstrated a stricture in the sigmoid colon. Biopsies from both the stomach and sigmoid colon demonstrated a diffuse, poorly differentiated carcinoma with signet ring cells. A CT scan of the abdomen and pelvis demonstrated diffuse wall thickening of the stomach (Fig. C) and the rectum. The patient was diagnosed with linitis plastica with metastases to the colon. The patient decided to pursue hospice care.

Conclusion: In the setting of mucosal inflammation, endoscopic forcep biopsies may not reveal an underlying layer of malignant tissue, which can lead to a delay in diagnosis as in the case presented. However, the combination of a poorly distensible stomach, a diffuse loss of rugal folds in the body of the stomach and a history of weight loss should raise suspicions of malignancy, and specifically linitis plastica. Although a relatively uncommon malignancy, a high index of suspicion and recognition of the characteristics of this malignancy aid earlier diagnosis.


Robert Siwiec, MD*, Baseer Qazi, MD, Marc Fine, MD. Gastroenterology, Internal Medicine, Advocate Lutheran General Hospital, Park Ridge, IL.

Purpose: Clozapine is an atypical antipsychotic commonly prescribed for treatment-resistant schizophrenia. The adverse effect profile is considerable, including hematologic risks, cardiomyopathy, seizures, weight gain, venous thromboembolism, metabolic syndrome and hypotension. Less well recognized is clozapine's potential to impair motility throughout the gastrointestinal tract, causing dysphagia, intestinal obstruction, bowel ischemia, and megacolon. There have been eight reported cases in the English literature of death from clozapine-induced gastrointestinal hypomotility (CIGH). We report a case of death from CIGH, accompanied by a brief review of the available literature.

Methods: A systematic review of the medical literature using Medline was performed.

Results: A 48 year old man with schizophrenia treated with clozapine 400 mg daily presented with a one day history of nausea, vomiting and abdominal pain. Physical examination revealed a distended rigid abdomen with pain to palpation in the epigastric region. Laboratory evaluation revealed an anion gap metabolic acidosis with a lactate level of 7.8 mg/dL, creatinine of 2.9, and white blood cell count of 11,100 with 22% bands. Computed tomography (CT) scan of the abdomen and pelvis revealed extensive fecal impaction extending from the rectum to the splenic flexure along with gas and feces in a markedly distended right colon. Intravenous fluids along with broad-spectrum antibiotics were administered. Manual disimpaction was performed with removal of numerous hard stools. The patient was transferred to the medical intensive care unit (MICU) for further management. Within hours of arrival to the MICU, the patient developed respiratory distress and underwent rapid sequence intubation for impending respiratory failure. Low systolic blood pressures prompted the initiation of vasopressors. A repeat CT scan of the abdomen and pelvis showed increased colonic distention and new ascites, but remained negative for free air. Despite the use of three vasopressors and drotrecogin alfa, the patient remained hypotensive. The family decided to withdraw support and the patient expired within minutes. Post-mortem examination revealed toxic megacolon with bowel ischemia and infarction.

Conclusion: Gastrointestinal hypomotility is a serious side effect of clozapine that may result in bowel obstruction, ischemia and necrosis, perforation, or aspiration pneumonia. The mechanism is likely to be anticholinergic and antiserotonergic. The scarcity of literature on CIGH suggests that the significance of this uncommon but important and frequently fatal side effect has not been recognized. A patient receiving clozapine and presenting with vomiting and abdominal pain should raise immediate concern for the physician.


Uzma Abbasi, MD*, Rishi Pawa, MD, Vishal Gupta, MD, PhD, Hashim Nemat, MD, Jay Cowan, MD. Gastroenterology, Columbia University College of Physicians and Surgeons, Harlem Hospital Center, New York, NY, Geriatric Medicine, Long Island Jewish Medical Center, New York, NY.

Purpose: Pylephlebitis or septic thrombophlebitis of the portal vein, a precursor of hepatic abscesses, is an extremely rare and frequently fatal complication of diverticulitis. The following report describes a patient presenting with pylephlebitis and complicated diverticulitis. The patient had a favorable outcome with medical and surgical therapy, prompting us to evaluate historical treatment of pylephlebitis.

Methods: Chart review and review of available literature using Medline and relevant bibliographies of published articles.

Results: A 57-year-old woman presented with complaints of abdominal pain, fever and vomiting. Physical examination was significant for abdominal tenderness in the left lower quadrant. Laboratory tests revealed leucocytosis with bandemia and blood cultures were positive for Basteriodes Caccae. She underwent abdominal CT scan which showed acute sigmoid diverticulitis and thrombophlebitis of portal vein and hepatic septic emboli. She was subsequently started on broad spectrum antibiotic therapy and anticoagulation. Her course was further complicated by the development of peridiverticular abscess and sigmoid perforation for which she underwent a Hartmann procedure. Patient was discharged after 35 days of hospitalization after the resolution of her septic status. Six weeks after the initiation of medical therapy, anticoagulation and surgery, a repeat CT scan showed resolution of portal vein thrombus and hepatic emboli.

Conclusion: This is a description of a rare association of septic thrombosis within the portal vein and septic hepatic emboli during acute sigmoid diverticulitis with abdominal abscesses. The patient was successfully treated with broad spectrum antibiotics and a Hartmann procedure.


Nan Sandar, MD*, Mojdeh Momeni, MD, Jeremiah Kurz, MD, Michelle Dahdouh, MD, Frederick Fallick, MD. Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Infectious Disease Department, Gastroenterology, St. Barnabas Hospital, Bronx, NY.

Purpose: While disseminated MAC infection in AIDs patients is common, MAC peritonitis is a relatively rare phenomenon. Chylous ascites as a complication of MAC is very rarely encountered. We report a case of chylous ascites associated with MAC peritonitis in an AIDs patient.

Methods: A 41 year old male with advanced AIDS, a CD4 count of 34 and recurrent MAC infection was admitted for cough with blood tinged sputum and a 10 pound weight loss over 3 weeks. He was non-compliant with his anti-HIV medications. He had no history of liver disease and denied drinking alcohol. He was afebrile but appeared cachetic with a distended abdomen. Abnormal laboratory values included a white blood cell count (WBC) of 22 x 106/L, albumin 1.4 g/dL and alkaline phosphatase 350 U/L. Viral hepatitis serologies were negative. Echocardiogram was normal. Computed Tomography (CT) of the abdomen and pelvis revealed diffuse ascites with retroperitoneal and portacaval adenopathy. Paracentesis revealed cloudy ascitic fluid with WBC 1880/mm3 (73% neutrophil), albumin 1 g/dl, total protein 3.5 g/dl and negative cytology. His sputum, blood, ascitic fluid cultures and stool concentrate smear were all positive for MAC. The patient was started on ethambutol, amikacin, ciprofloxacin and azithromycin for treatment of MAC. Repeat paracentesis four weeks later demonstrated resolving peritonitis (WBC 119/mm3) but the ascitic fluid appeared milky. The ascites triglyceride level was 780 mg/dl. Repeat cultures were negative. He was started on a low fat diet and spironolactone in addition to intensive MAC treatment. The patient's overall general condition improved and he was discharged to a short term facility to complete treatment for MAC infection.

Results: A 6-month follow up CT scan revealed complete resolution of ascites.

Conclusion: Our case highlights the point that paracentesis should be performed in all patients with ascites for fluid analysis and further management. In patients with MAC peritonitis, if ascites does not improve with MAC therapy and diuretics, paracentesis should be repeated to re-evaluate the ascitic fluid for the possibility of chylous ascites or superimposed bacterial infection. Even though the long term prognosis for patients with chylous ascites is poor, complete resoluation of chylous ascites can be achieved as in our case with aggressive MAC therapy and additional dietary management such as medium chain triglyceride or total parenteral nutrition. Finally, MAC infection should be considered in the differential diagnosis of chylous ascites.


Ruben Ramirez, MD*, Marc Zuckerman, MD, Sita Chokhavatia, MD. Medicine, Texas Tech University Health Sciences Center, El Paso, TX, Medicine, Mount Sinai School of Medicine, New York, NY.

Purpose: Acute colonic pseudo-obstruction is characterized by symptoms, signs and radiological appearance of acute large bowel obstruction in the absence of a true mechanical obstruction. The pathophysiology is not well understood. A proposed theory involves transient impairment of the sacral parasympathetic nerves causing atony of the distal large bowel resulting in functional obstruction.

Methods: We present a case of a patient with Guillain-Barre syndrome complicated by acute colonic pseudo-obstruction, in whom neostigmine could not be used.

Results: A 57 year old man with Guillain-Barre syndrome and progressive ascending muscular weakness was hospitalized for significant autonomic dysfunction and pronounced muscular weakness. He developed diffuse abdominal pain and distension, and was unable to pass gas or feces on hospital day 5. The physical exam was significant for abdominal distension, hyperactive bowel sounds, and diffuse abdominal tenderness. An abdominal CT showed dilated colon and cecum with a maximum diameter of 8.3 cm without associated abnormality of the bowel wall or proximal bowel dilation, consistent with acute colonic pseudo-obstruction. Successful endoscopic colonic decompression was performed the next day and supportive measures continued, including nasogastric (NG) suction and maintaining electrolyte balance. The patient developed recurrent distension within 24 hours. Neostigmine was contraindicated because of autonomic dysfunction and he failed to respond to erythromycin. Tegaserod 6 mg was given every 12 hours per NG tube and within 14 hours the patient started passing gas and had a spontaneous bowel movement. Abdominal pain and distension resolved, confirmed by an abdominal film. The patient continued to receive tegaserod until discharge 7 days later with no recurrence of obstructive symptoms.

Conclusion: Treatment options for acute colonic pseudo-obstruction have had variable outcomes and include medications (neostigmine and erythromycin), endoscopic decompression, percutaneous tube cecostomy and colectomy. To our knowledge, this is the first case report of acute colonic pseudo-obstruction with a clinical response to treatment with tegaserod, a partial 5-HT4 receptor agonist. 5-HT4 receptor agonists may be a viable option in the treatment of acute colonic pseudo-obstruction.


Nan Sandar, MD*, Jeremiah Kurz, MD. Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Gastroenterology, St. Barnabas Hospital, Bronx, NY.

Purpose: Enteral nutrition is a major component of therapy in critically ill patients. Feeding tubes passed through the nose or mouths are commonly used to administer medications and enteral nutrition, as well as to manage post-operative ileus. We report a case of an unusual complication associated with an orogastric tube (OGT).

Methods: A 45 year old man with Hepatitis C, HIV, rectal squamous cell carcinoma status post radiotherapy was electively admitted for abdomino-perineal resection because of recurrent cancer. Post operatively, he was being maintained on mechanical ventilation. He was receiving intravenous midazolam for sedation, intramuscular ketorolac for pain management and enteral nutrition via OGT for nutritional support. On day 6, the patient had a self-limited episode of hematamesis. The ketorolac was discontinued and he was put on intravenous esomeprazole. Endoscopic investigation was deferred as the patient was febrile, hemodynamically stable and had OGT aspirate revealing clear bilious fluid. The next day, he was found to have chewed through the OGT; the external piece of the tube was found outside his mouth. Radiographs confirmed the presence of the rest of the tube in the esophagus and stomach. EGD was performed. The tip of the remnant OGT was seen at 24 cm in the esophagus. It was pushed into the stomach, snared and removed through an overtube. A large ulcer was noted beginning 2 cm above the gastroesophageal junction (GEJ) and extending into the cardia of the stomach. A visible vessel was noted in the ulcer which was injected with epinephrine and cauterized using a gold probe.

Results: The patient had no further bleeding episodes but succumbed to his other comorbidities the following week.

Conclusion: In our case, even though the patient was intubated and sedated, he managed to chew through the OGT and swallow the tube remnant. This case highlights the point that care must be taken to prevent damage to the OGT by placing a bite block or oral airway, despite the fact that the patient might be mechanically ventilated and sedated. Another important point to note is that even though the OGT had been in place for a short duration prior to endoscopic evaluation, this patient had developed a large ulcer at the GEJ along the course of the tube. While NSAID administration may have played a significant role in causing the ulcer, the case nonetheless emphasizes the importance of prescribing proton pump inhibitors to critically ill patients to protect against GI bleeding, particularly in patients with additional risk factors for mucosal injury.


Deerajnath Lingutla, MD*, Kirti Joshi, MD, Michael DiSalle, MD. Medicine, Unity Health System, Rochester, NY.

Purpose: Varices in the distal esophagus are a commonly seen complication of portal hypertension; these are termed "uphill" varices, based on the direction of flow to the superior vena cava from the portal venous system. Proximal esophageal varices are termed "downhill" varices, referring to flow from above downwards and are usually associated with upper body venous obstruction. We report a case of bleeding downhill esophageal varices as a complication of upper extremity hemodialysis access.

Methods: A 62 year old male with ESRD on hemodialysis secondary to polycystic kidney disease presented with hematemesis. Due to failures of upper extremity dialysis fistulae, he underwent repeated placement of dialysis catheters into the central venous system. This resulted in bilateral innominate vein occlusion, and led to balloon angioplasty with the insertion of stents to maintain flow and hemodialysis access. In the present admission, EGD after initial resuscitation with IV fluid and blood transfusion showed grade 3-4 varices in the proximal and mid esophagus, including one varix with fresh clot in mid esophagus. Band ligation of this varix was successful.

Results: Doppler ultrasound of the abdomen did not suggest portal hypertension. Proximal esophageal varices were felt to be due to bilateral innominate vein occlusion causing SVC syndrome.

Conclusion: Felson and Lessure in 1964 first coined the term downhill varices because the direction of blood flow is from above downwards. Most downhill varices results from superior venacaval syndrome/occlusion either by intrinsic or extrinsic causes. In our patient, longstanding complications of recurrent bilateral innnominate vein occlusion and SVC occlusion resulted in downhill esophageal varices in the proximal and mid esophagus. Although downhill varices are usually limited to the upper esophagus they can present in entire length of esophagus depending on the site of obstruction. If the occlusion appears proximal to the azygous vein, blood will be diverted via collaterals through the internal mammary, vertebral and patent azygous vein and downhill varices will be confined to the proximal esophagus. If SVC obstruction occurs beyond the confluence of the azygous vein, blood is diverted via collaterals along the entire length of the peri-esophageal plexus to the portal vein and inferior vena cava before reaching the heart, thus the varices can be seen in the entire esophagus. Diagnosis is by endoscopy. Treatment may include banding of varices, SVC stent/innominate vein stent and grafting. In the case of bleeding downhill varices, banding is the treatment of choice. Sclerotherapy is not recommended as it may cause severe complications such as vertebral infarction and pulmonary embolism.


Rizwan Ahmed, MD*, William Gallahan, MD, John Long, MD. Gastroenterology, Wake Forest University Baptist Medical Center, Winston Salem, NC.

Purpose: Case: A 51-year-old female presented to Gynecology with feculent vaginal discharge, concerning for a recto-vaginal fistula. Flexible sigmoidoscopy and barium enema were normal. Gynecology instilled a saline-peroxide solution into her rectum via rigid sigmoidoscopy to assess for effervescence into the vagina. No fistula was found. The day after, she had mild rectal bleeding. The hematochezia worsened, followed by tenesmus and abdominal pain, prompting admission five days later. Abdominal CT revealed circumferential thickening and inflammatory stranding involving the descending and sigmoid colon. Flexible sigmoidoscopy revealed severe proctitis and distal colitis with friable, erythematous mucosa covered with whitish exudates (Fig. A). Pathology showed mucosal erosion, hemorrhage, and inflammation, consistent with chemical colitis. With IV antibiotics and bowel rest, her abdominal pain and hematochezia resolved. She was discharged on antibiotics and was asymptomatic one month following her procedure. Discussion: Fewer than 100 cases of chemical colitis have been reported. Most have involved the inadvertent contamination of endoscopes with hydrogen peroxide and/or glutaraldehyde during the disinfection process. Peroxide mixtures are also used in the diagnosis of recto-vaginal fistulae. Other implicated agents include alcohol, radiocontrast agents, formalin, ergotamine, hydrofluoric acid, acetic acid, ammonia, and sodium hydroxide. There are reports of these agents being used intentionally in bowel cleansings and suicide attempts. Patients typically present with abdominal pain, rectal bleeding, and diarrhea, making the diagnosis challenging if a thorough history is not obtained. Persistent symptoms warrant diagnostic endoscopy. Instantaneous effervescence and blanching with saline lavage can be observed endoscopically, known as the "snow white sign." Histology often reveals "pseudolipomatosis," in addition to hemorrhage and inflammation. Depending on the depth and extent of injury, patients can develop colonic strictures, fistulae, ischemic colitis, and even peritonitis requiring colectomy. Most patients improve with conservative medical management. Chemical colitis should be highly suspected in patients presenting with acute colitis following lower endoscopy.


Mark Brewster, MD*, Daryl Hutchinson, MD, Satish Maryala, MD, Milton Mutchnick, MD. Department of Gastroenterology, Wayne State University School of Medicine/Detroit Medical Center, Detroit, MI.

Purpose: Small bowel diverticula are more common than intuition would suggest. As described, a case that was increasingly suggestive of serious pancreatic or biliary disease was the result of bezoar impaction of a juxta-ampullary duodenal diverticulum, also referred to as Lemmel's Syndrome.

Methods: A 50-year-old Caucasian female is referred to Gastroenterology for evaluation of 3 months of intermittent abdominal pain associated with nausea, vomiting, and acholic stools. Laboratory studies revealed abnormal transaminases and an elevated alkaline phosphatase, convincingly suggestive of biliary disease. Synthetic liver function appeared to be intact and abdominal ultrasonography revealed a dilated common bile duct to 1.2 cm without visualization of gallstones or sludge. Intrahepatic ducts were within normal limits and thus ultrasound was suggestive possibly of an obstructive lesion. HIDA Scan was negative.

Results: Direct visualization with upper endoscopy and endoscopic ultrasonography was initially planned. Endoscopically, a very large, smooth rimmed juxta-ampullary diverticulum was visualized, measuring 3.0 x 3.0 x 2.6 cm, with what appeared to be a large food bezoar bulging from the aperture. Using careful dissection and an endoscopic irrigation device the bezoar was broken up and dislodged from the diverticulum. Proteinaceous material was snared and removed to the lumen and the diverticulum was cleared. Follow-up clinical assessment revealed complete resolution of all abdominal symptoms including the intense pain and nausea with vomiting. Laboratory parameters subsequently normalized briefly thereafter.

Conclusion: This case illustrates an unusual etiology for a commonly encountered clinical scenario. Direct endoscopy proved to be the most effective means to evaluate this patient and simultaneously provided the modality for treatment. Small bowel diverticula are not vastly prevalent in our population. As in this case, these lesions have an unexpected ability to mimic many other physiologic, pathologic and/or anatomic conditions. The rarity of juxta-ampullary diverticulum may very well contribute to an expensive and at often times, unfocused workup.


Jae Geun Hyun, MD*, Sita Chokhavatia, MD, Xianyong Gui, MD, Noam Harpaz, MD, PhD, Lloyd Mayer, MD. Pathology, Gastroenterology, The Mount Sinai hospital, New York, NY.

Purpose: A 61-year-old female with history of bronchiectasis and resection of benign thymoma presented to The Mount Sinai Hospital with severe weight loss and malnutrition. She reported having chronic watery diarrhea and lower abdominal pain since 2004. A diagnosis of celiac disease was made based on an extensive work up at an outside hospital, which included abnormal small intestinal biopsies, but she had minimal clinical response to a gluten free diet. After a repeat colonoscopy 9 months later, Crohn's disease was diagnosed and she was treated with 4-5 courses of steroid tapering and 6-MP until February 2007, when she was hospitalized twice for severe constipation. On presentation to the Mount Sinai Hospital, she had persistent abdominal pain and reported weight loss of 45 lbs, despite continued gluten restricted diet. On examination, she appeared malnourished and had severe tenderness in left lower quadrant but no palpable mass. Lab data included Hb 10 g/dl, ESR 83, CRP 20.5, albumin 3.5 g/dl and negative HLA-DQ2/DQ8. Immunoglobulin quantitation and absolute T and B cell counts were within normal range. Small bowel series and abdomen CT were normal. On colonoscopy, the colon and terminal ileum appeared normal. Random colonic biopsies revealed loss of goblet cells and Paneth cells, presence of lymphocyte infiltrates in the lamina propria and and multiple apoptotic bodies. The findings were interpreted as autoimmune enteritis (AIE). Indirect immunofluorescence using patient's serum and frozen section of normal small bowel showed linear staining along the gut epithelium, consistent with anti-enterocyte antibodies. The patient resumed a gluten unrestricted diet and started oral prednisone and 6-MP. Her abdominal pain and diarrhea promptly improved and oral prednisone was successfully tapered over the next two months. Clinical remission of GI symptoms was maintained with 6-MP for over 1 year. Worsening bronchiectasis due to recurrent pseudomonas infections resulted in multiple hospitalization and the patient succumbed to respiratory failure in April, 2008. AIE was first described in 1982 by Unsworth and Walker-Smith and characterized by protracted diarrhea, circulating enterocyte antibody and associated autoimmune conditions. Only 3 of 30 reported cases had associated with thymoma. No standard approach for the treatment has not been established and immunosuppressive treatment is required in most cases. 60% of patients respond to steroid and 2/3 of steroid responders require additional immunomodulators for maintenance of remission. AIE should be considered in the differential diagnosis of malabsorption and refractory celiac disease.


Wendy Mikulski, DO*, Teresa Fergus, LPN, John Long, MD. Internal Medicine, Wake Forest University, Winston-Salem, NC, Internal Medicine, Drexel University, Philadelphia, PA.

Purpose: Rumination syndrome is the effortless regurgitation of recently ingested food which is not preceded by retching. The diagnosis of rumination syndrome is challenging and is based on Rome III criteria which rely on symptoms alone. Objective confirmation of the findings has been shown using antroduodenal manometry or esophageal manometry-impedance, but the sensitivities and availability in clinical practice of these modalities are lacking. We report a case of a patient with rumination syndrome documented by Rome III criteria and confirmed by findings on esophageal pH-impedance (IMP) monitoring.

Methods: A 23 year old female was referred with complaints of worsening regurgitation for 6 years. The patient indicated that regurgitated material comes up after nearly every meal without retching or nausea and that episodes began immediately after or sometimes during a meal. She denied heartburn, dysphagia, or vomiting and reported minimal weight loss. She had no improvement with several proton pump inhibitors (PPI) or with metoclopramide. An upper endoscopy, upper GI series, and gastric emptying study were all unremarkable. Esophageal manometry revealed a low LES pressure but was negative for a primary motility disorder. The patient was considered to have "refractory" gastroesophageal reflux disease (GERD) and so an ambulatory pH-IMP study was performed.

Results: The study performed off PPIs showed normal esophageal acid exposure (EAE) with a distal total time pH < 4.0 of 0.4% (NL < 4.2%) and a composite score of 3.2 (NL < 14.7). However, the total number of reflux episodes was elevated at 118 (NL < 73), with 79 (67%) occurring within 60 minutes of a meal. The patient reported 70 episodes of regurgitation with a symptom index of 99% (69/70), 40 occurred with non-acid reflux (NAR) and 29 with acid reflux (AR). The study was then manually analyzed and both reflux and symptom episodes were assigned to four time periods: Early (0-30 min) or late (31-60 min) Postprandial (PP), other Upright, and Supine. This nicely showed a predominance of symptomatic NAR in the early PP period with transition to AR in the late PP and non-meal periods (see Table).

Conclusion: The 24-hour pH-IMP study performed off PPI therapy on a patient with suspected rumination syndrome showed normal EAE but frequent episodes of symptomatic NAR in the early PP period, which gradually became acidic as food is cleared from the stomach by regurgitation or via gastric emptying. This pattern of reflux is characteristic for rumination and is distinct from the pattern expected in GERD. Documentation of this pattern is possible with impedance monitoring which allows detection of NAR. We believe that pH-IMP testing off PPIs can be used to confirm the diagnosis of rumination syndrome.


Neeraj Anand, MD*, Neil Herbsmann, MD, Leanne Cronin, MD, Sammy Ho, MD. Montefiore Medical Center, Bronx, NY.

Purpose: To describe a case of sigmoid schwannoma detected on colonoscopy.

Methods: Case report, review.

Results: A 62 year old woman with history of DM and HTN had a colonoscopy for a lower GI bleed. The patient had an unremarkable physical exam and laboratory tests. During colonoscopy, she was found to have a submucosal mass at the recto-sigmoid junction with a superficial ulceration; a biopsy was not diagnostic. The patient was sent for rectal EUS to further evaluate the lesion. On EUS, the lesion appeared to be originating from the muscularis propria. The mass was measured to be 2.7 cm x 1.8 cm and appeared to be consistent wih a GIST. The patient was referred to surgery and the mass was resected. It was found to be consistent with a schwannoma. The tumor stained strongly for protein S100 and negative for KIT, CD34 and desmin. The margins were negative and 7 lymph nodes were negative for involvement.

Conclusion: Schwannomas are benign tumors derived from the cells of Schwann that form the neural sheath, which can become malignant. Schwannomas have been documented as primary tumors in the gastrointestinal tract, but are usually found in the stomach. There is an equal incidence in men and women and the median age of presentation appears to be 65 years. These tumors appear to grow very slowly. Patients are usually asymptomatic but can present with rectal bleeding, constipation, obstruction, and abdominal pain. A variety of imaging modalities have been used to investigate schwannomas such as CT, MRI, colonoscopy and endoscopic ultrasound. Endoscopic ultrasound has been suggested to be reliable in predicting malignant potential; the predictive features being irregular margins, depth of penetration, cystic spaces and lymph nodes with a malignant pattern. Treatment usually consists of surgical excision although these tumors are benign and usually do not recur.


Maqsood Khan, MD*, Burns Meredith, BS, Jack Leya, MD, FACG, Sonu Dhillon, MD, FACG. Internal Medicine, West Suburban Medical Center, Oak Park, IL, Medicine, Loyola University Medical Center, Maywood, IL.

Purpose: Introduction: Suppurative gastritis (SG) is an uncommon often-fatal condition characterized by suppurative bacterial infection of the stomach. Here we describe a case of recurrent gastric abscess (GA). Case report: 28 year old female presented with severe epigastric pain for 6 days. Her past medical history was significant 2 previous episodes of similar abdominal pain for which she was treated with IV antibiotics for gastritis and discharged. In this episode she was referred for endoscopic ultrasound. Physical examination revealed tenderness to palpation in left upper quadrant. Diagnostic investigation with CT scan, Upper endoscopy and Endoscopic Ultrasound demonstrated GA (Fig. 1) which was opened and drained with a cystotome. Patient's pain rapidly resolved after drainage. Patient was started on IV piperacillin/tazobactam. Aspirate cultures were positive for streptococcus species. She was discharged home on oral antibiotics. Patient had a recurrent abscess 2 months later and had distal gastrectomy with roux-en-y gastrojejunostomy. Patient recovered postoperatively and was discharged in a stable condition and since then has been doing well. Discussion: Two types of suppurative gastritis have been described -a diffuse or "phlegmonous variant" and the localized or "intramural gastric abscess". A review of English-language publications since 1972 identified only 18 reported cases of intramural gastric abscess. The pathogenesis of intragastric mural abscess is thought to involve a focus of injury to the gastric mucosa because of penetrating trauma from an ingested foreign body or an endoscopic biopsy. The most commonly reported pathogen is Streptococcus, which is implicated in up to 75% of cases. Today, intramural gastric abscess is being diagnosed with increasing frequency by endoscopic ultrasonography Diagnosis of intramural gastric abscess is not difficult but requires a high degree of suspicion because of its rarity. Early diagnosis is important, as it may obviate a needless gastrectomy and even death.


Michael Harris, MD*, Ravi Ainapudi, MD, Prakash Viswanathan, MD. Gastroenterology and Hepatology, Stony Brook Medical Center, Stony Brook, NY.

Methods: Case Report An 85-year-old female with history of hypertension was admitted to the hospital with a three day history of nausea and vomiting. An abdominal CT was performed and revealed a large calcified mass (Fig. 1) and pneumobilia. A large obstructing duodenal gallstone (Fig. 2) located in the third portion was found on upper endoscopy. Attempts to remove the object endoscopically were unsuccessful. An apparent fistula was found in the duodenal bulb. An enterolithotomy was performed where a 5 cm gallstone was extracted and she did well post-operatively.

Conclusion: Discussion Bouveret's syndrome is characterized by gastroduodenal obstruction secondary to an impacted duodenal or pyloric channel gallstone via a cholecysto-duodenal or cholecysto-gastric fistula. Clinically patients present with symptoms of obstruction and radiographic studies reveal pneumobilia, cholelithiasis, and a distended stomach. Endoscopic findings include retained food, an impacted stone, and occasionally a fistula which was seen in our patient. Treatment is usually surgery, consisting of an enterolithotomy with or without concomitant cholecystectomy and fistula repair. Recently there have been reports of endoscopic therapy disintegrating gallstones including intracorporal laser lithotripsy, endoscopic mechanical lithotripsy, and electrohydraulic lithotripsy (1). Reference: 1. Gemmel G, Weickert U, Eickhoff A, et al. Successful treatment of gallstone ileus (Bouveret syndrome) by using extracorporal shock wave lithotripsy and plasm coagulation. Gastrointest Endosc 2007;65:173-175.


Michael Harris, MD*, Peter Ells, MD. Gastroenterology and Hepatology, Stony Brook Medical Center, Stony Brook, NY.

Purpose: Most etiologies of ascites can be divided into cardiac, renal, or hepatic in origin. Diagnostic paracentesis is the gold standard in initial evaluation. We present a case where additional testing was needed.

Methods: N/A

Results: Case Report A 48 y/o male with history of non-ischemic cardiomyopathy (LVEF of 16%), s/p AICD, who was admitted to the medical service with increasing abdominal girth, lower extremity edema, and worsening dypsnea on exertion. He had been admitted several times in the past year with similar complaints and has had LVP performed repeatedly. His medications were furosemide, spironolactone, and accupril. He used to be a bartender and drink alcohol, admitting up to 10-12 shots/night for [proportional to] 12 years, however he has been sober for over one year. He has no family history of liver disease. Physical exam was notable for a blood pressure of 86/61. He appeared older than his stated age. His neck exam was significant for JVD. Skin exam revealed spider angiectasias. His chest was clear, cardiovascular exam with loud apical systolic murmur. His abdomen was tense with fluid wave and palpable spleen noted. There was peripheral edema in his lower extremities. Neurologic exam failed to show asterixis and the patient was alert and oriented. Pertinent labs include a prolonged PT at 17 seconds, total bilirubin of 1.7 mg/dl, alkaline phosphatase of 166 U/ml, and normal transaminases and platelets. A CT scan revealed a large heart and extensive ascites. Cardiology consultation questioned the possibility of underlying cirrhosis given his history of alcohol abuse. Diagnostic paracentesis revealed a total protein of 3.5 and a SAAG > 1.1 compatible with portal hypertension. The elevated protein and pattern of LFT abnormalities suggested cardiac ascites, but since SAAG was elevated the diagnosis of underlying cirrhosis was entertained. A HPVG was performed to answer this question which yielded a gradient less than 5 mmHg suggestive of both increased portal and hepatic venous pressures, consistent with our suspicion of right sided heart failure with hepatic congestion and protein rich ascites. He was then referred for possible cardiac transplantation.

Conclusion: Measuring the HPVG can be useful in differentiating the etilogy of ascites as described in the above vignette.


Houssam Al Kharrat, MD*, Omar Shoukfeh, Medical Student, Luke Brown, Senior College. West Texas Digestive Disease Center, Lubbock, TX, Texas Tech University Health Sciences Center, Lubbock, TX, Abilene Christian University, Abilene, TX.

Purpose: First described by Rudolf Virchow in 1857, retroperitoneal liposarcoma is the most common retroperitoneal sarcoma and accounts for about 0.1% of all cancers. It is a slow occupying space tumor, that presents after involvement of adjacent organs, or incidentally during PE. We are presenting a patient with an unusual size mass presenting as inguinal hernia.

Methods: The patient is a 64 year old male who noticed an increase and fullness in the right scrotum. He first had this complaint 10 years prior to presentation. At that time he had lipomatous tissue surgically removed as part of inguinal hernia repair. Three years later, the fullness returned and has been progressively worsening. PMH is significant for hepatitis B surface antigen positive, mild hypertension, cervical disc fusion, and colon polyps. Medications are Benicar and ASA. Social history smoker 1/2 pack/day for 20 years. On PE: the right scrotum had a non-reducible mass. Blood count and chemistry panel, including tumor markers, were normal. CT showed a large 25 cm x 15 cm fatty mass with two solid components in the right abdomen displacing the colon and small bowel to the left abdomen. The mass extended into the right scrotum. No lymphadenopathy was present. The CT results were suspicious for a large liposacroma. Surgery was performed and a 52 lb mass was removed. Pathology confirmed the mass as a well differentiated liposarcoma. CT imaging at 6 months did not show any tumor recurrence.

Results: Although a total of 4 similar cases of liposarcoma presented as inguinal hernia have been reported on OVID between 1950-2008, this is the only case that has this tumor size and bulk on presentation.

Conclusion: This is a unique case because of the size of the tumor and the unusual presentation as an inguinal hernia.


Steve Egwuonwu, MD*, William Chamberlin, MD, FACG. Department of Gastroenterology, Internal Medicine, Texas Tech University Health Science Center, Elpaso, TX.

Purpose: To describe a rare complication of sigmoid diverticulitis.

Methods: Pyogenic liver abscess often manifests as fever and right sided abdominal pain. Sigmoid diverticulitis may be a source of bacterial invasion of the liver via the portal venous system.

Results: A 52 year old male presented with a 1 month history of generalized malaise and 3 day history of fever, chills and vomiting. Abdominal distention was noted on physical examination. An Abdominopelvic CT revealed a 10.9 cm multiloculated fluid density in segment 6, 7 and 8 of the liver. Mural thickening involving the sigmoid colon and diffuse adynamic ileus were additional findings on Computed Tomography. An assessment of liver abscess was made and patient had CT guided drainage of liver abscess. He was also also started on Imipenem. Liver abscess cultures were negative. A repeat abdominopelvic CT 6 days later showed persistent liver abscess. Colonoscopy was performed. Findings on colonoscopy was severe stenosis in the distal sigmoid colon. Patient had exploratory laparotomy which reveled perforated sigmoid diverticulitis and liver abscess. He had sigmoid resection, incision, drainage and debridement of liver abscess. He was discharged home on antibiotics.

Conclusion: This is a rare case of pyogenic liver abscess complicating sigmoid diverticulitis. The colon therefore should be considered as a possible source of infection in cryptogenic liver abscesses.


Neeraj Anand, MD*, David Greenwald, MD. Gastroenterology, Montefiore Medical Center, Bronx, NY.

Purpose: A case of a patient with gastric cancer presenting with Sweet's syndrome.

Methods: case report; review

Results: A 52 yr old Dominican man, with a history of HTN and PUD, presented to our institution complaining of nausea, vomiting, abdominal pain and a rash for 3 months. The rash was a tender erythematous rash that had appeared at the base of his neck. The patient underwent an EGD with endoscopic ultrasound, which demonstrated gastric cancer, stage T3N1. A biopsy was done and the pathology was consistent with poorly-differentiated adenocarcinoma. An exploratory laparotomy revealed diffuse cancer with extension to the peritoneal cavity. In addition, dermatology was consulted and a biopsy of the rash present on the upper chest revealed Sweet's syndrome or acute febrile neutrophilic dermatosis. The patient was treated with topical steroids with resolution of the rash. He had a lengthy hospital stay, but ultimately was discharged to follow-up for palliative chemotherapy.

Conclusion: Sweet's syndrome was originally described in 1964. It now is commonly divided into classic Sweet's syndrome and a malignancy-associated form. It appears that about 10-20% of patients with Sweet's syndrome have an associated malignancy. Of these, about 85% are associated with hematologic malignancies and 15% are associated with solid tumors. Sweet's syndrome is characterized by fever, neutrophilic leukocytosis, painful erythematous cutaneous plaques, neutrophilic infiltration of the dermis, and a rapid therapeutic response to steroids. The skin lesions typically are tender, gradually enlarge and are located on the upper extremities, head and neck. The treatment of choice is corticosteroids.


Danny Yen, MD*, Surinder Mann, MD, Virmeet Singh, MD. University of California, Davis, Sacramento, CA, VA Mather Medical Center, Sacramento, CA.

Purpose: Case: A 60 yo man presented with 2 days of abdominal pain post-screening colonoscopy. Patient was asymptomatic and in good health prior to the procedure. He denied any prior surgical history. The colonoscopy exam demonstrated sigmoid diverticula and 3 descending colon polyps. These polyps were removed by snare polypectomy. One day after the colonoscopy exam, he complained of diffuse abdominal pain that eventually localized to right lower quadrant (RLQ). He also complained of fever and anorexia, without nausea or vomiting. He had passed flatus but reported no bowel movements, since the colonoscopy procedure. Upon examination, he was febrile to 101F, with a heart rate of 104 beats/minute. The remainder of the vitals was normal. Cardiac exam confirmed sinus tachycardia; abdominal exam was significant for tenderness in the RLQ with rebound tenderness. Laboratory evaluation was significant for leukocytosis of 17,000. Abdominal x-ray did not reveal free air. CT of the abdomen/pelvis revealed acute appendicitis. A surgical consult was obtained. Intraoperative findings included a contained perforated appendix with appendiceal abscess and terminal ileum obstruction. 40 cm of terminal ileum was removed along with the appendix. Patient had an unremarkable postoperative course. Discussion: The overall complication rate with screening colonoscopy is less than 1%. Appendicitis is a rare, but known complication associated with colonoscopy. To the best of our knowledge, there have only been 10 such reported cases in the English language medical literature. Although the exact mechanism is unknown; excess pressure from the endoscope, excessive air insufflation/ barotrauma or impaction of stool; have all been proposed as possible injury mechanisms to the appendiceal orifice. Early recognition of this uncommon complication is imperative in order to expedite surgical intervention and ensure a good clinical outcome.


Danny Yen, MD*, Surinder Mann, MD. University of California, Davis, Sacramento, CA.

Results: Case: 71 yo man with intermittent "black" colored stools for several months underwent capsule endoscopy after an unremarkable EGD and a colonoscopy evaluation. He denies any abdominal pain, nausea, hematochezia, and is unaware of any weight loss. Medical history includes diabetes and hyperlipidemia, which he is on the appropriate medications. There is no iron supplementation, but he is on a daily baby aspirin. His family history is negative for IBD and celiac disease. He has a 120 pack-year history of nicotine abuse, but quit 10 years ago. Laboratory evaluation was pertinent for microcytic anemia. Capsule endoscopic exam revealed an ulcer in the distal small bowel. Double balloon enteroscopy and surgery were discussed with the patient after the capsule endoscopy findings. Patient elected laparotomy, and a 9 cm x 4 cm x 2 cm segment of the small bowel was resected. Within the specimen was a 6 cm x 3 cm polypoid, fungating mass. Mass was consistent with high grade, poorly differentiated malignant neoplasm, favoring metastasis as there lacked mucosal dysplasia. Immunohistochemical staining of the neoplasm indicated the primary source to be the lung. CT of the chest revealed a 4 cm mass at the left upper lobe (LUL) with suspicious lymph nodes. Consequently, patient underwent a LUL lobectomy with node sampling, confirming the primary source. Discussion: Small bowel malignancies are rare and account for 0.4% of all cancers. In addition to melanoma, breast, lung, and renal cancers can metastasize to the small bowel by hematogenous spread. Cervical, ovarian, and colon cancers can involve the small bowel by direct extension. In this case, we describe the first case of metastatic lung cancer to the small bowel diagnosed by capsule endoscopy.


Danny Yen, MD*, Homayoun Shojamanesh, MD. University of California, Davis, Sacramento, CA, VA Mather Medical Center, Sacramento, CA.

Purpose: Case: 71 yo M presented for colonoscopy screening after found to have FOBT positivity. He denied having any abdominal pain, changes in bowel habits or stool caliber, flushing or obvious bleeding. There is no family history of colorectal cancer. CBC did not reveal any anemia. Colonoscopy exam was significant for an erythematous, friable mucosa at the ileocecal valve. Attempts to intubate the TI were made, but they were unsuccessful. Biopsy of the abnormal mucosa confirmed carcinoid tumor with invasion into the muscularis proposa. Post-colonoscopy and pre-surgery laboratory evaluation was significant for a serotonin level of 381 ng/mL (normal <321 ng/mL), a chromogranin level of 6 nmol/L (normal <5 nmol/L), and a normal gastrin, 24 hour 5HIAA levels and LFTs. A small bowel follow-through was unremarkable. CT of the abdomen and pelvis did not reveal liver lesions, but did show a soft tissue density at the TI with enlarged surrounding lymph nodes. Octreoscan study was unremarkable. A surgery referral was made, and the patient underwent a laparoscopic right hemicolectomy. Surgical specimen was of a 2 cm carcinoid tumor at the ileocecal valve with 4/6 positive lymph nodes. Patient has since been followed by Oncology. Discussion: We present a case of carcinoid tumor at an atypical location with uncharacteristic features, diagnosed by screening colonoscopy. Carcinoid tumors are commonly located in the small bowel, rectum, colon, stomach, and appendix. Tumors located at the colon and equal to or larger than 2 cm are typically metastatic by the time of diagnosis and can be associated with carcinoid syndrome. Furthermore, carcinoid syndrome is typical for lesions at the midgut distribution. With our patient, his tumor did not have distant metastasis nor did it have any manifestations of the syndrome.





Oksana Anand, MD*. Gastroenterology and Hepatology, Kansas University Hospital, Kansas City, KS.

Purpose: Since the original description in 1887, dermatomyositis (DM) has become a well-recognized entity, characterized by nonsuppurative inflammation of skeletal muscles, pain and proximal muscle weakness with or without cutaneous lesions and sympathetic hyperactivity. In 1916 Stertz first called attention to DM coupled with visceral malignancy with most common sites being stomach 15.6%, breast 13.8%, lung 12.9%, ovary 9.2%, colon 3.7%. The onset of DM may precede, coincide or follow the diagnosis of malignancy.

Methods: An 82-year-old otherwise healthy Caucasian male presented with a 3-week history of fevers, weight loss, drenching night sweats, severe proximal leg muscle weakness and pain, yet minimally elevated CPK and aldolase. Symptoms began shortly after right hemicolectomy for a superficially invasive, well differentiated, nonmetastatic adenocarcinoma of the colon. Physical exam was remarkable for symmetric 3+ leg edema with exquisite tenderness to palpation, proximally diminished motor strength with no other neurological deficits. Thorough skin exam revealed no lesions, however patient reported having facial rash a few weeks prior to the onset of muscle weakness, attributed to a sunburn. Laboratory testing showed leukocytosis of 46K, anemia, CRP 29.8, LAP score 158K, ferritin 1259; fluctuating troponins; mildly elevated CPK and aldolase. Extensive workup with autoimmune, paraneoplastic, tumor marker panels, SPEP/UPEP, TSH, PSA, cortisol, HIV Ab, blood, sputum and urine cultures, PET/CT, MRI of the spine, ECHO was unrevealing. BM biopsy showed hypercellular (80%) marrow consistent with a reactive process, Philadelphia chromosome negative. EMG was consistent with inflammatory myopathy. MRI showed increased T2 signal intensity within multiple leg muscles and edema consistent with myositis. Open muscle biopsy revealed perimysial lymphohistiocytic inflammation with perivascular atrophy, strongly suggestive of DM. Muscle weakness dramatically improved after initiation of a high-dose steroid therapy.

Results: N/A

Conclusion: Based on temporal relationship between the diagnosis of colon cancer and onset of severe proximal muscle weakness, preceded by characteristic facial rash in an otherwise healthy man, we hypothesize that in our case DM represents a paraneoplastic syndrome rather than idiopathic inflammatory myopathy. Multiple studies demonstrated that patients with tumor-associated DM are less likely to have myositis-specific autoantibodies, so do our patient. Gastrointestinal involvement in DM ranges from severe inflammatory disease resulting from myoenteric dysmotility to colon cancer. Cutaneous paraneoplastic lesions of colon cancer are nonspecific immune type reactions and warrant further workup for an underlying malignancy.


Swapna Reddy, MD*, Kashyap Trivedi, MD, Yevgeniy Karamurzin, MD, Wan Jun Bae, MD, Gregory Albers, MD, Nimisha Parekh, MD, MPH. Department of Internal Medicine, Division of Gastroenterology, University of California, Irvine, Orange, CA.

Purpose: Cytomegalovirus (CMV) is known to cause significant enterocolitis in immunocompromised people. We describe pseudotumors of the ileum caused by CMV enterocolitis in a patient with metastatic melanoma. A 67-year-old man with metastatic malignant melanoma status post biochemotherapy one week ago presents with two days of diarrhea, anorexia, abdominal pain, and fevers. On presentation T 38.1[degrees]C, BP 89/49, P 102 bpm, RR 44, SaO2 98% on 2 lpm. Patient was tachypneic, abdomen without bowel sounds, tympanic, diffusely tender to palpation, and normal rectal exam. Blood: WBC 100, Hb 10.4, Hct 29, Plt 14,000, lactate 4. Stool studies were negative. Imaging: cecal pneumatosis intestinalis and transverse colon distention. Blood cultures: Streptococcus Viridans and Citrobacter Braackii. Patient treated for neutropenic typhlitis with flagyl and meropenem. He developed melena and recurrent fevers on hospital day #24. Esophogastroduodenoscopy (EGD) revealed Dieulafoy's lesion, treated with hemoclips. Hematochezia occurred 3 days later. Repeat EGD showed clips in place over previous lesion without bleeding. Colonoscopy revealed dark clots in terminal ileum (TI), no active bleeding, and friable cecal mucosa. Tagged RBC scan and push enteroscopy to mid-jejunum were negative for active bleed. Cecal biopsies had intranuclear and intracytoplasmic viral inclusions and positive stain for CMV antigen. CMV serologies positive with viremia. Intravenous ganciclovir started, however hematochezia continued. Visceral angiography showed extravasation from distal branch of ileocolic artery localizing to cecum and TI. Twelve hours post-embolization recurrent hematochezia caused hemodynamic instability. Exploratory laparotomy showed several masses in the TI, so ileocecetomy with diverting ileostomy done. Final pathology: CMV without malignancy. Patient recovered post-operatively without further episodes of GI bleed. CMV enterocolitis presents with abdominal pain, bloody diarrhea, weight loss and fever. Diagnosis is made by symptoms, visualization of ulcers, and intranuclear viral inclusions in mucosal cells. CMV of the GI tract usually involves esophagus, colon, and less commonly small intestine. Ganciclovir is the treatment of choice for 3-6 weeks. Surgical intervention is necessary with signs of peritonitis, free perforation or persistent GI bleed. This case shows CMV enterocolitis can develop life-threatening complications such as hemorrhagic ulcerations causing GI bleed and inflammatory pseudotumors contributing to adhesions, and perforation. Failure of patient to improve with appropriate medical therapy should prompt clinicians to further investigate the presence of complicating factors, such as CMV masses.


Sofia Novak, MD*, Andrea Tieng, MD, Kostas Sideridis, DO, Simmy Bank, MD. Gastroentorology, Internal Medicine, Long Island Jewish Medical Center, New Hyde Park, NY.

Purpose: NA

Methods: 30 year old Indian male with no known prior medical history was admitted for total colectomy with ileorectal anastomosis for FAP syndrome. His father was diagnosed with colon cancer (ca) at the age of 52, prompting a colonoscopy in his brother that demonstrated multiple (>50) colonic polyps. The patient's colonoscopy found over 100 polyps ranging from 2 mm to 3 cm, tubular with tubular-villous adenomas on pathology. A presumed diagnosis of attenuated FAP was made.

Results: Genetic testing for FAP was positive while mismatch repair gene was negative. Post surgery, the patient had nausea and abdominal pain. An upper endoscopy demonstrated esophagitis, gastric erosions, and clean-based duodenal ulcers, with subtotal villous blunting on biopsy. Celiac markers were found to be positive: anti-tissue transglutaminase antibody (AB)(TTG IgA) 65-100 units, anti-endomysial IgA AB positive (1:20). Antigliaddin AB IgG/IgA were negative. Patient was found to have microcytic anemia (H/H 11/36 with MCV 75) due to iron deficiency (iron 15, iron saturation 4%) and diarrhea (nonbloody, loose, 5-6 BM/day). HLA DQ8 was detected while HLA DQ2 was not present. The patient was instructed to go on a gluten-free diet. A repeat upper endoscopy demonstrated an atrophic duodenum with preserved villi architecture and focal mild intraepithelial lymphocytic infiltrate. On follow-up, the patient had improvement of diarrhea (2 BM/day).

Conclusion: This case presents a patient with attenuated FAP syndrome and celiac sprue, both known for their strong genetic predisposition. There have been no known documented cases reported from an extensive literature search. Celiac disease (CD) is an under diagnosed problem that has a 95% genetic predisposition. It can be associated with other autoimmune conditions. 95% of patients with CD have a particular HLA class II genotype - encoded by chromosome 6: 6p21.3. The disease is genetically complex. A recent study (1) indicated that CD is more prevalent in females and has a strong paternal inheritance of predisposing haplotypes. It also found that HLA negative patients were more likely to be male. FAP is an autosomal dominant inherited disease that has a strong association with the APC gene located on chromosome 5, between p21 and p22. Attenuated FAP is characterized by a significant risk for colon ca, but fewer polyps (avg. 30) than classic FAP, more proximally located polyps, and diagnosis of colon ca at a later age; management may be substantially different. (2) It would be interesting to know if both diseases were transmitted through paternal transmission and if there is a role of disease accumulation or co-transmission. The immunologic bases for the co-conditions are not evident and this could represent a random occurrence.


M Babitha Reddy, DO*, Michael Frank, MD. Gastroenterology, Lenox Hill Hospital, New York, NY.

Purpose: Airway obstruction is a well known complication of propofol. The mechanism of action is related to laryngopharyngeal musculature relaxation. We report a case of large meat impaction in the distal esophagus that could not be extracted until a single dose of propofol was administered, which facilitated temporary laryngopharyngeal musculature relaxation.

Methods: Case Summary A 50-year-old man was evaluated in the emergency room with a symptomatic foreign body impaction making it difficult for him to manage his secretions. He reported eating steak prior to the onset of symptoms. Upper endoscopy with standard monitoring was employed, performed after admisitering midazolam 5 mg and miperidine 50 mg. A collection of food debris was found in the mid-esophagus and a large piece of meat was impacted in the distal esophagus. The endoscope could not be advanced beyond the impaction. The size of the meat precluded the use of an over tube. The meat was firmly held by a snare wire but despite adequate sedation could not be extracted beyond the proximal oropharynx without significant resistance. Multiple attempts at extraction had failed. A bolus dose 50 mg of propofol was administered to allow for relaxation of the laryngopharynx and to provide short-term deep sedation. The meat was then easily withdrawn in one attempt without resistance. The foreign body was a solid piece of meat that measured 6 cm in length and 2 cm in width. The patient maintained his respiratory status throughout the procedure and recovered consciousness within thirty seconds.

Results: NONE

Conclusion: Propofol may offer better laryngeal relaxation than midazolam and meperidine and should be considered an important agent that can allow for the safe extraction of a large foreign body. Future research to evaluate its safety profile and the efficacy in an emergency situation for foreign body removal should be studied.


Richard Blatt, MD*, Jennie Law, MD, Tanvi Dhere, MD, Marney Goldstein, MD, Henry Olejeme, MD. Emory University, Atlanta, GA.

Purpose: A 20-year-old Guatemalan male with no significant past medical history presented with complaints of one week of abdominal pain, nausea and vomiting. Labs were unremarkable. A CT scan of the abdomen and pelvis revealed evidence of a small bowel obstruction. After the patient showed no improvement in symptoms with bowel rest and decompression, a small bowel enteroscopy was performed. The enteroscopy showed a stricture within the proximal jejunum, ulcerations distal to the stricture, and diverticulae proximal to the stricture. Biopsies of the ulcerations revealed noncaseating granulomas. Acid fast bacilli (AFB) and fungal stains were negative. Based on the biopsy, there was a concern for the possibility of Crohn's disease so the patient was started on steroids and antibiotics. When the patient did not improve over the next 48 hours, he was referred for a surgical evaluation. A laparotomy revealed the presence of multiple peritoneal nodules, and lysis of adhesions was performed without bowel resection. Biopsies showed caseating granulomas with positive AFB stains. The patient's PPD, HIV test, and chest X-ray were all negative. The patient was started on rifampin, ethambutol, pyrizinamide, and levofloxacin. He showed an improvement in symptoms within six weeks. This case highlights the need for a high index of suspicion for tuberculous enteritis when evaluating patients with possible Crohn's disease, especially HIV patients and immigrants from areas where TB is endemic. Tuberculous enteritis rarely causes a small bowel obstruction. However, in cases where it causes strictures, obstruction is a common complication. Tuberculous enteritis is the most common extrapulmonary manifestation occurring in 25% of patients with pulmonary TB. Although our patient presented with proximal small bowel involvement, the majority of patients (75%) have distal small bowel and ileocecal involvement. As highlighted in this case, diagnosis is often difficult because common screening methods and microbiological diagnostics often fail to detect gastrointestinal TB. However, a prompt diagnosis can help prevent the development of serious complications such as intestinal fistulas, obstruction, and perforations.


Kiran Rao, MD*, Eric Rosendorf, MD. Internal Medicine, UMDNJ, Newark, NJ, Gastroenterology, Hackensack University Medical Center, Hackensack, NJ.

Purpose: Superior mesenteric artery (SMA) syndrome is a rare disorder that results in proximal small bowel obstruction caused by the trapping of the third portion of the duodenum between the SMA and aorta. This is often due to the loss of the intervening mesenteric fat pad. The use of endoclips to anchor an enteral feeding tube and ensure nutrition beyond the ligament of Treitz in patients with abnormal anatomy has only been described in 1 case report. We report a case where a nasojejunal tube was placed and anchored beyond the 3rd portion of the duodenum by an endoclip to ensure enteral nutrition in small bowel obstruction secondary to SMA syndrome.

Methods: We present a case of SMA syndrome in a 22 year-old male with a history of mental retardation and attention deficit hyperactivity disorder who presented with nausea, vomiting, progressive fatigue, weight loss and vague abdominal pain for 1 week. The diagnosis of SMA syndrome was made with an abdominal CT, which revealed complete duodenal obstruction at the level of the third portion of the duodenum. An elective push enteroscopy confirmed an extrinsic compression at the 3rd portion of the duodenum. An attempt for conservative treatment allowing for decompression of the stomach and maintance of nutrition was attempted with endoscopic placement of a "STAY-PUT" nasojejunal tube with a gastric venting port. The distal portion of the tube was secured with an endoclip.

Results: Unfortunately the patient was unable to tolerate conservative treatment and ultimately required a laparoscopic duodenojejunostomy.

Conclusion: SMA syndrome is a rare condition with an incidence of 0.013-0.3%. Compression of the duodenum by the SMA is an unusual cause of proximal small bowel obstruction which may result in malnutrition and weight loss. Secure placement of a nasojejunal tube with an endoclip is an option to ensure enteral nutrition with hopeful weight gain and restoration of the mesenteric fat pad, thus possibly avoiding surgical intervention.


Charles Koczka, MD*, Alejandra Castillo-Roth, MD, Adam Goodman, MD. SUNY Downstate Medical Center, Brooklyn, NY.

Purpose: Portal Cavernoma, also known as cavernous transformation of the portal vein, is a rare condition consisting of formation of multiple portoportal collateral vessels around a previously stenosed or occluded portal vein. It is classically described as a consequence of portal vein thrombosis (PVT).

Methods: A 53-year-old Haitian male with a history of diabetes mellitus and hypertension presented with one month history of lower abdominal pain. The pain was crampy in nature, intermittent, exacerbated after meals, and improved with rest. The patient also noted increased abdominal girth and bilateral lower extremity edema. He took Pioglitazone/Metformin and Triameterne/Hydrochlorothiazide on a daily basis, but denied smoking or alcohol use. He denied personal or familial history of hypercoaguable states or chronic liver disease. On presentation, he was afebrile and normotensive. No jaundice or stigmata of chronic liver disease was noted. His abdomen was distended with shifting dullness, diffuse tenderness, and normoactive bowel sounds. Bilateral 3+ pitting edema of lower extremities was also noted.

Results: Laboratory data, including hepatic panel and coagulation profile, were unremarkable, except for a CBC showing thrombocytopenia (78,000/[mu]L). Viral hepatitis B and C panels were negative; alpha-fetoprotein and iron panel were normal; autoimmune work-up unrevealing. Contrast enhanced CT scan of the abdomen revealed moderate-sized ascites along with multiple tortuous collateral vessels in the porta hepatis and gallbladder fossa, consistent with cavernous transformation of the portal vein. The splenic vein was dilated and tortuous, consistent with portal hypertension. No thrombi or intra/extrahepatic biliary tree dilatation were seen. Hepatic vessels were patent. On esophagogastroduodenoscopy, three columns of medium sized esophageal varices were noted. Liver biopsy showed normal hepatic liver parenchyma with significant dilation of the sinusoids. The patient is currently on Propranol and Spironolactone, with improvement of his symptoms.

Conclusion: Cavernous transformation of the portal vein usually occurs after PVT secondary to cirrhosis, abdominal infections or neoplastic processes, hypercoaguable states, myeloproliferative disorders, or surgery. Our patient did not have any of the above conditions. We, thus, report a rare case of idiopathic cavernous transformation of the portal vein.


Jahnavi Naik, MD*, Yan Li, MD, Nicole Griglione, MD, Qiang Cai, MD. Division of Digestive Diseases, Emory University, Atlanta, GA.

Purpose: A 26 year old man presented with 3 day history of severe bright red blood per rectum and dizziness. Pt had multiple hospitalizations since age of 7 for lower GI bleedings. In addition to orthostatics hypotension and tachycardia, his physical examination findings were remarkable for asymmetry left shoulder hypertrophied than right, hypertrophy of first 3 digits on left hand and 2nd and 3rd digit on right hand, as well as cutaneous cafe au lait laced spots extending from the right forearm to chest and hemangiomas in low extremities. His laboratory data revealed severe microcytic anemia with hemoglobin of 2.7 g/dl (normal = 12.9-16.1) with mean corpuscular volume of 58.0 fl (79.3-94.8). Others were normal After successful resuscitation with blood transfusion, patient underwent a colonoscopy that revealed extensive stage IV varices in the rectum. MRI/MRA demonstrated large hemangiomas in anterior and superior pelvic veins, extensive varices and dilatation of the abdominal IVC that were consistent with multiple vascular malformations. AVMs in the mesentery, the spleen, and the kidneys were identified. Portogram revealed normal portosystemic gradient of 2 mmHg. Arteriogram was normal. Patient underwent successful embolization of a middle sacral artery AVM with good collateral flow to the distal rectum.

Conclusion: Based on the above finding, the diagnosis was Klippel-Trenaunay Syndrome (KTS). KTS is a congenital disorder characterized by the triad of port wine stains, varicosities and venous malformation and limb hypertrophy (98%, 72%, 67% frequency seen, respectively). Most cases are sporadic and the pathogenesis remains unclear. GI manifestations, found in less than 1% of KTS, include cavernous hemangiomas of the distal colon and rectum and rarely of the jejunum, and esophageal and rectal varices secondary to prehepatic portal hypertension from hemangiomas or hypoplasia of portal vein. These hemangiomas and varices are susceptible to bleed leading to massive hematemesis or hematochezia, which was seen in this patient. Radiological investigations are vital in evaluating the location, severity and management of these bleeding GI. Management of nonsignificant bleeding is conservative with iron supplementation. In cases of recurrent and/or severe bleeding, management with either embolization of the bleeding site or surgical resection. However, resection is not curative due to extensive visceral hemangiomas. Endoscopic argon laser and photodynamic therapies have been utilized in a few cases of refractory post-resection localized bleeds.


Scott Pollack, MD*, Virendra Joshi, MD. Gastroenterology, Tulane University School of Medicine, New Orleans, LA.

Purpose: Annular pancreas (AP) is a rare congenital abnormality in which the ventral portion of the pancreas fails to rotate with the duodenum during embryological development, thus causing the ventral portion to remain partially or fully enveloped around the duodenum. The incidence of AP is unknown, as many cases are asymptomatic and undiagnosed. Adults with AP may present with a variety of symptoms suggestive of gastric outlet obstruction, or may present with gastrointestinal bleeding, pancreatitis, or biliary obstruction. Although as many as 50% of patients present in adulthood, there have been no published reports of cases above the age of 76. Surgery continues to remain the diagnostic "gold standard" for AP, but imaging techniques such as computed tomography (CT), magnetic resonance imaging, endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasound (EUS) can now be used to make the diagnosis. We report the case of an 85 year old gentleman who presents with symptoms of partial gastric outlet obstruction who was diagnosed with AP by EUS and secretin magnetic resonance cholangiopancreatography (MRCP).

Methods: N/A

Results: An 85 year old gentleman with a past medical history of hypertension, diabetes, and cerebrovascular disease was admitted to the hospital for the evaluation of intermittent abdominal pain, nausea, vomiting, and weight loss. CT of the abdomen revealed a soft tissue mass surrounding the second portion of the duodenum causing duodenal compression. Esophagogastroduodenoscopy revealed a narrowed duodenal lumen as well as the presence of a duodenal diverticulum. EUS was performed revealing the soft tissue mass to be pancreatic tissue of normal echogenicity with the presence of an annular duct confirming the diagnosis of AP. ERCP was unable to be performed as the major papilla was within the duodenal diverticulum and could not be cannulated. Dynamic MRCP, with the intravenous administration of secretin, was performed to evaluate both the pancreatic and biliary ducts revealing no ductal dilatation but again confirming the diagnosis of AP.

Conclusion: AP is a rare presentation in the elderly, yet a high index of suspicion needs to be maintained in elderly patients with a presentation of gastric and duodenal outlet obstruction. We highlight the role of EUS and secretin MRCP as highly sensitive and safe modalities compared to standard ERCP, with its associated risk of pancreatitis, to diagnose AP and its associated ductal abnormalities.


Arun Srivatsa, MD*, Judy Liu, BS, Joel McFarland, MD, Vivek Kaul, MD. University of Rochester, Rochester, NY.

Purpose: We describe a patient with black tarry stools & an elevated INR after eating a pound of Black Licorice. Although literature describes the effects of Licorice root on the cardiovascular & renal systems, there is a paucity of data on interactions between Black Licorice & warfarin. Furthermore, eating Black Licorice colors stools black & may be mistaken for melena in the absence of true bleeding. Vice versa, the patient with true melena may be falsely reassured that the stools are black because of the Licorice.

Methods: An 80-year-old woman with atrial fibrillation anti-coagulated with warfarin ate a pound of Black Licorice 4 days prior to presentation. She then noted black tarry stools but did not seek medical attention because she attributed this to the Licorice. Eventually she developed dizziness, subsequently collapsed & was brought into the Emergency department. There was no hematemesis or abdominal pain. Warfarin had been dosed at 1 mg daily. She had maintained a therapeutic INR, checked weekly for a long time. She was hypotensive & tachycardic, Hematocrit was 14 (baseline 34) & INR 5.5 (baseline 12 days prior was 2.1). The patient had a similar episode related to Black Licorice ingestion in 2004, when she was admitted with black stools & weakness. INR was 9.1 & hematocrit was 16 at that time. She received fresh frozen plasma & packed red blood cells & underwent upper endoscopy. A prepyloric gastric ulcer with a visible vessel at the base was seen & 2 clips were placed. She had an uneventful hospital course & was discharged with a stable hematocrit & therapeutic INR & instructions to avoid Black Licorice.

Results: Black Licorice is derived from the root of the plant, Glycyrrhiza glabra & is known for its anti-inflammatory & mineralocorticoid inducing properties. Licorice has also been implicated for interacting with a number of medicines, e.g. digoxin, thiazides & spironolactone. Gliabridin present in Licorice inhibits the P450 system which metabolizes Warfarin. Glycyrrhizin, also present in licorice, is a thrombin inhibitor & prolongs fibrinogen clotting times. Hence, the anti-thrombotic activity & inhibition of warfarin metabolism may synergistically amplify anti-coagulation.

Conclusion: Black licorice is a commonly available food product. This case report illustrates how Black Licorice may potentiate or cause GI bleeding especially in patients on warfarin. The presence of Black Licorice in stool can obviously mimic melena & confound its clinical presentation. Therefore, till more data is available, health care providers should caution patients who are at risk for bleeding or on warfarin to avoid black licorice.


Kumaravel Perumalsamy, MD*, Muthukumar Muthusamy, MD, Muhammad Abdullah, MD, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD. Division of Gastroenterology, Division of Medicine, Maimonides Medical Center, Brooklyn, NY, Divison of Surgery, Coney Island Hospital, Brooklyn, NY.

Purpose: Roux-en-Y gastric bypass (RYGBP) is a mainstay of bariatric surgical therapy. A Gastro-Gastric Fistula (GGF) is an infrequent but potentially serious complication of gastric bypass, and clinicians often have difficulty establishing the diagnosis. We report a novel endoscopic technique of successful management of GGF using APC and endo-clips.

Methods: A 31-year-old woman with a BMI of 44 underwent a laparoscopic divided ante-colic Roux-en-Y gastric bypass (RYGBP), with creation of a 30-cc gastric pouch. Her immediate post-operative course was unremarkable. She was discharged home on the 6th post-operative day. Two months later, she complained of persistent postprandial nausea and emesis. An upper GI series performed revealed a GGF, with preferential flow into the bypassed stomach (Fig. 1). Despite this finding, she has achieved a 70% excess weight loss. The patient had elected not to pursue revisional surgery. Upper Endoscopy was performed. No marginal ulcerations noted. GGF was identified at the cardia. Twice daily PPI's did not improve her symptoms. Two weeks later repeat endoscopy was perfomed. A guide-wire was passed through the fistula. Fluoroscopy confirmed the position of the cannula in the distal stomach pouch. APC of the fistula tract was done. Two Boston Scientific Resolution Clips were used to close the fistula after APC of the tract. The patient was sent home on twice daily PPI. Her symptoms improved. Repeat upper GI series three weeks later showed closure of GGF (Fig. 2).

Results: Although a gastro-gastric fistula is currently an uncommon complication of RYGBP, historically GGF was one of the most common complications after undivided RYGBP, occurring in up to 50% of patients. This complication rapidly declined with the introduction of laparoscopic gastric bypass with an incidence ranging from 0-6%. Multiple factors likely to play a role in the formation of a GGF. Failure to completely transect the gastric pouch from the bypassed stomach, gastrojejunal anastomotic leak, anastomotic or marginal ulcerations, and obstruction of the Roux-limb distal to the anastomosis is few of the causes of formation of GGF. In patients with a clearly identifiable GGF on contrast study and/or endoscopy who demonstrate poor weight loss, revisional surgery should be considered. In patients with demonstrable GGF but good weight loss, PPI therapy should be used to treat symptoms.

Conclusion: In symptomatic patients, as we have shown, obliterating the fistula tract using APC and closure of GGF using endo-clips should be considered safe and effective.


Harpriya Singh, MD*, Aparna Kulkarni, MD. Gastroenterology, Allegheny General Hospital, Pittsburgh, PA, Gastroenterology, Baylor College of Medicine, Houston, TX.

Purpose: Crohn's Disease is a chronic, idiopathic, inflammatory bowel disease (IBD) that can often present a diagnostic dilemma due to a nonspecific clinical presentation and the lack of sensitive and specific serologic, radiographic and pathologic findings. A 29 year old female presented to our institution with a 10 day history of nausea, vomiting, abdominal pain and diarrhea which started 2 weeks after an uneventful cesarean section. She had no significant past medical, social or family history. Initial evaluation revealed an elevated C-reactive protein, bandemia and diffuse small bowel thickening on a CT scan of the abdomen and pelvis. Stool studies were negative for Clostridium difficile, Salmonella, Shigella, Campylobacter, Giardia and Yersinia. Enteroscopy demonstrated diffuse granularity, erosions, erythema from the second part of the duodenum upto the proximal jejunum. Biopsies showed nonspecific inflammation, villous blunting, and ulceration. Gram's stain and fungal stain on the biopsies were negative. Additional testing included a Magnetic Resonance Angiogram of the abdomen, anti-neutrophilic cytoplasmic antibodies, tissue transglutaminase immunoglobulin A, anti-neutrophilic antibody, anti-double stranded DNA antibody, serum complements and lactic acid, which were all negative. A presumptive diagnosis of Crohn's enteritis was made and steroid therapy resulted in partial resolution of her symptoms. Over the next few months, she had multiple admissions for recurrent symptoms while on a steroid taper. Further evaluation included IBD serologies (anti-saccharomyces cerevisiae antibody, anti-Outer membrane porin C, antibody to CBir1 flagellin), a small bowel follow-through, human leukocyte antigen typing for DQ2 and DQ8, serum Entamoeba histolytica antibody, a repeat upper endoscopy with duodenal biopsies including smear for acid fast bacilli, colonoscopy with terminal ileal evaluation and a mesenteric angiogram which were all unrevealing. A diagnosis of Crohn's Disease was established after a Virtual Capsule Endoscopy showed patchy mucosal changes of erythema, fold thickening and fissuring, villous blunting, erosions and linear ulcerations in mid and distal small bowel with luminal stenoses at two sites. She was then started on azathioprine with good response. To our knowledge, six cases of new-onset Crohn's Disease in the postpartum phase have been previously described in the literature. However, this is the first case of Crohn's Disease with such a severe early onset presentation in the puerperium.


Suhail Salem, MD*, Omar Lateef, DO, Joseph Ahn, MD, MS, Stanley Cohen, MD, David Van Thiel, MD. Section of Pulmonary/Critical Care Medicine, Section of Hepatology, Rush University Medical Center, Chicago, IL.

Purpose: Background: Shy Drager syndrome or multiple system atrophy (MSA) is a neurodegenerative disorder characterized by any combination of autonomic failure, parkinsonism, cerebellar ataxia and pyramidal signs which is progressive until death, with a mean survival of 9 years. Orthostatic hypotension affects the majority of these patients. Supportive therapy including fluids, high salt intake, and vasopressor medications are the mainstays of treatment. This is the first reported case of MSA in a liver transplant recipient.

Methods: A case report is presented.

Results: Clinical History: A 63 year old male with hepatitis C cirrhosis post-OLT presented with mental status changes and hypotension. He was treated with lactulose, aggressive hydration, and dopamine. He was evaluated for re-transplantation for recurrent hepatitis C and allograft failure. The first attempt at re-transplantation was cancelled due to hypotension, but after subsequent workup, hydration, and cardiology clearance, the patient was taken for OLT. His post-operative course was complicated by another episode of hypotension. He was treated supportively, subsequently improved, and was eventually discharged. Six weeks later, he was again found to be hypotensive. 14 months later, he was admitted again with refractory hypotension, which persisted despite maximal supportive care including broad spectrum antibiotics, intravenous fluids, steroids, and multiple vasopressors. He had a prolonged 3 month hospital course and failed multiple attempts at pressor weaning. During this hospitalization, he was noted to have pupil abnormalities, an absence of sweating, and persistent diarrhea. A pulmonary artery catheter demonstrated normal to high cardiac index, low systemic vascular resistance, normal pulmonary capillary wedge pressure, and low mixed venous O2 saturation. This was consistent with neurogenic shock. A CT of the head demonstrated an old infarct in the center of the pons. The clinical history and CT findings were consistent with a diagnosis of Shy Drager syndrome. The family of the patient decided to withdraw care after he failed to improve and he expired shortly afterwards.

Conclusion: This case serves to illustrate several points: First, in a post-OLT patient, hypotension can occur and cardiac, hepatic, or infectious etiologies must first be considered. If the hypotension is refractory to maximal supportive therapy, then alternative diagnoses should be considered. Second, if the diagnosis of Shy Drager syndrome had been diagnosed prior to repeat OLT, it would have been inappropriate to proceed with the transplant as this condition is universally fatal.


Jason Gutman, MD*, Thalia Mayes, MD, Asad Ullah, MD, Linda Schiffhauer, MD. DiviDivision of Pathology, Division of Gastroenterology & Hepatology, University of Rochester, Rochester, NY.

Purpose: Breast cancer is the most common female cancer in the U.S., with 1 in 8 women developing invasive disease. Most often metastatic disease is found in lungs, bones, liver, and brain. Here we present a rare case of invasive ductal breast cancer with metastatic lesions to the rectum confirmed by endoscopic ultrasonography and biopsy.

Methods: This is a retrospective chart review of a single case.

Results: A 59 year old female with a history of metastatic breast cancer, was referred for constipation and lower quadrant abdominal pain. She was originally diagnosed with Stage IIA (T2N0M0) ER positive invasive ductal breast cancer in 1997. A lumpectomy was performed and she completed 5 cycles of adjuvant chemotherapy followed by 5 years of Tamoxifen. In 2004, she had a surgical resection of a metastatic right adnexal mass. In 2006, she was started on Arimidex and a re-staging CT scan did not show any metastatic disease. Over the next 18 months she complained of worsening lower quadrant abdominal discomfort and constipation. Abdominal exam revealed mild lower quadrant tenderness. Rectal exam was normal. CEA was elevated. CT scan showed multiple small liver lesions and rectal wall thickening. Barium enema confirmed circumferential rectal wall thickening. Flexible sigmoidoscopy with endoscopic ultrasound showed a single small rectal ulcer with sonographic thickening of the rectal wall, loss of normal layers, and no abnormal lymph nodes. Biopsy revealed metastatic carcinoma of breast origin with immunohistochemical staining positive for cytokeratin 7/ER and negative PR/HER2/cytokeratin 20.

Conclusion: Metastatic breast cancer to the GI tract is quite rare, and is more common in the upper intestine. The rate of metastatic breast cancer to the lower GI tract on autopsy series is 8-12%, but only case reports or series have been reported in live patients. Most cases of rectal involvement are found with synchronous lesions and after a latent period of 4-10 years from initial diagnosis. Primary colorectal cancer is more common in breast cancer patients compared to metastases to this area, making it difficult to differentiate the two on initial presentation. Endoscopically, these lesions are usually indistinguishable; however metastatic lesions are usually intramural. Thus endoscopic ultrasonography can help with localization and characterize this intramural pattern. In patients with a history of breast cancer and a new colorectal lesion, differentiating between metastatic disease and a new primary can be aided by endoscopic ultrasonography, histologic appearance on biopsy, and use of immunohistochemical stains for cytokeratins, tumor markers, and estrogen/progesterone receptors.


Mustafa Tiewala, MBBS, MD*, Gerold Fruchter, MD. Gastroenterology, SUNY Downstate Medical Center, Brooklyn, NY, Gastroenterology, VA NY Harbor Healthcare System, Brooklyn, NY.

Purpose: To highlight mucormycosis with cranial nerve involvement presenting with dysphagia in an immunocompromised cirrhotic patient.

Methods: A 59 year old male with Laennec's cirrhosis, diabetes mellitus, and coronary artery disease presented to the emergency department with left sided facial pain following a tooth extraction 2 days earlier. His facial swelling was initially attributed to the tooth extraction. He had left sided facial numbness and drooping, with flattening of the left nasolabial fold. The Head CT and MRI on admission were essentially unremarkable. In view of dysphagia to both solids and liquids, with inability to swallow and choking on liquids, the GI team was consulted. He denied any nausea, vomiting, odynophagia, or abdominal pain. The following day he developed diplopia, and the next day became blind in the the left eye. On exam he was tachycardic, Tmax 100 F, 120/60 mm of Hg, and respiratory rate of 16 per minute. He had slurred speech, was unable to open left eye and had no vision in that eye. Pupils were sluggish in response to light and poorly reactive bilaterally with bilateral ptosis. Absent left ocular motion. Poor gag reflex was present; tongue movements were fine. Abdominal exam was significant for moderate ascites. During hospital stay he developed a white count of 24,000, and became hemodynamically unstable requiring ICU monitoring. A repeat CT of the sinuses now showed bilateral mucosal thickening of the ethmoid, frontal and maxillary sinuses, with frothy mucous in the sphenoid sinus. On nasal endoscopy a necrotic left middle turbinate was seen with white spores in the posterior nasopharynx, biopsies positive for mucor like fungus. The patient was started on amphotericin B and an emergent tracheostomy, radical maxillectomy, and left orbital exenteration was performed. Post-op the patient continued to deteriorate and he expired two days later.

Results: NA

Conclusion: Mucormycosis in cirrhosis is rare and has a poor prognosis. The immunocompromised state present in cirrhotics as well as the underlying diabetes represented risk factors in our patient. This case highlights a rapidly progressive fatal case of rhinocerebral mucormycosis presenting with dysphagia due to cranial nerve neuropathy. Literature search reveals a small case series of cirrhotics with mucormycosis presenting with upper motor neuron signs, but this case is unique in its presentation with dysphagia. In view of the immunocompromised state of cirrhotics, it is important to maintain vigilance for an opportunistic infection. Furthermore, oropharyngeal dysphagia warrants a full neurological evaluation to assess for presence of cranial neuropathy.


Joel McFarland, MD*, Ashok Shah, MD, FRCP, MACG. Gastroenterology and Hepatology, University of Rochester, Strong Memorial Hospital, Rochester, NY.

Purpose: We describe a patient previously known to have unicornuate uterus and fertility difficulties leading to successful in vitro fertilization who was later found to have agenesis of the dorsal pancreas presenting with recurrent acute pancreatitis.

Methods: Retrospective review of a single case

Results: A 40 year old woman presented as an inpatient with recurrent acute pancreatitis without evidence of immediate etiology. She had no significant alcoholism and no biliary disease. She had normal calcuim levels, normal triglycerides, no history of traumatic injury or family history of disease. Abdominal CT scan showed inflammation of the pancreatic head with non-visualization of the body and tail. She was supported through the acute episode with resolution of symptoms and normalization of laboratory values. ERCP was performed at a later date and was significant for a short, dilated ventral pancreatic duct with extensive side branching. There was no extension of dye across the midline on pancreatogram prompting search for an accessory ampulla give the possibility for pancreas divisum. After extensive searching, the accessory ampulla was not found and thought likely to be congenitally absent. MRCP was performed and confirmed the suspicion for agenesis of the dorsal pancreas.

Conclusion: Agenesis of the dorsal pancreas is a rare congenital anomaly. It is even less likely to present with acute pancreatitis as it is typically asymptomatic and found incidentally on imaging studies. There have been no reports of associated congenital anomalies with agenesis of the dorsal pancreas, while abnormalities of the ureteropelvic system have been described with pancreas divisum. While the Mullerian ductal system is of mesodermal origin, it is possible that this tubular structure shares embryonal transcription factors with the pancreaticobiliary system. This could represent a potential pathophysiological mechanism resulting in the concomitant presentation of agenesis of the dorsal pancreas and unicornuate uterus.


Jason Gutman, MD*, Asad Ullah, MD, Joel McFarland, MD. Division of Gastroenterology & Hepatology, University of Rochester, Rochester, NY.

Purpose: We present a case of a patient presenting with dysphagia, who was found to have a large tracheo-esophageal fistula due to recurrent squamous cell carcinoma of the lung. Palliative treatment was achieved with placement of a covered esophageal wall stent.

Methods: This is a retrospective chart review of a single case.

Results: A 51 year old male presented to our hospital with dysphagia. Six years prior he was diagnosed with Stage I squamous cell carcinoma of the lung. He underwent right upper lobectomy and adjuvant chemoradiation therapy due to positive margins. After completion of chemoradiation, he was deemed to be disease free. He then presented to our hospital with 2 weeks of dysphagia secondary to coughing fits associated with swallowing. Over this time he lost 15 pounds and became dehydrated necessitating admission. On exam he appeared dehydrated with dry mucous membranes and a mild tachycardia. On attempting to drink water he developed a severe coughing fit. Barium swallow showed possible upper esophageal diverticulum. CT scan showed an irregular tracheal lumen at the carina, narrowing of the right mainstem bronchus, and a fleck of gas extending from the right mainstem bronchus into the esophageal wall. Upper endoscopy demonstrated a large tracheo-esophageal fistula at 30 cm in which the endoscope could be passed into the airway, along with a mass involving the trachea. Biopsy demonstrated squamous cell carcinoma of the lung consistent with his previous cancer. He underwent repeat endoscopy with placement of a covered self-expanding metal stent for palliative treatment with resolution of his symptoms.

Conclusion: Acquired tracheo-esophageal fistulas can be a rare complication of either malignant or non-malignant causes. The most frequent malignant causes are esophageal and lung cancers, accounting for 77% and 16% of malignant TEF's respectively. The incidence of TEF in esophageal cancer is 4.5%, compared to 0.3% in primary lung cancer. Mean survival after diagnosis and treatment is 13.4 weeks. Thus the goal of care is to minimize pulmonary complications and maintain nutritional support. In small studies, endoscopic approach with placement of a wall stent has provided an 80% success rate of complete obliteration of TEF's. Complication rates range from 15-40% and includes perforation, stent migration, and incomplete closure, while surgical options have a peri-operative mortality rate of 29-47%. In patients with successful placement of a wall stent mean survival improves to 15.1 weeks compared to 6.2 weeks in those with failed attempt. Thus the use of self-expanding metal or plastic wall stents can provide a relatively safe and effective alternative to palliative surgery in malignant conditions.


Joel McFarland, MD*, Jason Gutman, MD, Arthur DeCross, MD. Gastroenterology and Hepatology, University of Rochester, Strong Memorial Hospital, Rochester, NY.

Purpose: A case report of diverticular-associated colitis presenting with a stricture, mimicking Crohns Disease.

Methods: Case review.

Results: A 56 year old woman presented with crampy, bloody diarrhea up to 8 times daily for the last six months. No nausea, vomiting, fever or chills. No recent antibiotic use, or travel history. She did not smoke and had no family history of IBD. Vital signs were unremarkable; exam revealed only mild lower abdominal discomfort. Screening colonoscopy 18 months earlier showed mild sigmoid diverticulosis and a fixated sigmoid colon requiring a pediatric colonoscope in order to reach the cecum, probably due to prior hysterectomy. There was no mucosal inflammation. Colonoscopy performed at the time of presentation with bloody diarrhea showed erythema from the proximal rectum to 40 cm, mild sigmoid diverticulosis, and stricturing at 40 cm preventing advancement with even an upper endoscope. Stool cultures were negative; serum CRP was 17 mg/L. Sigmoid biopsies showed moderate active chronic colitis with acute cryptitis, and moderate architectural distortion without granulomas identified. She began mesalamine 1600 mg PO BID with partial resolution of symptoms. CRP measurements were decreasing and symptoms resolved completely with increase in mesalamine dosage to 2400 mg PO BID. Barium enema showed a 7.5 cm sigmoid stricture which did not allow barium to pass. Repeat colonoscopy 18 weeks later was performed after normalization of the CRP and relief of her symptoms, and showed improved mucosal erythema, but no change in the stricture. Biopsies taken then from 10 cm, 20 cm, and 30 cm showed mild active chronic colitis with much less acute inflammation compared to prior, but no change in the degree of architectural distortion. She then had sigmoid colectomy to remove the stricture. Pathology showed active chronic colitis with moderate architectural distortion without granulomas, and mild diverticulitis. Mesalamine was tapered off after surgery. Colonoscopy was performed 9 months after stopping mesalamine, and this revealed completely resolved inflammation, with completely normal biopsies from terminal ileum, right colon, 30 cm, and rectum.

Conclusion: Diverticular-associated colitis may present with a stricture, which can mimic Crohns disease. The colitis improved with mesalamine, although there was no improvement in the stricture. Of particular interest, after segmental colectomy of the strictured, diverticulosis-affected sigmoid, the colitis vanished completely - including the histological signs of architectural distortion traditionally associated with chronic inflammatory bowel disease - even though the mesalamine had been withdrawn 9 months earlier.


Marc Hopkins, MD*, Kathy Bull-Henry, MD, Kirti Shetty, MD, Stanley Benjamin, MD. Gastroenterology, Georgetown University Hospital, Washington, DC.

Purpose: Case: A 43 year old African-American male presented with multiple episodes of frank hemetemesis and hematochezia. Initial evaluation revealed hemodynamic instability, a hematocrit of 29% (which fell to 18%), normal platelets, and normal coagulation profile. He was resuscitated aggressively; intravenous proton pump inhibitor was started. Intubation was performed for airway protection prior to endoscopic examination. Esophagogastroduodenoscopy (EGD) revealed large blood clots in the esophagus which were removed. The stomach and duodenum contained blood, but thorough irrigation and visualization showed no abnormalities. Fresh blood was seen oozing from the esophagus on retroflexion; esophageal examination revealed multiple sub-centimeter diverticula in the mid to lower esophagus with small punctate lesions consistent with intramural pseudodiverticulosis. No diverticula were actively bleeding; therefore, no therapeutic intervention was undertaken and the patient was extubated and managed conservatively. Barium esophagram showed small outpouchings of the esophageal wall, but no stricture was present. The patient was discharged to home two days later and has had no recurrent bleeding as per a telephone conversation one month after discharge. Symptoms such as dysphagia and pyrosis were never present. He had no prior history of esophageal infection, motility disorders, or gastroesophageal reflux disease. Discussion: Esophageal intramural pseudodiverticulosis (EIP) is an unusual condition characterized by small outpouchings of the esophageal lumen which can involve any segment of the esophagus and typically are less than 5 mm in diameter. Histologically they are not true diverticula, but rather pathologic dilations of excretory submucosal glands. Although the pathogenesis is unclear, it is thought to be an acquired disorder usually associated with abnormal esophageal motility, strictures, or mucosal inflammation. The most common presenting symptom is dysphagia; however, EIP may be an incidental finding in asymptomatic patients. Diagnosis can be made using a combination of endoscopy and radiologic imaging. Treatment should focus on the underlying disorder. The disease typically follows a benign course, but severe complications such as esophageal perforation or fistula resulting in mediastinitis have been reported. Only one other case report exists of upper gastrointestinal bleeding in a patient with EIP, although the authors attributed the bleeding to an esophageal web. The case described here is unique in that his presenting symptom was severe hemorrhage due to EIP. In addition, no other associated esophageal abnormalities were present.


Kevin Jo, MD*, Ashok Shah, MD, MACG. Gastroenterology, University of Rochester, Rochester, NY.

Purpose: Post endoscopic biliary sphinterotomy bleeding is a frequent and life threatening complication associated with ERCP. Multiple risk factors have been identified. We describe a case of post endoscopic biliary sphinterotomy bleeding in a patient with both duodenal diverticulae and abnormal vascular anatomy.

Methods: N/A

Results: A 75 year-old with a history of CVA, COPD, and GERD presented to the hospital with intermittent abdominal pain. The patient reported subjective fevers and chills and was noted to have elevated LFTs. The patient's LFTs peaked at an AST of 494, ALT of 541, T. bili of 4.2, and alkaline phosphatase of 278. An MRCP revealed a 1 cm filling defect in the distal common bile duct (CBD) with mild extra-hepatic ductal dilatation. Additionally, multiple duodenal diverticulae were noted. An ERCP was performed given the findings on MRCP. Upon visualization of the ampulla, the anatomy of the ampulla was noted to be altered due to large diverticulae bilaterally. The ampulla was cannulated, and the subsequent cholangiogram revealed a large filling defect in the distal CBD. Initial sphincterotomy was performed with a 20 mm wire sphincterotome. Due to both the inadequacy and inability to extend the sphincterotomy, a 25 mm wire sphincterotome was used to further extend the sphincterotomy. Upon extension of the sphincterotomy, rapid arterial bleeding was noted. The endoscopic field was quickly and completely obscured with blood preventing any endoscopic intervention. The patient was emergently transferred to interventional radiology due to the profuse ongoing bleeding. Initial angiogram at the celiac axis revealed active bleeding from the gastroduodenal artery (GDA). Deep cannulation of the GDA revealed that the bleeding source was supplied by the GDA and a collateral branch. Multiple coils were placed across the extent of the GDA which resulted in hemostasis. Post embolization angiogram revealed a small collateral branch off of the hepatic artery in the region of the previously seen bleeding site. Due to the possibility that this was the collateral branch contributing to the bleeding, this was also embolized. Following angiography, the patient did not have any further bleeding. After close monitoring, the patient was discharged. An outpatient ERCP performed one month later resulted in the removal of the retained CBD stones.

Conclusion: Hemorrhage is a well known complication of endoscopic biliary sphincterotomy during ERCP. Risk factors for post sphinterotomy bleeding are well described. While the presence of duodenal diverticulae is a well documented risk factor for post sphinterotomy bleeding, we present a case of severe bleeding in a patient with both duodenal diverticulae and abnormal vascular anatomy.


Kevin Jo, MD*, Thomas Park, MD, Asad Ullah, MD, Ashok Shah, MD, MACG. Gastroenterology, University of Rochester, Rochester, NY.

Purpose: The development of small bowel imaging and endoscopic techniques has contributed to the ability to more completely evaluate the small intestine. Classically, small bowel lesions were diagnosed latter in their course leading to poor outcomes. We describe a case of multiple, large small bowel hyperplastic polyps in a patient with recurrent colon cancer.

Methods: N/A

Results: A 57 year-old Caucasian male with a history of colon cancer, atrial fibrillation on anticoagulation, congestive heart failure, and diabetes mellitus presented to an OSH with iron deficiency anemia requiring transfusion of 6 units of pRBCs. The patient's colon cancer was diagnosed in 2002 requiring a sigmoid resection with a recurrence in 2004 requiring a hemicolectomy. An EGD and colonoscopy performed at the OSH were negative. The patient was taken off of anticoagulation with cessation of his anemia. The patient was referred to our institution for further management. Our initial evaluation included a CT scan of the abdomen/pelvis which was unremarkable. Subsequently, an enteroclysis was performed that revealed multiple polyps throughout the small bowel. Therefore, a wireless capsule enteroscopy was performed to better visualize these lesions. The wireless capsule enteroscopy revealed greater than 15 polyps, mainly in the proximal jejunum. The polyps were of varying sizes, with one that was nearly lumen occluding. A double-balloon enteroscopy was then performed. Multiple, large polyps were visualized and biopsied. A 1 cm polyp was removed by snare polypectomy. Histologic evaluation of the specimens was consistent with hyperplastic polyps. The patient was evaluated by surgery who felt that given the number and location of the polyps a segmental small bowel resection would not be possible. Therefore, the decision was made to follow the patient conservatively off of anticoagulation for any evidence of further bleeding or bowel obstruction that would necessitate intervention.

Conclusion: We present a case of multiple, large small bowel hyperplastic polyps in a patient with recurrent colon cancer. The natural history of these lesions is not well described, including possible malignant potential. The long term surveillance of these lesions has also not been well outlined.


Praveen Guturu, MD*, Shaad Abdullah, MD. Internal Medicine, UTMB, Galveston, TX.

Purpose: 59 year old lady, who lives alone, was bought to Emergency Department by ambulance after neighbors found her confused. Emergency contact could not be reached. On admission she was only oriented to person and her vital signs were stable. Laboratory work up revealed CBC and chemistry panel at base line and her liver function tests were slightly deranged with mildly elevated Alkaline Phosphatase/Aspartate aminotransferase and normal Alanine aminotransferase. Her ammonia levels were high on admission (96 mmol/L). Initially she was thought to have Hepatic encephalopathy and over next 24-48 hours she deteriorated clinically and even with regular bowel movements her ammonia levels went up to >150 and her urine grew E. Coli for which she was started on Cefotaxime. She did not have any stigmata of chronic liver disease and her Hepatitis serology's were negative. We searched for alternate causes of hyperammonemia and plasma amino acid profile was sent to rule out Urea Cycle disorder and Urinary tract infection with urease splitting organism as cause of high ammonia is ruled out with urine culture on admission. Her plasma amino acid profile returned with high glutamine and low citrulline, consistent and urine orotic acid was elevated and so she was diagnosed with partial Ornithine Transcarbamylase deficiency and treatment was initiated with Sodium Phenylbutrate, low protein diet and Arginine supplementation. Her ammonia levels came down but before her mentation improved, patient developed Methicillin Resistant Staph. Aureus sepsis and multi organ failure and family wanted conservative approach and she passed away in less than 48 hours after diagnosis of multiorgan failure. An autopsy was not authorized family members. Most often, urea cycle disorders present as hyperammonemia in the newborn period; however, urea cycle disorders can present at almost any age in individuals who have milder urea cycle defects when severe stress triggers a hyperammonemic crisis. So alternate cause for high ammonia should be sought in all patients with high ammonia and no liver disease. High degree of suspicion and prompt initiation of treatment is very important in managing patients with urea cycle disorders because patients experiencing acute elevations of ammonia present to the ICU with encephalopathy, which may progress quickly. Management includes combination of sodium phenyl butyrate and sodium phenyl acetate/benzoate as a glutamine trap, diverting nitrogen from urea synthesis to alternatives routes of excretion. Urea cycle a disorder causing fatal illness is reported but one recent article gives encouragement with 84% survival rate with prompt correction of the metabolic abnormalities


Praveen Guturu, MD*, Advitya Malhotra, MD, Alex Hewlett, MD. Internal Medicine, UTMB, Galveston, TX.

Purpose: A 77-year-old Caucasian female patient presented to emergency department (ED) with acute onset of vomiting and epigastric pain. Vomiting was coffee-ground in color and her abdominal pain which started in epigastrium was now more diffuse in character. She denied any melena. Her medications at the time of presentation include bactrim, prilosec and atenelol. She denied any recent NSAID use. Her past medical history was significant for vertebral fracture, osteoporosis and recurrent UTIs. On physical examination, vital signs were stable. She was tender to palpate in the epigastric and umbilical regions. Abdominal x-rays obtained in ED showed air filled sac in the mediastinum, raising a possibility of gastric volvulus. Esophagogastroduodenoscopy revealed a twisted hiatal hernia and scope could not be advanced through the hernia. A follow-up barium swallow revealed mesentero-axial gastric volvulus and gastric obstruction. Patient underwent emergency laparoscopic surgery with reduction of volvulus, repair of diaphragmatic defect and fixation of the stomach. Gastric Volvulus is a rare disorder but it can be potentially fatal and mortality has reported to be up to 30-50% in acute gastric vovulus. Stomach is relatively mobile and so asymptomatic and transient rotations of stomach do occur. This abnormal rotation of stomach can be longitudinal (organoaxial) or transverse (mesenteroaxial) or a combination of both. The classic triad of symptoms is epigastric pain, vomiting and difficulty or inability to pass nasogastric tube. Early diagnosis and prompt initiation of treatment is very important as volvulus can be fatal. Upper GI contrast studies and upper endoscopy are the most important investigations useful in the diagnosis. Acute gastric volvulus is a surgical emergency and treatment generally involves reduction of volvulus, repair of diaphragmatic defect and fixation of stomach (gastropexy). The surgical options available have changed greatly over the last decade and with developments in laparoscopic surgery, it now takes preference over laparotomy for both acute and chronic gastric volvulus.


Byron Cryer, MD*, David Peura, MD, Francis Chan, MD, Lee Simon, MD, Gurkirpal Singh, MD, Martin Stillman, MD, C. Mel Wilcox, MD, Manuela Berger, MD. Division of Gastroenterology, University of Texas Southwestern Medical Center, Dallas, TX, Health Sciences Center, University of Virginia, Virginia, VA, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, Department of Medicine, Stanford University School of Medicine, Stanford, CA, General Internal Medicine, Hennepin County Medical Center, Minneapolis, MN, Division of Gastroenterology & Hepatology, University of Alabama at Birmingham, Birmingham, AL, Global Medical, Pfizer Inc, New York, NY.

Purpose: Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed; however, their use is limited by gastrointestinal (GI) side effects. Randomized clinical trials of medicines affecting the GI tract have focused primarily on damage to the upper GI tract. Recent studies have demonstrated a significant risk for serious GI events occuring in the lower GI tract. A measure to capture damage to the entire GI tract (both upper and lower) could help improve understanding of this problem by validating a method to look at the GI effects of various therapies, both in and outside of clinical trials.

Methods: A new composite endpoint of GI safety addressing this need is CSULGIEs, or Clinically Significant Upper and/or Lower GI Events. This measure provides a more comprehensive evaluation of therapeutic toxicity through the entire GI tract. The measure extends the traditional "perforation, obstruction, and bleeding" (POB) assessment of upper GI complications by including events in the lower GI tract, such as small/large bowel perforation, lower GI bleeding, and clinically significant anemia. Two ongoing randomized clinical trials-the Celecoxib vs Omeprazole aNd Diclofenac for at-risk Osteoarthritis (OA) and Rheumatoid arthritis (RA) patients (CONDOR) trial, and the GastroIntestinal Randomized Events And Safety Open-label NSAID Study (GI-REASONS)-have been designed with CSULGIEs as a primary end point, with events being adjudicated by separate GI Events Committees, blinded to treatment.

Results: These studies may provide a better outcome to evaluate potential adverse events induced by NSAID treatments across the entire GI tract, and will include >12,000 OA and RA subjects of moderate to high GI risk.

Conclusion: The CSULGIEs end point allows for the collection of more complete and clinically relevant GI safety data for a range of therapies, and has the potential to yield a new descriptive language for adverse events through the entire GI tract. The CONDOR and GI-REASONS studies will use CSULGIEs to help further define patient risk factors associated with increased NSAID risk, and will help improve patient care by providing a more complete evaluation of GI toxicity.


Joel Pekow, MD*, Charles Dye, MD, Eugene Chang, MD. Department of Medicine, Section of Gastroenterology, University of Chicago, Chicago, IL.

Purpose: To describe a case of gastric outlet obstruction and multiple carcinoid tumors in a patient with metastatic gastrinoma.

Methods: A 58 year old man with past medical history significant for multiple endocrine neoplasia type 1 who had a pancreatic tail resection 25 years ago for a gastrinoma presented to our hospital with intractable nausea and vomiting. Two months prior to his current admission, a EGD done for workup of anemia showed diffuse nodularity (Image 1) involving the body and fundus of the stomach with antral sparing as well as smaller nodules in the duodenal bulb and 2nd portion of the duodenum. Gastric pH was 6 on proton pump inhibitor therapy. Multiple biopsies of the gastric nodules exhibited well differentiated neuroendocrine tumors in the setting of foveolar gland hyperplasia; duodenal and antral biopsies revealed metastatic gastrinoma.

Results: Two month later, he returned with intractable nausea and vomiting. A repeat EGD showed nodules that were partially obstructing the pylorus as well as a high grade non-transversable stenosis of the pylorus. Gastric pH was 7. Incremental balloon dilation to 20 mm was then performed resulting in decreased resistance to scope passage. Antral biopsies from the procedure were positive for H. Pylori for which he received treatment. Two months following the procedure, the patient has had no recurrence of nausea and vomiting is tolerating a full diet.

Conclusion: Carcinoid tumors arise from enterochromaffin-like cells in oxyntic glands of the stomach, of which gastrin is a potent stimulant. The antrum is relatively void of these glands, which explains the antral sparring of carcinoid tumors on endoscopy in our patient. The dramatic nodular appearance on endoscopy likely represents carcinoid tumors and foveolar hypertrophy accompanied by areas of glandular atrophy due to chronic H. pylori infection. We have two potential explanations why our patient would have developed a gastric outlet obstruction after several years on proton pump inhibitor therapy. First, active H. pylori infection may have caused significant acute edema in the setting of chronic fibrosis. In addition, partially obstructing metastatic gastrinoma nodules deforming the prepyloric area may have contributed to the obstruction.


Jeffrey Laczek, MD*, Roy Wong, MD. Department of Gastroenterology, Walter Reed Army Medical Center, Washington, DC.

Purpose: Gastroparesis is a disorder characterized by symptoms of gastric retention and evidence of delayed gastric emptying in the absence of mechanical obstruction. Established causes of gastroparesis include systemic disease (such as diabetes mellitus) and abdominal surgery. There are also three reported cases of gastroparesis occurring following vaccination. We present an additional case of post-vaccination gastroparesis, occurring following a smallpox vaccination.

Methods: A 37-year-old Caucasian woman in her normal state of good health underwent smallpox vaccination. Within 24 hours, she developed a globus sensation and facial flushing, which were treated with corticosteroids and antihistamines. Over the next three weeks, she was seen multiple times for dysphagia, nausea, headaches, and a sensation of her throat closing. She was treated with epinephrine, H1 and H2 receptor antagonists, and a prolonged course of corticosteroids. Her symptoms further evolved to include dyspnea, chest tightness, palpitations, dizziness, and elevated blood pressure. One month after the onset of her symptoms, pulmonary consultation was obtained; laryngoscopy revealed denuded epithelium on her vocal cords, consistent with GERD. Two months after the onset of her symptoms, she was seen in our GI clinic. A review of gastrointestinal symptoms was notable for persistent nausea, frequent vomiting, heartburn, and regurgitation. An EGD was normal and 24-hour ambulatory pH testing showed significant acid reflux (JD score 86). A nuclear medicine gastric emptying study showed 93% of gastric contents retained at 90 minutes. Based on these findings and the temporal relation of her symptoms to her smallpox vaccination, she was diagnosed with post-vaccination gastroparesis. Her GERD was treated with a PPI. She was unable to tolerate metoclopramide for treatment of her gastroparesis, while domperidone (20 mg po qid) and erythromycin (250 mg po tid) were ineffective. Her symptoms have persisted for more than eight months and nonpharmacological treatment is being considered.

Results: To our knowledge, this is the fourth reported case of post-vaccination gastroparesis. Tetanus, anthrax, and hepatitis B vaccinations were implicated in the previous three reports, making this the first reported case of gastroparesis following smallpox vaccination.

Conclusion: This case demonstrates that gastroparesis is a potential adverse effect of vaccination. Although exceedingly rare, post-vaccination gastroparesis can significantly impair patients' quality of life. Physicians should consider this diagnosis and investigate accordingly when patients present with compatible symptoms after receiving a vaccination.


Timothy Duncan, MD*, Jonathan Koff, MD, Frank Moses, MD. Gastroenterology, Walter Reed Army Medical Center, Washington DC, DC.

Purpose: A 76 yo African American man presented with a 10 year history of constipation. He also had described numerous evaluations for multiple episodes of partial bowel obstructions, with symptoms consistent with obstipation. His only surgical history was a right nephrectomy for renal cell carcinoma. Colonoscopy was extremely technically difficult due to severe tortuosity of the colon. Advancement in the area of the hepatic flexure was difficult and the Olympus OPD positioning detecting unit was inserted, the scope tip appeared to be in the area of the right nipple. The procedure was aborted out of concern for a diaphragmatic hernia, and a virtual colonography was performed to evaluate the remainder of the colon for pathology and to define the anatomic layout of the colon. Virtual colonography demonstrated the hepatic flexure colon segment passing lateral, then superior and finally anterior to the liver. In addition, there was 12 x 5 mm pedunculated polyp in the ascending colon. There was no evidence for a diaphragmatic hernia. A double balloon colonoscopy was the performed with the intent of polyp removal. The cecum was comfortably reached without fluoroscopy. The ascending polyp was more easily approached in the retroflexed position and was removed using a saline lift piecemeal polypectomy. Final pathological diagnosis was tubular adenoma. Chilaiditi's syndrome is defined as interposition of bowel between the liver and right hemi-diaphragm. The syndrome has a low prevalence rate, which has been estimated to be between 0.1-0.25% of reviewed chest x-rays. It is associated with a number of abnormalities including chronic constipation, absence of transverse colon or falciform ligaments, chronic lung disease, hemi-diaphragm paralysis, ascites and/or cirrhosis. Complications can range from bowel puncture during liver biopsy, misdiagnosis of pneumoperitoneum or large bowel volvulus. There are few examples in the endoscopic literature to note that Chilaiditi's syndrome may be an unrecognized cause of a "difficult" colonoscopy. There are no prior examples of double balloon technique successfully facilitating colonoscopy completion with Chilaiditi's syndrome.


David Victor, MD*, Jacob Feagans, MD, Salima Haque, MD, Hana Safah, MD, Shobha Joshi, MD. Internal Medicine, Tulane University School of Medicine, New Orleans, LA.

Purpose: Background: Liver diseases are common after bone marrow transplant, the most common being graft versus host disease (GVHD) and hepatotoxicity due to drugs. Viral hepatitides are less common, usually caused by reactivation of or new infection with hepatitis B, C or herpesviruses. There are few descriptions of Coxsackie hepatitis in the literature. We report a patient who developed submassive Coxsackie hepatitis eight months following allogeneic stem cell transplantation. Case Report: A 54 year-old male with non-Hodgkin's lymphoma underwent allogeneic stem cell transplantation after failing chemotherapy. Immunosuppressive drugs and prophylactic antimicrobials and antivirals, including acyclovir, had been discontinued for two months when he developed flu-like symptoms, loose stools, painful oral apthous ulcers, jaundice, a maculopapular rash on the chest and abdomen, and nontender hepatomegaly. Serum alanine (ALT) and aspartate (AST) aminotransferases were elevated (1108 U/L and 1160 U/L, respectively); total bilirubin was 10.8 mg/dL and alkaline phosphatase was 402 U/L. A liver biopsy showed submassive hepatic necrosis with viral features, but no GVHD. Herpes simplex virus (HSV) and Coxsackie virus hepatitis were suspected based on clinical findings and recent discontinuation of prophylactic antivirals. Acyclovir treatment was restarted. Hepatitis A, B and C serologies and antibody titers were drawn for HSV, human herpesvirus (HHV)-6, HHV-8, adenovirus, Epstein Barr virus, cytomegalovirus, HIV, toxoplasma, and Coxsackie viruses. Weekly measurement of ALT, AST, bilirubin and alkaline phosphatase showed a gradual decline; his apthous ulcers healed. A Coxsackie A9 antibody titer was 1:256, Coxsackie B antibody titer was 1:160, and HHV-6 IgG titer was 1:43. Repeat titers after two weeks of acyclovir treatment showed no change in the Coxsackie B and HHV-6 titers, but the Coxsackie A9 titer declined to 1:64. At this point, the diagnosis of Coxsackie A9 hepatitis was confirmed. Viral suppression treatment with acyclovir was continued. Liver chemistries normalized over 12 weeks. Discussion: Coxsackie virus infections in patients undergoing bone marrow transplantation vary in severity from mild viral enteritis to severe fatal myocarditis. Hepatic involvement with Coxsackie infection has been reported, however, submassive hepatic necrosis has not been documented previously in a stem cell transplant recipient. This case illustrates the importance of considering Coxsackie viruses as etiologic agents when evaluating a patient with hepatitis after a bone marrow transplant. Treatment remains largely supportive but acyclovir can be used to prevent fulminant transformation of the disease.


Scott Pollack, MD*, Thomas Parambil, MD, Fredric Regenstein, MD, Shobha Joshi, MD. Internal Medicine, Tulane University School of Medicine, New Orleans, LA.

Purpose: Background: Post-transplant lymphoproliferative disorder (PTLD) is a serious and potentially fatal complication of chronic immunosuppression in organ transplant recipients. PTLD is usually characterized by large-cell lymphomas, a great majority being of the B-cell type. Waldenstrom's Macroglobulinemia (WM) is a disorder characterized by the production of excess IgM monoclonal proteins along with an underlying mostly indolent malignant lymphoproliferative disorder. WM is treated with chemotherapy, such as rituximab, alkylators, nucleoside analogues, or combinations that include rituximab. Hyperviscosity syndrome is present in approximately 30 percent of patients with WM, and is treated with urgent plasmapharesis. Although these disorders have been reported either by themselves or in combination, we report a patient with liver transplant who had PTLD, WM, and hyperviscosity syndrome. Case Report: A 55 year-old male with orthotopic liver transplant for cirrhosis secondary to hepatitis C, developed PTLD 15 months after transplantation. He was treated with rituximab. Twenty eight months after transplantaion, the patient developed altered mental status and respiratory failure requiring endotracheal intubation and mechanical ventilation. There was increased viscosity of blood on initial phlebotomy. Initial abnormalities in blood were: sodium 127 mmol/L, urea nitrogen 67 mg/dL, creatinine 4.5 mg/dL, total protein 11.2 g/dL, albumin 1.6 g/dL, platelet count 144,000/dL, uric acid 19.8 mg/dL, ammonia 25 mmol/L, viscosity 13.75 cP (centipoises), IgG 2,073 mg/dL, IgM 8,949 mg/dL and IgA 2,036 mg/dL. The patient underwent urgent plasmapharesis with improvement of mental status over the following 2-3 days, with successful extubation and return of baseline mental function. Serum protein electrophoresis showed a large monoclonal spike in the gamma region. Serum immunofixation electrophoresis (IFE) showed an IgM type kappa monoclonal protein with additional bands of IgG, IgA and lambda. Urine IFE was positive for monoclonal free kappa light chains (Bence-Jones protein) and monoclonal IgM heavy chain with associated kappa light chain and excess monoclonal free kappa light chains. Bone marrow biopsy was suggestive of a B-cell lymphoma. The patient was then diagnosed with WM and treated with rituximab. Discussion: As of now, there are no reports of Waldenstrom's macroglobulinemia and hyperviscosity syndrome associated with post-transplant lymphoproliferative disorder in a liver transplant recipient. Our case is an example of a patient who benefited from prompt recognition of this disorder and urgent plasmapharesis.


Shannon Chang,*, David Victor, MD, John Kalarickal, MD, Scott Pollack, MD, Nadret Copur, MD, Fredric regenstein, MD. School of Medicine, Department of Gastroenterology, Tulane University, New Orleans, LA.

Results: Sarcoidosis is a disease characterized by noncaseating granulomas found in any organ, most commonly the lung, lymph nodes, skin, liver, eyes, and bones. (1). The clinical course can vary from self-limiting to chronically incapacitating (1). Gastrointestinal tract involvement is rare (0.9-1%) and most patients with gastric sarcoidosis are asymptomatic (2-4). We report two unusual cases of symptomatic anemia resulting from previously undiagnosed gastric sarcoidosis. The first patient is a 22 year-old previously healthy African-American male who presented with progressive weakness and fatigue over the preceding seven months. He noted gradual weight loss and episodes of epigastric abdominal pain refractory to Omeprazole. Initial evaluation was notable for hemoglobin of 7.4 mg/dL. Further work-up revealed an iron deficiency anemia. Upper gastrointestinal endoscopy showed nodular, friable gastric mucosa with superficial ulceration and hyperemic, thickened gastric folds. Endoscopic biopsies of the gastric mucosa revealed severely active noncaseating chronic granulomatous gastritis. Transbronchial lung biopsy showed noncaseating granulomatous inflammation of bronchial mucosa with no signs of infection, clinically consistent with the diagnosis of sarcoidosis. The second patient is a 46 year-old African American female with a history of presumed idiopathic granulomatous hepatitis who presented with abdominal pain, fatigue, anorexia, nausea, hematemesis, and melena. Her hemoglobin, which had previously been normal, had fallen to 9.7 mg/dl. Upper gastrointestinal endoscopy to investigate the bleeding showed erosive gastritis with hyperemic gastric folds with atypical appearing superficial one by two centimeter ulcerations with adherent exudate. Biopsies of the ulcerated mucosa showed noncaseating granulomatous gastritis with areas of erosion. She improved dramatically with steroid therapy. In both cases other causes of granulomatous disease was ruled out. Sarcoidosis manifesting as symptomatic anemia is rare. Most patients with gastric sarcoid will be asymptomatic and those that seek attention will have vague complaints of abdominal pain or gastrointestinal bleeding (5). Therefore, gastric sarcoidosis must be considered in the differential of gastrointestinal bleeding in patients known to have sarcoidosis and in those with suggestive clinical features. Typical endoscopic findings include hyperemic, thickened gastric folds and/or superficial ulcerations with histologic evidence of non-caseating granulomas on biopsy specimens. The prognosis of gastric sarcoid is typically favorable, with improvement of the endoscopic and histopathologic findings in response to treatment of the underlying disease.


Sharmeel Wasan, MD*, Christopher Huang, MD. Gastroenterology, Boston Medical Center, Boston, MA.

Purpose: Agnogenic myeloid metaplasia (AMM) is a rare myeloproliferative disorder characterized by bone marrow fibrosis, marked splenomegaly, and extramedullary hematopoeisis (EMH). EMH can occur in almost any organ, but clinically significant involvement of the gastrointestinal (GI) tract is very rare.

Methods: A 62-year-old female with AMM with myelofibrosis was transferred to our institution for evaluation of overt gastrointestinal bleeding of obscure origin. She presented with a six-month history of recurrent hematochezia. Her extensive previous workup had included six negative upper endoscopies and three colonoscopies, which were unremarkable except for the presence of blood throughout the colon. Three nuclear medicine bleeding scans had also been performed, two of which showed active bleeding arising from the right lateral hemipelvis. Subsequent angiograms, however, were negative. The patient had received 17 units of PRBC over the two weeks prior to her transfer to our institution.

Results: Physical exam revealed a chronically ill patient with marked hepatosplenomegaly. Laboratory data showed a hemoglobin of 7.9 mg/dL and platelet count of 46,000/uL. CT enterography demonstrated an abnormal focal accumulation of intravenous contrast in the wall or lumen of a loop of mid-to-distal ileum, without mass or abnormal wall thickening. Angiography was again negative, and retrograde double balloon enteroscopy was nondiagnostic. Video capsule endoscopy visualized a small, smooth, dome-like protuberance arising from otherwise normal appearing small bowel mucosa at 4 hours and 40 minutes. At the apex of the lesion, there appeared to be a small umbilication, and possibly an adjacent clot. Due to the severity of her bleeding, she underwent exploratory laparotomy with intraoperative enteroscopy. A lesion was palpated in the jejunum, and endoscopically identified as the same lesion seen on capsule study. This was resected, and on gross pathology was described as a 0.7-cm submucosal nodule with mild erythema and umbilication. Histology and immunoperoxidase studies revealed a cluster of erythroid cells, granulocytic and myeloid precursors, and megakaryocytes, consistent with focal EMH. Postoperatively, the patient had no further bleeding.

Conclusion: EMH is common in patients with myelofibrosis, affecting organs containing tissue of mesenchymal origin. However, clinically significant GI tract involvement is very rare. GI bleeding from EMH in the esophagus, small bowel, and colon has been described in a small number of case reports. To our knowledge, this is the first case of GI bleeding arising from a single focus of small bowel EMH visualized on video capsule endoscopy.


Samantha Scanlon, MD*, Karthik Ravi, MD, Mark Topazian, MD. Internal Medicine, Mayo Graduate School of Medical Education, Rochester, MN.

Purpose: A 76 year old female presented with jaundice and twelve pound weight loss over one month. Liver function tests (LFTs) were notable for total bilirubin 8.5, direct bilirubin 6.8, AST 106, ALT 119, and Alkaline phosphatase 617. An abdominal and pelvic CT showed a 5.5 cm predominantly low-density porta hepatic and hepatic hilar mass as well as a 4.2 x 6.7 cm heterogeneously enhancing mass in the right pelvis. The patient was admitted to a local hospital for percutaneous transhepatic cholangiogram with percutaneous drain placement. Two days later, she required revision of the drain leading to a steady decline in LFTs. On the subsequent day, she developed fever, rigors, and leukocytosis. She received Levaquin 750 mg by mouth daily for suspected acute cholangitis. She underwent a CT guided liver biopsy which was inconclusive and was transferred to a tertiary care center for ERCP. During routine ERCP for brush biopsies and plastic biliary stent placement, a communication was appreciated between the biliary system and the hepatic vein with reversal of flow consistent with a biliary venous fistula. This was not previously seen on prior cholangiograms. Given concern of ongoing bacteremia, she completed a two week course of Levaquin 750 mg by mouth daily and Flagyl 500 mg by mouth three times daily. Four weeks later she underwent repeat ERCP with stent removal and replacement with an uncoated Flexxus biliary stent. A biliary venous fistula was not seen during this exam. Fistulas between the biliary tree and the hepatic vein are typically produced during percutaneous drain placement. It is rare for such communications to become clinically evident. In this case, the obstructed bile duct created a pressure gradient favoring reversal of flow and consequently bilhemia. Treatment of bilhemia was previously limited to surgery involving resection of the involved liver. Endoscopic interventions have become the procedure of choice to treat bilhemia associated with obstructive common bile duct lesions. However, there have been few cases which examine the need for antibiotics when such fistulas are discovered. Theoretically bile is sterile, however in the case of biliary duct obstruction, recent percutaneous interventions, and presence of SIRS criteria, when is it indicated to treat? Some authors surmise that prompt resolution of the obstruction and reversal of the gradient may be sufficient since this will normalize the pressure gradient, however the role for antibiotics is unclear in a situation like above when SIRS criteria are present, but source of infection is uncertain. In conclusion, we present a rare case of biliary venous fistula and bilhemia with response to endoscopic intervention and antibiotics.


Rishi Pawa, MD*, Zion Oshikanlu, MD, Vishal Gupta, MD, PhD, Uzma Abbasi, MD, Hashim Nemat, MD, Jay Cowan, MD. Gastroenterology, Columbia University College of Physicians and Surgeons, Harlem Hospital Center, New York, NY, Geriatric Medicine, Long Island Jewish Medical Center, New Hyde Park, NY.

Purpose: We report a rare case of a patient who presented with obstructive jaundice from a pancreatic tumor metastasizing from breast cancer and gastrointestinal bleeding secondary to esophageal and gastric metastasis. Gastrointestinal tract metastasis from primary breast carcinoma is present in 14% to 35% of cases in autopsy series, with gastric involvement in 6% to 18% of cases. Management of these metastasis differs from the management of conventional primary cancers.

Methods: Chart review and review of available literature using Medline and relevant bibliographies of published articles.

Results: A 52-year-old woman presented with complaints of melena, painless jaundice and fatigue. Her past medical history included a modified radical mastectomy three years ago for invasive ductal carcinoma. Physical examination was remarkable for pallor and scleral icterus. Laboratory work-up was consistent with anemia and marked elevation in total bilirubin (19.3 mg/dl) and alkaline phosphatase (2933 U/L). Abdominal and pelvic CT scanning (with oral and intravenous contrast) showed dilated intrahepatic and extrahepatic bile ducts and a rounded soft tissue mass in the head of the pancreas. Esophagogastroduodenoscopy (EGD) was performed which revealed a 4 mm non-bleeding lesion in the distal esophagus and a 1 cm bleeding lesion at the cardia which was treated with endoscopic therapy and esomeprazole. Biopsies were obtained from the esophageal and gastric lesions. Endoscopic retrograde cholangiopancreatography (ERCP) with contrast medium showed a diffusely dilated biliary tree. A sphincterotomy was performed, brush cytology obtained and a stent was placed in the common bile duct. Immunohistochemical analysis of the biopsy specimens tested positive for cytokeratin 7 and ERBB-2. Further immunostaining of the original breast tumor specimen was consistent with the same immunophenotype.

Conclusion: As the prognosis of cancer patients has been improving gradually, gastrointestinal metastasis will be encountered more often. The goals of therapy (i.e., cure, palliation, quality of life) should be clear in each case and survival expectancy from the primary disease and associated conditions estimated.


Arvind Reddy, MD, MPH*, Johnny Altawil, MD, Fadi Antaki, MD. Medicine, Gastroenterology, Wayne State University, Detroit, MI.

Purpose: Gastrointestinal involvement in amyloidosis is well recognized and involves infiltration of the muscularis propria with amyloid leading to dysmotility. While the oral cavity, small bowel and rectum are most commonly affected, gastric involvement is rare, more likely to be of lambda subtype, and usually presents with symptoms of gastroparesis. We present a 59 yr old male with a recent diagnosis of end-stage renal disease who was evaluated for progressive nausea, vomiting and weight loss. Endoscopy revealed a fungating circumferential mass in the antrum with near complete gastric outlet obstruction, very suspicious for malignancy. Forceps biopsies taken on 2 separate occasions showed an inflammatory process with granulation tissue formation and focal eosinophilic deposition. Congo red staining suggested amyloid material in the deep parts of the biopsies. CT scan showed antral mucosal thickening with luminal narrowing. Due to persistent suspicion for malignancy, the patient was referred for surgery. An antral mass was palpated and antrectomy with Bilroth-II gastrojejunostomy were performed. Pathology showed infiltration of the muscularis propria with amyloid material. Workup revealed increased kappa light chains in the urine and a monoclonal spike on serum protein electrophoresis. Bone marrow analysis confirmed multiple myeloma.

Conclusion: Although gastrointestinal amyloidosis is well known, gastric involvement is uncommon. So far, only two other cases of gastric outlet obstruction from amyloidosis have been reported. This case illustrates an unusual presentation with gastric outlet obstruction and a mass lesion mimicking malignancy in association with multiple myeloma.


Maya Mathew, MD*, John Kalarickal, MD, Scott Pollack, MD, Virendra Joshi, MD. GI, Tulane University, New Orleans, LA.

Purpose: Sarcoidosis is a chronic multisystem disease characterized by the presence of noncaseating granulomas in various organs most commonly involving the lungs. Pancreatic involvement is rare. It typically presents as an asymptomatic pancreatic mass diagnosed incidentally during surgery or autopsy. We present a case of pancreatic mass presenting as recurrent acute pancreatitis in a patient with quiescent pulmonary sarcoidosis.

Methods: N/A

Results: The present case is a 39 year old African-American female with a past medical history of previously treated pulmonary sarcoidosis confirmed by bronchoscopic biopsy, a prior episode of acute pancreatitis of uncertain etiology, diabetes, and hypertension. She presented with non-radiating, sharp, post-prandial low back pain associated with emesis for three days. There was no history of weight loss or steatorrhea. Initial evaluation revealed an elevated amylase 390 U/L (N: 25-115) and lipase 261 U/L (N: <61) consistent with the diagnosis of acute pancreatitis. Review of her history revealed no alcohol use, medication changes, abdominal trauma or pancreatic surgery. Further work-up showed normal liver chemistries, serum calcium and triglyceride level. The patient underwent computed tomography of the abdomen with intravenous contrast which revealed a 2.2 cm mass within the head of the pancreas. These findings were associated with dilation of the main pancreatic duct and parenchymal changes suggestive of chronic pancreatitis (CP). Endoscopic retrograde pancreatography showed multiple strictures of the main pancreatic duct and dilation of the secondary branches as seen in CP. Serologies including CA 19-9 and quantitative measurements of serum IgG4 subclass were unremarkable. Subsequent endosonography revealed a 3 cm hypoechoic mass arising from the head of the pancreas associated with changes of the pancreatic parenchyma suggestive of an infiltrative process but did not meet endosonographic criteria for CP. Fine needle aspiration (FNA) of the mass revealed clusters of epithelioid cells consistent with non-caseating granulomas. Stains for acid-fast bacilli were negative. A diagnosis of recurrent acute pancreatitis secondary to granulomatous disease, likely sarcoidosis, was made. The patient was placed on steroid therapy.

Conclusion: The clinical presentation of recurrent pancreatitis associated with a pancreatic mass due to sarcoidosis has never been reported and can only be established at laparotomy. To our knowledge this is the first report of granulomatous pancreatitis (presumably sarcoid of the pancreas) diagnosed using endoscopic ultrasound with FNA. We highlight the role of endoscopic ultrasound with FNA as a safe, minimally invasive alternative to surgery to aid in this diagnosis.


Joseph McKinley, MD*, Steven Kucera, MD, Yasser Saloum, MD, H. Worth Boyce, MD. Gastroenterology, University of South Florida, Tampa, FL.

Purpose: An 83 year old healthy female presented with one episode of hematemesis. She denied prior episodes of hematemesis, abdominal pain and melena. She c/o acute onset solid food dysphagia but denied odynophagia, recent trauma and retching. She was on no medications, did not smoke or drink etoh and had no family history of GI malignancies. An EGD revealed a large mass in the proximal esophagus that was thought to be composed of blood vessels. The endoscopists were concerned for the presence of esophageal varices, but were unsure and transferred her to our tertiary care center. We repeated the upper endoscopy on her arrival; at 20 cm within the proximal esophagus we encountered a large submucousal mass that extended continuously to 40 cm. The lesion was on the posterior wall of the esophagus, was 2 cm wide and 20 cm long. It appeared beefy red in color with multiple areas of purple discoloration and ulceration. CT scan of the thorax revealed a large submucousal mass within the esophagus which was concerning for malignancy, however a definitve diagnosis could not be made. Conservative management was undertaken with plans for repeat endoscopy as we entertained a diagnosis of esophageal apoplexy. Repeat endoscopy was performed two weeks later with near resolution of the findings thus confirming our suspicion. Esophageal apoplexy, also known as esophageal intramural hematoma is a rare cause of hematemesis. Patients usually present with retrosternal chest pain, dysphagia and hematemesis. Frequently the patient is an older female on anticoagulants. Precipitating events include food bolus impactions, vomiting with recurrent retching, recent esophageal instrumentation including dilation and biopsy. Occasionally esophageal apoplexy occurs with no identifiable trigger. EGD helps with diagnosis and is especially useful to rule out esophageal cancer. Barium esophagram may show the "double barrel sign" suggesting intramural dissection. EUS and CT are useful to help confirm the diagnosis. Management is generally conservative as the hematoma usually resolves in 1-3 weeks. Prompt recognition is critical as the prognosis is excellent and the need for more invasive investigation and surgery is unnecessary.


Gennadiy Bakis, MD*, Eiad Nasser, MD, Shahid Mehboob, MD. Medicine, SUNY at Buffalo, Buffalo, NY.

Purpose: To characterize elastofibromatous polyp as a hypoechoic lesion in the second endosonographic layer

Methods: We performed an endoscopic ultrasound of a subepithelial colonic lesion and a subsequent endoscopic resection

Results: Elastofibromatous change presenting as a hypoechoic lesion in the second endosonographic layer. We performed endoscopic resection of the polyp, pathology revealed dilated mucosal capillaries consitent with prior erosion, expansion of the submucosal layer by largely acellular palestaining material wich extended into the overlying muscularis mucosa. Verhoeff elastic stain of the amorphous material was positive and outlined dense, diffusely arrayed serpinginous fibers such consistent with elastofibromas. Desmin D33 stain showed no evidence of smooth muscle tumor. CD 117 stain showed numerous mast cells and no evidence of stromal tumor. Congo red stains for amyloid were negative.

Conclusion: Elastofibromatous change should be in the differential diagnosis of hypoechoic change in the second endosonographic layer


Harshna Patel, MD*, Maria Cino, MD. Department of Medicine, University of Toronto, Toronto, ON, Canada, Department of Medicine, Division of Gastroenterology, University Health Network, University of Toronto, Toronto, ON, Canada.

Purpose: Ulcerative colitis (UC) is an inflammatory bowel disease (IBD), which can have many systemic complications. We present a case of UC with systemic vasculitis involvement of skin, lungs, and central nervous system.

Methods: A case report of a patient seen in the outpatient Gastroenterology Clinic.

Results: A 35 year old Caucasian man presented with non-blanching, non-pruritic, annular skin lesions, myalgia, and arthritis that preceded the onset of his intestinal illness. Complete blood cell count, electrolytes, and renal function tests were within normal limits. Inflammatory markers were elevated: C-reactive protein 65 mg/L and erythrocyte sedimentation rate 47 mm/hr. Rheumatoid factor, anti-DNA antibody, antinuclear antibody, immunoglobulins, peroxidase-antineutrophil cytoplasmic antibodies were negative. CT of the neck showed C4-C5 disc herniation. Electromyography studies revealed axonal injury consistent with brachial neuritis. Flexible sigmoidoscopy revealed diffuse hemorrhagic mucosa, with loss of vascular pattern, mild edema, and preservation of haustral architecture compatible with moderate UC. The patient was started on Salofalk 4 g/day with complete resolution of rectal bleeding, diarrhea, arthralgias and skin lesions within 48 hours. He then developed hemoptysis and dyspnea, hemoglobin 85 g/L, elevated peripheral eosinophil count 1.5 x 10.sup.3/[mu]l and a right middle lobe consolidation on chest radiograph. CT of the chest confirmed an intrapulmonary hemorrhage. The question of Salofalk-induced pulmonary and skin complications was raised; therefore, Salofalk was discontinued. A muscle biopsy revealed necrotizing small vessel vasculitis with eosinophilia. After more than one month off Salofalk, the skin lesions, myalgias and arthralgias recurred. The patient remained asymptomatic from intestinal symptoms. Treatment with oral prednisone 40 mg/day was commenced with resultant improvement of the arthritis, skin lesions and brachial neuritis. Over the next year, the patient tapered prednisone slowly, with recurrence of rectal bleeding and diarrhea at prednisone dose of 20 mg/day. Salofalk was slowly re-introduced; however, in view of corticosteroid dependence, Azathioprine was introduced.

Conclusion: Vasculitis affecting multiple organ systems in a patient with UC suggests that IBD may be part of a larger inflammatory systemic illness as manifested by the extra-intestinal symptoms. The distinction between disease-related and drug-induced systemic symptoms in patients with IBD is a diagnostic challenge and complicates medical management. Early awareness of vasculitis as an extra-intestinal manifestation should be made, so that prompt treatment with a course of corticosteroid therapy may be initiated to prevent serious complications.


Siddharth Mathur, MD*, Niket Sonpal, BS, William Thelmo, MD, Yashpal Arya, MD, Mukul Arya, MD. Wyckoff Heights Medical Center, Brooklyn, NY.

Purpose: Half of all GI tract stromal tumors are gastric while approximately 80% of these are leiomyomas or leiomyosarcomas. The benign lesions are the most common; however the malignant type account for 1% of all gastric malignancies and can be difficult to distinguish via radiological methods. Since the growth of leiomyosarcoma can grow outward from the submucosa into adjacent structures CT scanning can yield results which are not in line with the tumors true anatomy.

Methods: Such is this case of a 55 year old female with no relevant PMH who presented to the ER with lower abdominal pain, loss of appetite, 32 pound weight loss over 4 months and sporadic vomiting. The patient also complained of lower back pain radiating her mid abdomen and varying in intensity. The patient's physical exam and lab results were remarkable for mild anemia; otherwise other values were all within normal. A CT of her Abdomen revealed a large tumor in the upper abdomen inseparable from the poster neck of the pancreas and extending into the porta hepatis; in addition to multiple metastatic lung nodules. The patient was then referred to GI service for staging; where a EUS yielded significantly different yet equally surprising results. Radial echoendoscopic examination from the stomach demonstrated a large 3.1 x 2.2. cm mass arising from the muscularis propria with an intact serosal layer suggestive of a leiomyoma or sarcoma. The lesion was diffusely hypoechoic, heterogeneous, and contained small cystic spaces which suggest areas of necrosis. Additionally several suspicious peri-gastric lymph nodes and measuring anywhere between 6-1.2 cm in size were noted. The biliary and pancreatic systems were noted to be free of malignancy. Findings were confirmed with a linear echoendoscopic fine need aspiration using a 19 and 22 gauge needle.

Results: Pathology demonstrated clusters of spindle cells while immunohistochemical staining for SMA disclosed positive reactivity and confirmed a smooth muscle tumor while CD 117, CD34, and S-100 were all negative. The patient was then referred for surgical and oncological management of a leiomyosarcoma.

Conclusion: In conclusion, EUS-FNA offers an invaluable approach for diagnostic and sampling of GI tract tumors and should always be considered as the surreptitious nature of smooth muscle tumors can lead diagnosticians astray.


Amel Karaa, MD*, Manish Tandon, MD, Julio Ayala, MD, Kinnari Kher, MD. Medicine, Mount Auburn Hospital, Harvard Medical School, Cambridge, MA.

Purpose: Since its first description in 1958 by Caroli around 150 cases of Caroli's disease (CD) have been reported in the literature. This is a rare congenital condition characterized by multiple polycystic malformations of the intrahepatic bile ducts involving a segment, a lobe, or both lobes giving rise initially to biliary stasis, intrahepatic lithiasis and subsequently recurrent secondary infection including cholangitis, septicemia and intrahepatic and subphrenic abscesses. This is different from Caroli's syndrome where the chronicity of the disease progresses into liver fibrosis and cirrhosis. Caroli's disease has been shown to have frequent association with other hereditary cystic diseases. We here report a case of a 75 year old woman with ADPKD diagnosed with CD at the age of 74. Our patient has longstanding ADPKD inherited from her mother with chronic renal failure on hemodialysis but she never experienced any hepatic or biliary symptoms throughout her life. She presented with her first episode of cholangitis at the age of 74. A right upper quadrant ultrasound revealed a slightly dilated common bile duct without evidence of cholelithiasis and CT of the abdomen confirmed the finding with evidence of intrahepatic duct dilation. Diagnosis of CD was final with MRCP showing numerous biliary cysts scattered in both lobes of the liver differentiating this from hepatic cysts usually present in patients with ADPKD. The patient had no evidence of liver cirrhosis by physical exam, labs or radiologic findings. She recovered with conservative management and is not a surgical candidate given the absence of cirrhosis and the diffuse nature of the disease in the liver. This patient is at higher risk of developing cholangiocarcinoma and will need close clinical and biological monitoring. Caroli's disease usually manifests during childhood and early adulthood. The mean age is generally 10 years old with extremes ranging from intrauterine diagnosis to the oldest case reported being 68. We believe that this is the oldest case report in the literature of new onset Caroli's Disease. Moreover, although the association of Caroli's disease with autosomal recessive polycystic kidney disease (ARPKD) is well established, the relationship with dominant polycystic kidney disease (ADPKD) like in this patient remains rare and warrants further studied to elucidate the genetic association.


Michelle Rivera, MD*, Ana Conde, MD, Jose De Jesus, MD, Jorge Santana, MD, Maria Correa, MD, Esther Torres, MD, MACP, MACG, AGAF. Gastroenterology Section, Department of Internal Medicine, UPR school of Medicine, San Juan, PR, Infectious Diseases Section, Department of Internal Medicine, UPR School of Medicine, San Juan, PR, Department of Pathology, UPR school of Medicine, San Juan, PR.

Purpose: Case Report of an unusual case of azathioprine induced eosinophic lung nodules in a patient with Crohn's Disease.

Methods: Clinical Vignette.

Results: Azathioprine- induced Eosinophilic Lung Nodules in a Patient with Crohn's Disease.

Conclusion: An 11-year-old girl with fistulizing Crohn's Disease (CD) for 18 months presented with multiple bilateral lung nodules. She was initially treated with metronidazole and methylprednisolone. Azathioprine was added after tapering down steroids and continued for 16 months. Two weeks after discontinuation of medications she developed abdominal pain, fever, weight loss, bloody stools, and active perianal disease. She was admitted to our center with active Crohn's Disease. On admission, she had leukocytosis with eosinophilia. A Chest X-ray showed bilateral nodular infiltrates. Chest CT scan revealed multiple scattered nodular infiltrates with cavitations within the soft tissue densities and no lymphadenopathy. Abdomino-pelvic CT scan showed diffuse thickening from the transverse colon to rectum. The patient received broad spectrum antibiotics. Infectious workup was negative. Echocardiogram showed no vegetations. Small bowel series, upper endoscopy and colonoscopy revealed focal active colitis with non-specific ileitis, and eosinophilia. Biopsy of the nodules revealed abundant micro-abscesses of eosinophils and macrophages. Immuno-histochemistry was negative for Langerhan's cell histiocytosis. The diagnosis was drug induced eosinophilic pneumonia. She was discharged on metronidazole, amoxicillin-clavulanate and mesalamine. After two weeks, eosinophilia resolved and a follow up chest CT scan demonstrated complete resolution of the nodules. Infliximab was started for the treatment of fistulizing CD. This is an unusual case of azathioprine induced eosinophic lung nodules in a patient with CD. The most common toxicity reported with this drug is a type 1 and 3 hypersensitivity reaction. Inflammatory bowel disease causes pulmonary complications; and the medications available for treatment are also associated to lung pathology. Multiple lung nodules with micro abscesses of eosinophils is an unusual finding in CD. In the absence of an infectious cause, the possibility of azathioprine induced EP was considered. Peripheral eosinophilia, the presence of eosinophilic nodules in relation to administration of the drug and radiologic resolution after removal of the medication support the diagnosis. No re-challenge was attempted.


Paula Dionisio, MD*, Kevin Ruff, MD, Holenarasipur Vikram, MD, Lucinda Harris, MD, Tisha Lunsford, MD. Infectious Diseases, Gastroenterology, Mayo Clinic Scottsdale, Scottsdale, AZ.

Purpose: Aeromonas species are a ubiquitous, hydrophilic, gram-negative rod. Reservoirs include a variety of water environments and vegetable produce with an increase in isolation during warm weather months. Originally thought of as a pathogen in the immunocompromised host only, these organisms are now recognized as a cause of a spectrum of disease in immunocompetent humans. The following is a case of diffuse colitis with deep ulcers secondary to Aeromonas sobria. A 76-year-old, previously healthy female presented with complaints of 2-3 months of nightly fevers up to 102 degrees Fahrenheit associated with sweats. She also complained of crampy abdominal pain and diarrhea intermittently associated with the passage of bright red blood over the previous two weeks and a 15 pound weight loss over the same time period. Evaluation in infectious disease clinic outside of our facility had not revealed a clear cause of her symptoms despite performing multiple blood and stool cultures. Examination revealed a febrile (38.8 C), thin appearing female with mild diffuse abdominal tenderness. Colonoscopy revealed erythema and deep ulcers throughout the entire colon (including rectum). Ulcers were deep, clean-based with undermined edges and surrounding hyperemia. Multiple biopsies were obtained throughout the patient's colon (from ulcers and surrounding tissue). Biopsies and stool cultures supported the diagnosis of an acute infectious colitis secondary to Aeromonas sobria. The patient was treated with ciprofloxacin and had an appreciable decline in her gastrointestinal symptoms prior to hospital discharge. Review of the literature revealed several case reports describing segmental colitis secondary to an Aeromonas species. Our case demonstrates an occurrence of a pan-colitis secondary to Aeromonas sobria and emphasizes the need to consider Aeromonas species in the differential diagnosis for colitis.

Methods: N/A

Results: N/A

Conclusion: N/A


Simon Chan, MD*, Jason Gutman, MD, Ashok Shah, MD, MACG. Department of Gastroenterology, University of Rochester Medical Center, Rochester, NY.

Purpose: Endometriosis is a common gynecological disorder characterized by the presence of functional endometrial glands outside of the uterus. It is thought to occur through either retrograde menstruation into the peritoneal cavity or metastases through blood and lymphatic vessels. Various radiographic studies including CT scan, MRI, transvaginal ultrasound, and rectal ultrasound have been used to detect peritoneal implants, but definitive diagnosis requires laparoscopy and biopsy. Endometriosis of the gastrointestinal tract most commonly involves the rectosigmoid colon due to its close proximity to the reproductive organs. Here we describe a rare case of endometriosis involving the appendix. The patient is a 56 year-old healthy woman with a history of prior hysterectomy and bilateral salpingo-oophorectomy for endometriosis who was found to have a 1 cm polypoid mass at the appendiceal orifice on screening colonoscopy. Endoscopic ultrasound of the mass with the miniprobe revealed a 10 x 7 mm anechoic structure suggestive of a cystic lesion. Biopsies of this lesion were nondiagnostic. A subsequent CT scan of the abdomen revealed a 9-10 mm area of decreased attenuation adjacent to the cecum, possibly representing the lesion of interest. The patient otherwise was asymptomatic and denied any abdominal pain, weight loss, night sweats, hematochezia, or diarrhea. The patient was referred to a colorectal surgeon, as a mucocele of the appendix was suspected. The patient underwent laparascopic right hemicolectomy several months later and the final pathology of the resected specimen revealed endometriosis. Appendiceal endometriosis is a rare phenomenon with a reported prevalence of 0.054%. Many cases are asymptomatic and pass undiagnosed. However, symptoms of acute appendicitis, chronic right lower quadrant abdominal pain, cecal intussusception, and intestinal perforation have been reported. Diagnosis is difficult as endometriosis of the gastrointestinal tract mimics other disorders such as irritable bowel syndrome and requires histological demonstration of ectopic endometrial glands and stroma.

Methods: N/A

Results: N/A

Conclusion: N/A


Thomas Parambil, MD*, Scott Pollack, MD, Fredric Regenstein, MD, Shobha Joshi, MD. Surgery - Abdominal Transplant, Tulane University School of Medicine, New Orleans, LA.

Purpose: Background: Ascites is a common finding in patients with cirrhosis. The non-hepatic causes of ascites include venous or lymphatic obstruction, nephrotic syndrome, and congestive heart failure. Constrictive pericarditis (CP) is characterized by pericardial inflammation and subsequent scarring and contracture of the pericardium. The clinical manifestation of CP is usually congestive heart failure (CHF) which results in a "nutmeg liver" due to chronic congestive changes in the liver. Histologic findings in the liver include sinusoidal dilatation, fibrosis around spared portal regions and hemorrhagic necrosis in zone 3 of the hepatic lobule. Recently, the prevalence of CP has declined significantly due to increased focus on preventive medicine and improved diagnostic capability. Thus, CP with congestive hepatopathy (CH) has not been reported. We report a case of CH with ascites caused by CP. Case Report: A 78 year-old male with history of hypertension, diabetes, and dyslipidemia presented with gradual increase in abdominal girth over 5-8 months; this was attributed to ascites. The patient denied dyspnea at rest or on exertion and orthopnea. He denied alcohol or drug use, and history of previous liver disease or radiation exposure. Patient's mild abdominal pain was relieved by a paracentesis; 5 liters of transudative fluid were removed. The serum ascites albumin gradient was 1.0. An abdominal CT scan showed cirrhosis and extensive calcification in the inferior pericardium. The latter finding was confirmed on a CT scan of the chest. Tuberculin skin test was negative. Platelet count was 270,000/[mu]L, sodium 137 mEq/L, creatinine 1.5 mg/dL, prothrombin time 22 seconds, aspartate aminotransferase 19 U/L, alanine aminotransferase 24 U/L, alkaline phosphatase 89 U/L, bilirubin 6.4 mg/dL. Hepatic sinusoidal pressure was 16 mmHg; liver histology was consistent with CH. Transthoracic Echocardiogram revealed biatrial enlargement and normal left ventricular ejection fraction. Right and left heart catheterizations indicated relative equalization of pressures in the cardiac chambers, restrictive physiology and a pulmonary artery wedge pressure of 62 mmHg. The patient underwent an anterior pericardiectomy; however, ascites reaccumulated requiring numerous paracenteses. Discussion: This case illustrates that CP needs to be considered as an etiology of CH, cirrhosis and ascites. In our patient, pericardiectomy was unsuccessful in completely resolving ascites, highlighting the importance of early pericardiectomy and appropriate CHF management to prevent cirrhosis. Although CHF has been associated with CH, this is the first case of CP and CH.

Methods: NA

Results: NA

Conclusion: NA


Muslim Atiq, MD*, Daniel Brown, MD, Muhammad Husain, MD, Kevin Olden, MD. Pathology, Gastroenterology, University of Arkansas for Medical Sciences, Little Rock, AR.

Purpose: To recognize esophageal cancer as a possible explanation for high Alfa fetoprotein (AFP).

Methods: Case review and review of literature.

Results: Alpha-fetoprotein (AFP)-producing esophageal tumors are extremely rare. AFP producing tumors with liver metastasis pose significant diagnostic dilemma with regards to delineating the primary. A 56 years old gentleman with no significant past history presented for evaluation of fatigue and weight loss. He did not complain of dysphagia, hematemesis or melena. Initial evaluation reveled iron deficiency anemia. A CT scan showed multiple liver lesions. Alfa-fetoprotein was elevated at >3000 ng/ml. Fine Needle Aspiration of liver was positive for malignant cells. Gastroscopy revealed a large fungating mass in lower esophagus, with yellowish colored debris. The biopsy material showed a malignant tumor with extensive necrosis. The tumor cells were large, had large nuclei and occasional prominent nucleoli. They were arranged in clumps, columns and vague acinar configuration intercepted by thin vascular channels. Many mitotic figures were present. By immunohistochemical stains, tumor was suggestive to be of hepatoid origin.

Conclusion: Primary tumors of the upper gastrointestinal tract showing hepatoid differentiation are very infrequent. Most have been reported as arising in the stomach. To our knowledge, this is the first case of hepatoid esophageal cancer to be reported from the United States.


Shyam Dang, MD*, Muslim Atiq, MD, Kevin Olden, MD, Ralph Panek, MD, Neelima Velchala, MD, Robert Svoboda, MD, Farshad Aduli, MD. Radiology, Internal Medicine, Gastroenterology, University of Arkansas for Medical Sciences, Little Rock, AR.

Purpose: 1-To describe comlications related to percutaneous liver biopsy 2-To be able to recognize hematochezia as a consequence of hemobilia after percutaneous liver biopsy.

Methods: Case presentation and literature review.

Results: A thirty-five year old woman underwent an ultrasound guided liver biopsy of the left liver lobe. One week later she returned to the emergency room with right upper quadrant abdominal pain, nausea and multiple episodes of bleeding per rectum. Patient was hypotensive and tachycardic. On exam a mild right upper quadrant tenderness was noted. Laboratory tests showed anemia and a cholestatic elevation of liver enzymes. Medical resuscitation allowed hemodynamic stabilization. Computed tomography (CT) of the chest, abdomen and pelvis was performed. It showed a possible arteriovenous (AV) fistula in the left liver lobe. CT did not reveal any other pleural, abdominal or pelvic abnormalities. Colonoscopy was normal. Upper gastrointestinal endoscopy showed ongoing blood flow through the ampulla of Vater. The diagnosis of hemobilia secondary to injury from liver biopsy was made. Angiography verified the presence of an arteriovenous fistula in the segment three of liver. Successful embolization of the bleeding artery was performed. Clinically, there was no further evidence of bleeding. Hemoglobin remained stable and liver enzymes normalized. She was discharged to home.

Conclusion: Liver biopsy is a commonly performed procedure. However, it may result in complications. Hematochezia post percutaneous liver biopsy could be a subtle finding, resulting from hemobilia. Prompt recognition of this entity may prevent frustration and facilitate measures to control bleeding.


Simon Chan, MD*, Parvez Mantry, MD. Department of Gastroenterology, University of Rochester Medical Center, Rochester, NY.

Purpose: Esophageal intramural pseudodiverticulosis is characterized by multiple flask-shaped outpouchings within the submucosa of the esophageal wall due to abnormally dilated mucus gland ducts. This disorder is thought to be the result of chronic esophageal inflammation, and has been described in association with Candidiasis, caustic ingestion, gastroesophageal reflux, and malignancy. Although many patients are asymptomatic, some present with dysphagia due to an associated stricture. Here we present a rare case of pseudodiverticulosis in the setting of HIV-associated ulcerations of the esophagus. The patient is a 48 year-old man with end stage liver disease secondary to HIV and hepatitis C who presented to hepatology clinic with dysphagia. He had been treated with efavirenz and tenofovir for eight years with poor compliance related to alcohol abuse. Laboratories one month prior to presentation revealed a CD4 count of 254 and an undetectable HIV viral load. He also had a history of Candida esophagitis two years ago which was treated successfully with Diflucan. An upper endoscopy revealed the presence of multiple deep ulcerations in the proximal to mid esophagus, the largest of which measured 8 cm in size. Biopsies were negative for a viral etiology. Repeat bloodwork demonstrated HIV viral breakthrough, and subsequent phenotype testing indicated the development of efavirenz resistance. The patient was placed on a new HAART regimen including atazanavir, emtricitabine, and didanosine, resulting in suppression of the HIV virus once again. A repeat endoscopy six weeks later revealed complete healing of the ulcers with multiple shallow pseudodiverticula remaining. To our knowledge, this is the first reported case of pseudodiverticulosis associated with HIV ulcerations of the esophagus. Treatment of the ulcerations with HAART therapy resulted in healing of the ulcers and resolution of his symptoms. This case highlights the fact that specific treatment for esophageal intramural pseudodiverticulosis is not necessary, though these lesions have been described to disappear after empiric dilation.


Afreen Khan, MD*, Vijay Mudunuri, MD, Milton Mutchnick, MD, Elizabeth Puscheck, MD. Gastroenterology, Wayne State University, Detroit, MI.

Purpose: Introduction: Ovarian hyperstimulation syndrome (OHSS) is a rare but serious complication of in-vitro fertilization and iatrogenic ovarian stimulation. Although OHSS has been reported widely in the literature, there is scant data about the hepatic manifestations of OHSS. Abnormalities of liver functions were first reported in 1988 and may be seen in 30-40% of patients. Our case is unique because it is the second reported case with very high aminotransferase levels and a favorable outcome.

Methods: Case Report: We report a 39-year-old woman who presented with dehydration, decreased urine output, nausea, vomiting, abdominal distension, pedal edema and weight gain 10 days after ovulation induction (using gonalef and menopur). She had a history of recurrent miscarriages, non alcoholic fatty liver disease (NAFLD) with normal liver enzymes and no pharmacotherapy, polycystic ovarian syndrome (PCOS). Physical exam revealed massive ascites and right sided pleural effusion. Patient's liver enzymes have always been within the normal range. During her 23 day hospital stay a gradual rise in liver enzymes was noted. AST showed an increase from 48 to 1132 units/L and ALT increased from 40 to 1604 units/L. Alkaline phosphatase, bilirubin and prothrombin time was normal. Albumin decreased from 2.7 gm/dl to1.4 gm/dl. All other causes of hepatic dysfunction were ruled out and treatment was directed to major manifestations of OHSS including ascites, hypoalbuminemia and hypovolemia. The liver enzymes started trending down and patient showed significant clinical improvement. The patient was discharged in stable condition with viable pregnancy with outpatient follow up.

Results: N/A

Conclusion: Conclusion Increased awareness of the hepatic manifestations of ovarian hyperstimulation syndrome is important as very few cases of this entity have been described thus far. All patients undergoing in-vitro fertilization should have close monitoring of liver functions to prevent such complications.


Kenneth Berman, MD*, Raj Vuppalanchi, MD. Medicine- Gastroenterology, Indiana University, Indianapolis, IN.

Purpose: Focal nodular hyperplasia (FNH) is a relatively rare benign tumor of the liver typically seen in young to middle aged women. It is usually an incidental finding, with most patients being asymptomatic. We describe a previously unreported presentation of a FNH causing a Mirizzi like syndrome.

Methods: An 18 year-old white female presented with two days of right upper quadrant and epigastric pain associated with nausea, vomiting and chills. She had no prior medical history other than eczema and asthma. She denied taking any prescription or over the counter medications including oral contraceptives. Liver biochemistries revealed elevated total bilirubin 2.9 gm/dL, alkaline phosphatase 270 U/L, AST 104 U/L, ALT 171 U/L and a normal alpha feto-protein. CT with contrast showed gallbladder thickening and a 9.0 x 7.4 cm mass in segment 4 of the liver demonstrating hyper enhancement on arterial phase with a central hypodense stellate focus (Fig. 1). An MRI revealed a 9.2 x 7.8 cm mass with a T2 hyperintense central scar with enlarged gallbladder with wall thickening. Finally, a hepatobiliary scan demonstrated radiotracer throughout the liver, prompt gallbladder visualization and a 0% gallbladder ejection fraction. Given the typical radiographic features of FNH seen with the above studies her mass was felt to be FNH presenting with a Mirizzi like syndrome.

Results: Due to the large size of FNH potentially leading to technical difficulty in performing a cholecystectomy, a cholecystostomy tube was placed to allow for gallbladder decompression. Subsequently, a right sided portal vein embolization was performed to allow left lobe hypertrophy of liver prior to successfully performing a right trisegmentectomy. The resected specimen revealed a 10.4 x 9.5 x 7.6 cm tan, heterogeneous, firm, diffusely nodular, well delineated mass with a central scar abutting the capsule and histology confirmed the presence of FNH. Gallbladder specimen did not reveal choleliths. Her post operative course was uncomplicated.

Conclusion: This is the first case reported of a giant FNH presenting with Pseudo-Mirizzi syndrome.


Vishal Gupta, MD, PhD*, Zion Oshikanlu, MD, Rishi Pawa, MD, Uzma Abbasi, MD, Jay Cowan, MD. Division of Gastroenetrology, Columbia University College of Physicians and Surgeons/ Harlem Hospital Center, New York, NY.

Purpose: Introduction: Metastatic spread of breast cancer to the upper gastrointestinal tract has been infrequently reported in the literature (1). The common sites of spread include bones, lung and liver. We report a rare case of metastatic lobular breast cancer to stomach.

Methods: Case: A 51 year-old African-american woman presented with complaints of dyspepsia and weight loss. She denied any melena, hematochezia or vomiting. Lab work revealed HB 7.6%; AST 129; ALT 125; Alk P 360; Direct/Total Bilirubin 1.3/2.5; Albumin/Protein 2.3/5.8; BUN/Creatinine 11/1.4; Amylase 102; Lipase 82; HAV and HBV immune and HCV negative. Contrast CT abdomen showed double duct sign with pancreatic head fullness, which were confirmed by MRCP. Bone scan revealed diffuse metastatic bone disease. Two years prior to this presentation, she underwent modified radical mastectomy with adjuvant chemotherapy and radiotherapy for Stage IIIa (ER/PR +ve HER 2 NEU -ve) invasive lobular carcinoma of the left breast. She subsequently was taking Tamoxifen and till recently remained symptom-free.

Results: EUS during this presentation revealed 12 mm antral mass which was biopsied; pancreatic head fullness which unfortunately could not be sampled due to technical difficulties. Antral biopsy immunohistochemistry demonstrated staining for AE1/AE3; cytokeratin 7 +ve/ cytokeratin 20 -ve. This immunoprofile pattern confirmed a metastatic breast carcinoma (Fig. a).

Conclusion: Discussion: Despite improvement in treatment of breast cancer, distant metastatic disease continues to occur. The incidence of breast cancer metastasis to the stomach, especially lobular cancer is higher then other variants including ductal cancers (2). A high index of suspicion for metastatic disease to the stomach of previous breast cancer should be maintained when new gastrointestinal symptoms develop. 1. Menuck LS, Amberg JR. Metastatic disease involving the stomach. Am J Dig Dis. 1975;20:903-13. 2. Taal BG, den Hartog Jager FC, Steinmetz R, Peterse H. The spectrum of gastrointestinal metastases of breast carcinoma, I: stomach. Gastrointest Endosc. 1992;38:130-135.


Vishal Gupta, MD, PhD*, Rishi Pawa, MD, Uzma Abbasi, MD, Hashim Nemat, MD, Raja Sabbagh, MD, Jay Cowan, MD. Division of Colorectal Surgery, Division of Gastroenetrology, Columbia University College of Physicians and Surgeons/ Harlem Hospital Center, New York, NY.

Purpose: Introduction: Trichuris trichiura, or whipworm is the third most common nematode infection worldwide. However, in United States it is exclusively seen in immigrants from tropical countries. Due to increased endoscopic examination of the gut, more cases of the infection have recently been diagnosed. We report an endoscopic extraction of whip worm while performing a screening colonoscopy.

Methods: Case: A 54 year old male from Puerto Rico who immigrated to United States presented for average risk screening colonoscopy. He denied any fever, rash, abdominal pain or diarrhea. Laboratory work up including Complete Blood Count, Blood Chemistry and liver function test were unremarkable.

Results: Colonoscopy performed revealed a thick straight white end of a worm looking object in the cecal lumen. The worm was gently extracted using biopsy forcep, which also freed the mucosal embedded whip like head of the worm from the colonic wall, and placed in saline container (Fig. 1). H&E staining revealed barrel shaped ova of Trichuris trichiura in a gravid female adult worm. The cecal wall biopsy revealed intense lymphocytic and eosinophilic infiltration. Mebendazole was prescribed for this asymptomatic infection.

Conclusion: Discussion: Trichuris trichiura which was first described by Roederer in 1761, is highly prevalent in tropical climates. Generally if less then 10 worms are present, the patient remains asymptomatic. However in those with symptoms, they present with diarrhea, anemia or malnutrition. Whip worm is whitish in color and typically measures 3 to 5 cm in size with a whip like anterior end which embeds into the colonic mucosa. The luminal posterior end is straight in males and coiled in females. In majority of cases they are seen in terminal ileum, cecum and sigmoid colon. The standard regimen is three day course of either Mebendazole 100 mg twice daily or Albendazole 400 mg once daily. With the increasing number of colonoscopy examination being performed for various indication, it seems prudent for endoscopist to be able to identify common worms which can be visualized by naked eye. 1. Blaser MJ, Smith PD, Ravdin JI and Greenberg HB. Infections of the gastrointestinal tract. 2nd edn. Philadelphia: Lippincott Williams & Wilkins, 2002;1085.


Nikila Ravindran, MD*, Maria Cino, MSc, MD. University of Toronto, Toronto, ON, Canada.

Purpose: Case Presentation: A 22 year old Vietnamese immigrant in Canada for 16 years presented with a 5 month history of abdominal pain, weight loss and diarrhea. History was negative for medical problems, medication and drug use, smoking, alcohol, gastrointestinal bleeding, constitutional symptoms, infectious contacts, recent travel and extraintestinal manifestations of inflammatory bowel disease (IBD). Family history was negative for tuberculosis, IBD and colon cancer. Physical exam showed a pale, cachectic, afebrile, hypotensive (88/54) man with no postural drop. There was mild left lower quadrant tenderness and no lymphadenopathy. Lab investigations revealed hemoglobin 117 g/L, white blood cell count 20.6 x 10.sup.9/L, neutrophil count 16.9 x 10.sup.∧9/L, mean corpuscular volume 79.1 fL and serum albumin 29 g/L. Remaining blood tests including electrolytes, creatinine, liver enzymes, amylase and TSH were within normal limits. Serum endomysial antibody and stool testing were negative. Colonoscopy showed a fistulous opening at the base of the cecum, marked mucosal nodularity with multiple pseudopolyps, deep ulcers and areas of denudation in the cecum, ascending and mid-transverse colon. Corticosteroid therapy was deferred due to possibility of tuberculosis. Intestinal biopsies showed moderate acid-fast bacillus with necrotizing granulomas. Nucleic acid amplification test was positive for Mycobacterium tuberculosis complex. The patient's gastrointestinal symptoms improved with antituberculous treatment and he made a full recovery. Discussion: Our case illustrates three important principles in the diagnosis and treatment of gastrointestinal tuberculosis (GI TB). First, tuberculosis infection should be considered in patients with clinical, endoscopic, radiological and histopathological features of Crohn's disease, especially where there is a predominance of ileal and cecal involvement. Immigration from a country with known endemic tuberculosis is an important risk factor, even if immigration is a remote event. Nonspecific symptoms of GI TB include fever, night sweats, weight loss, abdominal pain and diarrhea. Diagnosis of GI TB is based on detection of acid-fast bacilli in tissue or stool. Second, it is important to exclude the possibility of tuberculosis before the commencement of corticosteroid therapy, often used in the treatment of IBD, since corticosteroid therapy will increase morbidity of the patient with GI TB. Third, treatment of GI TB is primarily medical and although complications such as fistula formation, perforation and hemorrhage may require surgery, it is possible to treat gastrointestinal fistulae due to tuberculosis successfully with medical therapy alone.


Alastair Smith, MB, ChB*. Medicine, Eastbourne District General Hospital, Eastbourne, United Kingdom.

Purpose: Autoimmune hepatitis (AIH) is a chronic inflammatory disorder of unknown etiology arising in genetically susceptible individuals, typically women. Certain drugs e.g. minocycline and atorvastatin, have been reported in association with the onset of AIH, although the precise mechanism(s) for this are unclear. We describe the onset of AIH in a man ten months after he sustained cholestatic hepatitis following exposure to atorvastatin, and from which subsequent recovery appeared complete.

Methods: A 55 year old man with poorly controlled type 1 diabetes mellitus (DM) was prescribed atorvastatin 40 mg/day for hypercholesterolemia (other drugs were insulin, aspirin and nicorandil). Twenty weeks later he developed fatigue, generalized pruritus, pale stools and dark urine.

Results: Examination revealed jaundice and scratch marks, but no features of hitherto undiagnosed chronic liver disease, e.g. splenomegaly. Liver test and selected other results are tabulated at five different time points (months after index episode). Alternative causes of acute severe liver injury (viral, metabolic and alcoholic) were excluded as far as possible by history-taking and laboratory testing. Liver biopsy demonstrated portal tract expansion with lymphocytes, plasma cells and numerous eosinophils. Similar changes were present but to a lesser degree in the lobules, where acidophil bodies and perivenular cholestasis were evident also. Given the discrepancy between elevated aminotransferase (AST) and immunoglobulin G (IgG) concentrations, circulating antinuclear (ANA) and smooth muscle antibodies (SMA) on the one hand, and the markedly increased cholestatic liver tests, portal tract eosinophils and DM on the other, it was decided not to recommend prednisone. Liver tests became normal within three months. Seven months thereafter, the original symptoms returned and liver tests had relapsed (Table). Further liver biopsy revealed changes very similar to those present first time, with the exception that plasma cells were more conspicuous. Portal fibrosis was evident also. Prednisone resulted in normalization of liver tests, albeit at the expense of even poorer blood sugar control. Azathioprine was added to consolidate attainment of disease remission. It was well tolerated, thus allowing prednsione withdrawal in due course.

Conclusion: It is uncertain whether this man was destined to develop AIH regardless of exposure to atorvastatin. Conversely, the index episode may have represented AIH rather than drug-induced liver injury, although resolution in the absence of steroid therapy makes this more difficult to sustain. A third explanation is that atorvastatin exposure helped precipitate AIH albeit at a later date. No further exposure to the drug occurred to my knowledge.


Nikila Ravindran, MD*, Paul Kortan, MD. University of Toronto, Toronto, ON, Canada.

Purpose: Case Presentation: A 29 year old female immigrant from India presented with a 5 month history of recurrent abdominal pain. Past medical history was significant for vitamin B12 deficiency, iron deficiency anemia and acute pancreatitis. History was negative for smoking, alcohol, drug use, gallstone disease, constitutional symptoms and medication use. Lab work was unremarkable. Abdominal CT showed extensive calcification within the head, body and tail of the pancreas and dilated pancreatic ducts. Endoscopic retrograde cholangiopancreatography (ERCP) showed a pancreatic duct stricture in the neck of the pancreas. Stent placement did not relieve pain. Repeat ERCP showed multiple calcified stones with a large stone in the head of the pancreas causing obstruction. Endoscopic shock wave lithotripsy (ESWL) and ERCP were attempted for stone removal but were unsuccessful. Surgical decompression (lateral pancreaticojejunostomy) was effective in achieving pain relief. The patient was diagnosed with Tropical Pancreatitis (TP). Discussion: TP is a form of chronic pancreatitis (CP) found in people residing within 30 degrees of the equator (Asia, Africa, South America). It is the most common type of CP in India, accounting for approximately 70% of patients with CP. The etiology of TP is unknown. Environmental factors and decreased inhibitory capacity within the pancreas (SPINK1 mutation) have been implicated. Characteristic features of TP include young age at onset, residence in the tropics, absence of alcohol use, no other cause of CP, large duct disease with ductal dilatation, large pancreatic calculi (predominantly in the head) and chronic abdominal pain. Patients can develop nutritional deficiencies and insulin-requiring diabetes. They are at high risk of pancreatic cancer. Management is directed towards pain relief, and control of diabetes and steatorrhea. ERCP coupled with ESWL has been used for stone fragmentation and removal in patients unresponsive to medical therapy. Recently, surgical decompression and drainage have been shown to be more effective than endoscopic treatment in patients with obstruction of the pancreatic duct. TP is an important diagnosis to consider in an immigrant patient from the tropics with chronic abdominal pain and pancreatic calcification.


Justina Ju, MD*, Stephan Goebel, MD, John Shamma'a, MD, Uma Sundaram, MD. Division of Digestive Diseases, West Virginia University School of Medicine, Morgantown, WV.

Purpose: Endoscopic clips are designed to be temporary devices in the achievement of hemostasis. Having stopped the acute bleeding, they usually dislodge and pass through the gastrointestinal tract. Studies have looked at early clip dislodgement resulting in rebleeding and this appears to be rare. Whether clips can be retained for long periods of time (e.g. months) is unclear. We report here two patients who had clips retained for five to six months, one in the upper GI tract and the other in the lower GI tract. Patient 1 is a 47-year-old man who presented to WVUH with abdominal pain, nausea, and multiple episodes of hematemesis. On EGD he had a large visible vessel in the cardia just below the GE junction actively oozing fresh blood. Epinephrine was injected into the area and 2 clips (Boston Scientific Resolution clips) were deployed on the vessel. The patient did well and was discharged to home three days later. Six months after his initial presentation, he again presented to the hospital with nausea, vomiting, and abdominal pain. He denied hematemesis. An upper endoscopy revealed erosive gastritis and one retained clip. His symptoms improved with carafate and esomeprazole and he was discharged soon after. Patient 2 is a 64-year-old man with significant lower GI bleed. A colonoscopy revealed multiple polyps, pandiverticulosis and a visible vessel was found in a diverticulum, for which clips were deployed. The patient presented five months later to clinic complaining of intermittent streaks of dark blood in his stools. A repeat colonoscopy seven months after the clip was initially deployed revealed the clip was still present in the right colon. Although neither patients' symptoms were likely secondary to the retained clips, we report two cases of temporary clips remaining in place for several months. Review of the literature suggests that different clips remain attached for different periods of time. For example, in a study by Jensen et. al. Triclips fell off significantly faster than Resolution Clip or QuickClip2 and the Resolution Clips were retained significantly longer than the other two clips. Thus, while it appears that retained surgical clips did not lead to adverse effects in patients, it appears that different brands of clips carry different retention times, and caution should be used in applying clips to sites that are intended to be temporary.


Anthony Aghenta, MD*, Surinder Devgun, MD, Tarun Kothari, MD, FACG. Department of Medicine, Unity Hospital, Unity Health System, Rochester, NY.

Purpose: Dieulafoy's lesions are a rare cause of massive and often recurrent gastrointestinal (GI) bleeding. These lesions tend to occur in any part of the GI tract and there are several reports of sudden hemorrhage from rectal Dieulafoy's. While it is known that the bleeding results from an abnormally large submucosal artery, the exact trigger remains undetermined.

Methods: A 45 year old male with a history of Hepatitis C infection, alcohol abuse, liver cirrhosis with esophageal varices presented to the hospital with a 3 week history of upper abdominal pain, nausea, coffee ground emesis and passage of melena stools. His hemoglobin was 5.9, platelet count was 99,000. He had acute mental status changes and was admitted to the Intensive Care Unit (ICU). He received 6 units of PRBC and an upper endoscopy revealed non bleeding grade 1-2 esophageal varices. He was intubated and remained on ventilatory support for management of acute respiratory failure and alcohol withdrawal. His medications included ativan, multivitamins, vancomycin and piperacillin-tazobactam. He developed diarrhea on the 3rd day of admission and a rectal tube (Flexi-Seal) was inserted for ease of drainage. On day 14 of admission, as he was wheeled back to the ICU from an imaging study he was noticed to be passing bright red blood via the rectal tube. The tube was promptly taken off; he continued to bleed massively. Blood pressure dropped to 81/62, heart rate was 92. Nasogastric aspirate revealed no blood. Abdominal exam remained distended and soft. Examination of the anal region revealed active bleeding with clots. Hemoglobin was 6.7, platelets 43,000, PT 21.6 and APTT 36.3. He was aggressively resuscitated with intravenous fluids, 6 units of PRBC, 6 units of FFP and a unit of platelets. Urgent colonoscopy revealed fresh blood with large clots in the rectum. The ileum was clear of blood. An actively pulsating artery was identified 3 cm proximal to the anal verge. Hemostasis was secured by injecting a total of 17 cc of 1:10000 epinephrine interspersed with the application of 3 endoclips. No visible erosion or ulceration was identified.

Results: There were no further bleeding episodes. Unfortunately the patient was made comfort care by the family 3 days later and he passed peacefully.

Conclusion: The exact trigger for the bleeding from the abnormally large submucosal artery is unclear. Suggested causes include stercoral ulceration, thrombosis and NSAIDS. In this case, although no visible erosion was found on endoscopy, the bleeding might have been triggered by the presence of a rectal tube which might have resulted in mucosal erosion when the patient was wheeled out for a procedure. We suggest that rectal tubes could possibly trigger bleeding by a rectal Dieulafoy's lesion.


Krzysztof Kopec, MD*, Samir Shah, MD, Edward Feller, MD. Medicine, Divison of Gastroenterology, Gastroenterology Associates and Brown University, Providence, RI, Department of Medicine, Warren Alpert Medical School, Providence, RI.

Purpose: Eosinophilic esophagitis (EoE) is characterized by an eosinophilic infiltration of the esophagus and is increasingly recognized as a cause of dysphagia and heartburn unresponsive to antireflux therapy. We report a case of eosinophilic esophagitis that presented without dysphagia, heartburn or endoscopic abnormalities to alert clinicians to the importance doing of esophageal biopsies in atypical presentations of EoE.

Methods: A 19 yo college student presented with a 3 year history of anorexia and dyspepsia. Multiple foods and milk seemed to cause dyspepsia. However, his symptoms persisted despite avoiding milk and milk products. He had several episodes of minor hematemesis that led to an endoscopy at age 16 (by a different physician) showing only a small Mallory-Weiss tear and normal duodenal biopsies. Because of worsening symptoms and weight loss of ten pounds, he was referred for further evaluation. Family history was notable for mother with celiac sprue. A gastric emptying test was normal, LFTs and CBC were normal except for borderline eosinophilia; WBC = 7000/uL and 7.3% eosinophils (normal 0-7.0%). A full panel of celiac antibodies were negative except for an antigiadin IgG of 100.0 U/ml (normal <10.0 U/ml). A repeat endoscopy to assess for celiac sprue was normal except for slight gastric retention. Multiple biopsies were negative for celiac sprue and H. pylori. There was no eosinophilia in the duodenal or gastric biopsies. The esophagus was endoscopically normal without evidence of esophagitis, rings, or any other abnormalities. Biopsies from a normal appearing GE junction revealed a focal dense eosinophilic infiltration in the squamous epithelium ([greater than or equal to]28 eosinophils per high powered field) consistent with EoE. The patient was started on fluticasone swallowed twice a day with resolution of all symptoms within a few weeks.

Results: EoE is becoming more frequently diagnosed as a cause of dysphagia and heartburn and is predominantly considered in younger patients presenting with symptoms that are unresponsive to antireflux therapy or with endoscopic signs of EoE such as ringed esophagus. Diagnosis is by clinical features supported by esophageal biopsy with [greater than or equal to]15 eosinophils per HPF. Five biopsies (including proximal esophagus) have a sensitivity of 100%. Other bloodwork and endoscopic findings are neither sensitive nor specific.

Conclusion: This case highlights the importance of esophageal biopsies in the diagnosis of EoE in atypical presentations. We suggest that clinicians consider the possibility of EoE in patients with prolonged, non-specific upper GI complaints and biopsy the esophagus even if the mucosa appears normal on endoscopy.


Jonathan Hlivko, MD*, Olaronke Oshilaja, MD, Nibha Saxena, MD, Alfred Ciraldo, MD, Ghulam Mir, MD, FACG, Costas Kefalas, MD, FACP, FACG. Surgery, Pathology, Medicine, Summa Health System, Akron, OH, Medicine, Barberton Citizens Hospital, Barberton, OH.

Purpose: Malignancy is a major complication of celiac disease. Small intestine lymphoma and carcinomas of the oropharynx, esophagus, and small intestine are the most common malignancies associated with celiac disease. We report a neuroendocrine tumor of the jejunum. Case Report: An 84 Y/O man who had undergone right hemicolectomy for colon cancer 16 years prior was referred for a second opinion for iron deficiency anemia (IDA). The anemia required weekly blood transfusions. One year prior, he had undergone an evaluation elsewhere. Significant findings included: elevated anti-gliadin IgG antibody; unremarkable colonoscopy; normal appearing duodenal mucosa on EGD with Marsh III findings on duodenal biopsies; and focal villous blunting of the proximal small bowel on WCE. The patient was not on a gluten free diet (GFD) at the time of the second opinion. Because of persistent IDA and weight loss, a repeat evaluation was done. Significant findings included: normal serum IgA level and normal tissue trans-glutaminase antibody; positive HLA DQ2 and negative HLA DQ8; unremarkable colonoscopy; and normal appearing duodenal mucosa and normal duodenal biopsies on EGD. The patient was started on a GFD for celiac disease, based on prior evaluations. At a 3 month follow-up visit, he noted an additional 30 lb weight loss, despite adherence to a strict GFD. A CT of the abdomen revealed abnormal small bowel wall thickening in the left pelvis. A small bowel follow through x-ray confirmed abnormal small bowel loops and abnormal small bowel mucosa. Antegrade double balloon enteroscopy was done and revealed a 4 cm fungating, necrotic jejunal mass. Biopsies revealed poorly differentiated neuroendocrine carcinoma. The patient underwent surgical resection of the mass. Final pathology revealed high grade malignant neuroendocrine carcinoma (WHO grade IV) with lymph node metastasis. The patient tolerated surgery well, had return of bowel function, and was discharged. Chemotherapy was not offered due to poor functional status. Discussion: Celiac disease is associated with an increased risk of malignancy. Neuroendocrine tumors in patients with celiac disease are reported infrequently. This case reports the first neuroendocrine tumor of the jejunum in a patient with celiac disease.


Jeff Ye, MD*, Ronald Gaskins, MD, Jeff Stead, MD, Uma Sundaram, MD. Section of Digestive Diseases, West Virginia Univesity, Morgantown, WV, Department of Pathology, West Virginia University, Morgantown, WV.

Purpose: Granular cell tumor (GCT), also known as Granular cell Schwannoma or Abrikossoff tumor, is rare in the colon. It is commonly seen in the subcutaneous tissue and other soft tissue in the body. In the GI tract, it usually presents in the oral cavity or esophagus. Most GCTs are small submucosal benign tumors with maximal reported size of 1.5 cm in colon; however, a malignant counterpart has been reported. It is almost impossible to differentiate it from other benign or malignant epithelial cell tumors and other submucosal tumors by endoscopy. Here we report the first case of an aggregate of multiple GCTs with the largest tumor more than 1.5 cm in the ascending colon. A 39-year-old male patient underwent a screening colonoscopy. Two other polyps detected and removed from cecum and sigmoid had normal histology. Several large flat lesions in ascending colon with largest one of 1.5 x 2.0 cm were biopsied (Fig. 1). Pathological examination reported a benign submucosal granular cell tumor (Fig. 2). The tumor consisted of nests of neoplastic cells with abundant granular eosinophilic cytoplasm and strong expression of S-100 protein (Fig. 3). Since there were multiple GCTs in aggregates with benign histology, endoscopic removal did not appear feasible. It was elected to observe the patient with repeat colonoscopy in 2-3 years. GCT should be in the differential diagnosis of colonic tumors.


Jonathan Hlivko, MD*, Kimberly Eickholt, MD, Raymond Clarke, MD, Costas Kefalas, MD, FACP, FACG. Pathology, Medicine, Summa Health System, Akron, OH.

Purpose: Overlap syndromes of two autoimmune liver diseases are not uncommon and usually involve autoimmune hepatitis with either PBC or PSC. We describe a case of AMA negative PBC and small duct PSC overlap syndrome, an extremely rare cause of autoimmune liver disease. Case Report: A 58 year old male was referred for evaluation of elevated liver enzymes: total bilirubin 2.4 mg/dL, alkaline phosphatase 630 IU/L, AST 262 IU/L, and ALT 447 IU/L. These were associated with fever, night sweats, dark urine, and pruritis. Serologies revealed an elevated pANCA (1:1280) but negative ANA, AMA, and ASMA. Complete serologic evaluation, including viral and metabolic serologies, was otherwise negative. Abdominal ultrasound revealed a normal liver and gallbladder. MRCP revealed normal intrahepatic ducts, common hepatic duct, and common bile duct. No strictures or irregularities of the biliary tree were identified. Liver biopsy revealed features of both PBC and PSC: portal hepatitis, a florid duct lesion, granulomas, and loss of small bile ducts. There was also concentric periductal fibrosis ("onion skinning"), affecting multiple small bile ducts. Trichrome and reticulin stains noted periportal fibrosis. A repeat AMA was performed using the more specific mitochondrial M2 test; this was also negative. The patient was assigned the diagnosis of AMA negative PBC and small duct PSC overlap syndrome. He was started on ursodeoxycholic acid 1200 mg daily in divided doses. Liver enzymes returned to normal within 6 months of therapy and he has had no further symptoms. The patient had undergone a screening colonoscopy 1 year prior to the elevated liver enzymes. This had revealed a hyperplastic colon polyp with normal appearing colon mucosa. Discussion: Overlap syndromes are noted in approximately 18% of patients with autoimmune liver disease and usually involve autoimmune hepatitis and either PBC or PSC. The very rare variant of PBC and PSC overlap syndrome has been reported in 4 cases in the literature. Our patient with features of both AMA negative PBC and small duct PSC represents an additional case of this extremely rare overlap syndrome.


Ian Wall, DO*, Nison Badalov, MD, Jack Braha, DO, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD, MPH, Michael Bernstein, MD. Department of Internal Medicine Division of Gastroenterology, Maimonides Medical Center, Brooklyn, NY, Department of Internal Medicine Division of Gastroenterology, Coney Island Hospital, Brooklyn, NY.

Purpose: Hepatocellular carcinoma (HCC) that develops in non-cirrhotic HCV patients following SVR challenges the current dogma. Celiac disease has been shown to affect the liver. This case represents a HCV patient with F1 fibrosis and active Celiac disease (CD) who went on to develop cirrhosis and HCC 26 months after SVR. A 41 year old gentleman presented for evaluation of HCV. Evaluation revealed Genotype 3a HCV infection with a viral load of 372,000 IU/ml. Testing for other viral and metabolic liver diseases of the liver were negative. Computed tomographic scan showed no focal liver lesion. A liver biopsy revealed A1F1 disease (Fig. 1). Iron deficiency anemia (IDA) prompted endoscopy. Duodenal biopsies and serology were consistent with Celiac disease (Fig. 2). The HCV was treated with peg-interferon alpha 2b and ribavirin for 24 weeks achieving a SVR. Gluten free diet was also begun. The patient was lost to follow up for 2 years. Evaluation after 2 years revealed iron deficiency anemia. Serology and pathology showed active Celiac disease. The AFP was elevated at 6488 ng/ml. Testing for HCV and other viral or metabolic liver diseases remained negative. MRI revealed a nodular liver and a 2.6 cm lesion in the liver. Intra operative US revealed cirrhosis with a second lesion in the liver. DISCUSSION: It is believed that patients with HCV can only develop HCC in the setting of cirrhosis. It is also believed that non-cirrhotic patients who achieve an SVR do not need surveillance for HCC. This patient began therapy for HCV with A1F1 disease and achieved an SVR but went on to develop cirrhosis and HCC 26 months later. Celiac disease (CD) was prominent in this patient. The patient was noncompliant with a gluten free diet. CD can cause "Celiac Hepatitis" consisting of mild transaminitis and a continuum of histological changes from nonspecific to cirrhosis. This case could represent HCC developing in a non cirrhotic patient with successful HCV eradication but persistent Celiac hepatic inflammation.


Prashant Krishnan, MD*, Harprabhjit Singh, MD, Surinder Batra, MD. Gastroenterology, Henry Ford Hospital, Detroit, MI.

Purpose: A 36-year-old female from India was evaluated for intermittent, sharp, cramping abdominal pain and nausea of 3 weeks duration. The pain was initially in the epigastrium but migrated to the periumbilical region without radiation. Her pain was worse with food; there were no relieving factors. She had two episodes of emesis without blood. Her bowel habits alternated between diarrhea and constipation. She denied having fevers. Her appetite was poor; she had a 7 lbs weight loss over 3 weeks. She had no significant past medical history. Her vital signs and physical exam were normal. Her abdomen revealed normoactive bowel sounds and was soft, non-tender, and non-distended with no masses or organomegaly. A CBC, liver profile, electrolytes, amylase, and lipase were all normal. An ultrasound of the abdomen was unremarkable. An EGD was normal. She was treated with omeprazole for 6 weeks. At her follow-up visit, her pain migrated into the lower abdomen. She complained of excessive borborygmi and was having 1 bowel movement per day; her stools were hard so she was started on a stool softener. She lost 4 lbs between clinic visits. A CT of her abdomen and pelvis revealed a loop of bowel in the mid-pelvis with slight luminal narrowing, thickened wall, and enhancing mucosa. A small bowel follow-through revealed 3 contiguous abnormal areas in the terminal ileum: a 6 cm featureless segment distally, an 8 cm segment of luminal narrowing with ulcerations in the middle, and a 12.5 cm moderately dilated segment proximally. A colonoscopy revealed edematous, erythematous, friable, and granular mucosa in the terminal ileum; biopsies revealed no diagnostic abnormalities and were negative for acid-fast bacterial cultures. ASCA and p-ANCA were both negative. She was started on Pentasa and budesonide, and initially noted mild improvement. Within a month, she started noticing increased abdominal cramping, nausea, vomiting, and further weight loss. She was evaluated for partial small bowel obstruction by colon and rectal surgery. During the surgery, an 8 cm lobulated polypoid mass was seen 10 cm proximal to the ileocecal valve; approximately 22 cm of terminal ileum was resected. Histopathology revealed an 8 cm multi-lobulated cauliflower-like villous adenoma with focal high-grade dysplasia, obliterating the lumen completely. Surgical margins were negative for dysplasia; there was no evidence of Crohn's disease. She has done well post-operatively and is asymptomatic. Her most recent colonoscopy was completely normal up to 70 cm into the small bowel.


Thomas Park, MD*, Kevin Jo, MD, Ashok Shah, MD, MACG, Asad Ullah, MD. Gastroenterology, University of Rochester, Rochester, NY.

Purpose: Duodenal carcinoid tumors are rare, accounting for 2% of gastrointestinal carcinoid tumors. We review five cases of duodenal carcinoid tumors diagnosed at our institution from 2004-2008.

Methods: N/A

Results: Of the five cases, there were four men and one woman, with ages ranging from 50 to 73. Three patients were asymptomatic and discovered incidentally, and two presented with painless jaundice. None manifested symptoms of carcinoid syndrome. Two carcinoid tumors were located in the duodenal bulb, two in the periampullary area, and one in the second portion of the duodenum. The two periampullary carcinoid cases presented with symptoms of obstructive jaundice, and the others were asymptomatic. At the time of diagnosis, two patients had metastases. One of them presented with painless jaundice and was found to have a periampullary carcinoid and positive lymph nodes. The second patient had carcinoid in the second portion of the duodenum and liver metastases, but was asymptomatic. EUS with fine needle aspiration was performed on three patients and findings were accurate for carcinoid in all three. The three smallest tumors were removed endoscopically. These tumors ranged from 6 to 19 mm in greatest diameter. There were post-EMR (endoscopic mucosal resection) bleeding complications associated with one of the three cases, the 15 x5 mm carcinoid in the duodenal bulb. Two EGDs over the next few days performed for acute GI bleeding revealed a clot over the resection site and no intervention was performed. Of the two patients with large periampullary tumors, one patient without any metastases had a curative pylorus-sparing pancreatoduodenectomy. The other patient had positive lymph nodes and it was decided that surgical intervention was contraindicated due to the patient's portal hypertension from end-stage liver disease thought to be due to alcoholic liver disease. One patient who had EMR was lost to follow up. The two other patients with EMR were asymptomatic after 9 and 19 months of follow up. The patient who had a pylorus-preserving Whipple was asymptomatic after 12 months. The patient who had a periampullary carcinoid with metastases to lymph nodes but no surgical treatment has been doing well on treatment with octreotide alone after 28 months. His ALT was slightly elevated at 56. This clinical course is reflective of the usually indolent course of carcinoid tumors.

Conclusion: Duodenal carcinoid tumors are rare, and can be discovered incidentally or with symptoms, such as obstructive jaundice, when the ampulla is involved. The course is typically indolent, and the presence of metastases and co-morbidities can determine appropriate intervention. EUS is a useful diagnostic tool for suspected duodenal carcinoid tumors.


Thomas Park, MD*, Kevin Jo, MD, Ashok Shah, MD, MACG, Asad Ullah, MD. Gastroenterology, University of Rochester, Rochester, NY.

Purpose: GIST (gastrointestinal stromal tumor) of the pancreas is extremely rare, with only a handful of cases reported to date. GIST of the duodenum are rare, comprising 3-5% of all cases of GIST.

Methods: N/A

Results: A 72 y/o woman presented with 6 months of mild epigastric discomfort and fatigue. A CT of the abdomen revealed a 6.0 x 3.7 cm mass at the head of the pancreas with central low attenuation, interpreted as possible necrotic change. This was suspicious for a pancreatic head cancer. There was mild intrahepatic ductal dilation. A subsequent EGD was normal without suggestion of extraluminal compression. EUS revealed a 4.6 x 5.8 cm mass at the head of the pancreas that was thick-walled with an anechoic, necrotic-appearing center. FNA was performed, and cytologic analysis revealed a spindle cell neoplasm consistent with GIST. Immunohistochemical staining was strongly positive for c-kit (CD117) and focally positive for smooth muscle actin, supporting the diagnosis of GIST. At laparotomy, a large, soft tumor involving the uncinate process of the pancreas was visualized. It seemed to be closely intertwined with pancreatic tissue and appeared to cause some compression of the second and third portions of the duodenum. The pancreas appeared mildly calcified. There appeared to be no possibility of completely enucleating the tumor, so a Whipple procedure was performed. Pathologic analysis revealed a tumor 8 cm in greatest dimension with a thin capsule. It extended into the subserosa and muscularis of the duodenum without apparent invasion into the duodenal submucosa. It extended to the pancreatic serosa but not into the parenchyma. All surgical resection margins were negative. Six regional lymph nodes were negative. Immunohistochemical stains were strongly positive for c-kit but negative for S100, smooth muscle actin, and CD34. There was moderate to high cellularity and 3-4/50 HPF mitotic activity. Based on these findings, the patient was finally diagnosed with malignant GIST of the duodenum. She has been tolerating her planned year-long treatment with imatinib (Gleevec).

Conclusion: In sum, we present a rare case of extraluminal GIST of the duodenum that masqueraded as a pancreatic head tumor.


Ava Ankelsaria, MD*, Po Chu, MD, Ian Wall, DO, Nison Badalov, MD, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD. Department of Internal Medicine Division of Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Purpose: Percutaneous gastrostomy placed either radioglogically or endoscopically is a safe procedure with few well known complications. The following is a case of a T fastener gastropexy wire impaction and represents a newly described complication of radiological percutaneous gastrostomy. A 91 year-old male patient was admitted complaining of chronic pain around his gastrostomy site. He had a radiological percutaneous gastrostomy (PRG) placed 7 months prior. The gastrostomy tube was changed without relief of the pain. Physical exam revealed tenderness to palpation around the PRG site with voluntary guarding. The site lacked any erythema or induration. Upper endoscopy was performed. Beneath the gastrostomy balloon a wire was noted which originated in the stomach wall and stretched out roughly 10 cms into the lumen. Manipulation with biopsy forceps revealed that the wire was impacted in the stomach wall immediately adjacent to the gastrostomy tube (Fig. 1). The wire was unable to be removed endoscopically. A cat scan revealed a linear density between the anterior gastric wall and the abdominal wall musculature. The patient underwent surgical removal of the impacted wire. Pathological evaluation of the wire revealed it to be a T fastener wire used for gastropexy. The patient recovered well and no longer complains of pain. Endoscopically and radiologically placed gastrostomy share most of the same complications including bleeding, site infection, displaced tubes, and buried bumpers. PRG are preferred in the setting of oropharyngeal cancers to avoid tumor seeding, in patients who cannot tolerate an endoscopy, and in patients whose gastric or abdominal wall anatomy do not permit endoscopic placement. PRG utilizes wire T fasteners to tack the anterior gastric

wall against the abdominal wall during PRG insertion. These wires are left in place temporarily to hold the stomach affixed to the abdominal wall and facilitate the formation of a track. They are cut at the surface of the skin 10 to 14 days later. During insertion 3 T fasteners are placed in a triangular configuration and the tube is placed in the center of this triangle. In this case the impacted wire was noted to be just adjacent to the PRG tube. Presumably the tube was inserted too close to one of the T fastener wires trapping the wire and incorporating it into the tissue of the forming fistulous track.


Krishdeep Chadha, MBBS, MD*, Jan Novak, MD. Department of Gastroenterology and Hepatology, State University of New York, Buffalo, NY.

Purpose: 51 yr old Caucasian male with long standing Crohn's disease presented with 3 days history of epigastric pain, abdominal distension and obstipation. There was no history of nausea, vomiting, diarrhea or fever. Past history was significant for Crohn's disease for 16 yrs. Patient had an episode of small bowel obstruction and underwent stricturoplasty in 1995. Patient was taking prednisone 20 mg daily for Crohn's disease at the time of this presentation. General physical examination was remarkable for tachycardia with pulse of 110/mt. Abdominal examination showed tenderness to palpation in the epigastric region with no peritoneal signs. Abdominal x-rays showed no evidence of intra-abdominal free air. CT scan of the abdomen showed free air in the abdomen with partial small bowel obstruction. The patient underwent exploratory laparotomy and was found to have perforation of the small bowel at the previous stricturoplasty site with a distal small bowel obstruction. The perforated small bowel was removed and a repeat stricturoplasty was performed at the site of the distal obstruction. The perforation was presumably related to the distal small bowel obstruction as a result of Crohn's disease exacerbation. CT scans are often employed in Crohn's disease to rule out intra-abdominal abscesses. CT abdomen in this case diagnosed bowel perforation, which was apparently undetectable on physical exam and abdominal radiographs. To our knowledge, there are less than 10 cases of Crohn's disease reported in the literature with perforation at the stricturoplasty site secondary to a distal bowel obstruction.


Maria Moscandrew, MD*, Sunanda Kane, MD, MSPH. Gastroenterology, Mayo Clinic Rochester, Rochester, MN.

Purpose: Recurrent appendicitis is the clinical entity in which a patient with pathologically confirmed acute appendicitis describes one or more prior episodes with identical symptoms that resolved without surgical intervention. Although rare, patients report previous episodes of pain and then relief of their symptoms after appendectomy.

Methods: A 31-year-old man with a history of HLA-B27 spondyloarthropathy presented to the GI clinic with complaints of two weeks of sharp mid-abdominal pain associated with bloating and cramping. A laboratory evaluation (CBC, Chem 7, LFTs, amylase and sed rate) was within normal limits. A CT scan demonstrated bowel wall thickening and mural stratification in the distal terminal ileum. A colonoscopy showed "nodularity" in the TI to 15 cm but overlying mucosa appeared normal. Small bowel and colonic biopsies were normal. It was thought that the CT abnormalities showed more proximal small bowel disease and, therefore, were not seen on endoscopy. A diagnosis of Crohn's disease was made and the patient's symptoms completely resolved with Infliximab. In 3 months, he returned to the clinic complaining of one week of increasing periumbilical abdominal pain radiating to the RLQ, similar to but not as severe as the prior abdominal pain. Physical exam: +Rovsig's sign. CT enterography was consistent with acute appendicitis. No small bowel abnormalities were seen.

Results: The patient underwent a laparoscopic appendectomy that revealed pathologically confirmed acute appendicitis with a large amount of inflammation and adhesions around the appendix. The remainder of the bowel appeared normal. Since appendectomy, the patient has not had recurrent abdominal pain.

Conclusion: This case illustrates the importance of correlating endoscopic and CT findings as well as recognizing the existence of recurrent appendicitis. Although this diagnosis is rare, identifying this entity is critical to the institution of appropriate treatment and the prevention of possible peritonitis. This case serves as a reminder not to discount the diagnosis of appendicitis in patients with prior episodes of similar abdominal pain.


Dharshan Coomaraswamy, MD*, Ian Wall, DO, Michael Bernstein, MD, Nison Badalov, MD, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD, MPH. Department of Internal Medicine Division of Gastroenterology, Maimonides Medical Center, Brooklyn, NY, Department of Internal Medicine Division of Gastroenterology, Coney Island Hospital, Brooklyn, NY.

Purpose: Iron deposition in the gastric mucosa, or Gastric Siderosis (GS), is a rare clinical entity resulting from iron overload states, or iron pill ingestion. We present a patient who developed GI bleeding from a gastric ulcer secondary to GS. This rare complication of iron therapy likely occurred in the setting diabetic gastroparesis. A 46 year old woman presented with melena and increasing shortness of breath. Her past medical history was significant for hypertension, poorly controlled type two diabetes, osteoarthiritis, and iron deficiency anemia. The patient had been treated for diabetic gastroparesis in the past. More recently, she had been taking iron supplementation for anemia of unclear etiology. On admission, she was hemodynamically stable; physical exam revealed pale sclera, soft, non tender abdomen, and black tarry stool on rectal exam. Laboratory results showed severe anemia with a hemoglobin and hematocrit of 5.3 g/dl and 18.2% respectively. The iron profile was consistent with iron deficiency anemia. The patient was given intravenous fluids, pantoprazole, and four units of packed red blood cells. Upper endoscopy revealed a gastric ulcer in the body of the stomach along the lesser curvature. The ulcer was not actively bleeding, but had an abnormal dark brown metallic quality that did not wash with repeated flushing (Fig. 1). Biopsies revealed a gastric ulcer with superficial mucosal iron deposition consistent with Gastric Siderosis (Fig. 2). Secondary GS consists of superficial mucosal iron deposition in the epithelium and is related to oral iron supplementation. Endoscopic findings associated with this form are nonspecific ulcerations, "Iron Pill Gastritis", or dark pigmentation. In therapeutic doses the mechanism of cellular injury is not clearly understood. Likely high local concentrations of iron from pill stasis lead to excessive iron absorption into cells that then catalyzes reactive oxygen species causing localized mucosal injury. Stasis is an important component of the corrosive process of iron pill injury. This patient's underlying gastroparesis likely complicated the local effects of the iron supplementation, leading to localized iron injury to the gastric mucosa, ulceration and upper gastrointestinal bleeding. Clinicians should be aware of this potential complication of iron supplementation in patients with underlying diabetic gastroparesis.

Methods: N/A

Results: N/A

Conclusion: N/A


Deborah Flomenhoft, MD*, Nicholas Nickl, MD. Internal Medicine, Internal Medicine and Pediatrics, University of Kentucky, Lexington, KY.

Purpose: Description of endosonogrpahic doppler interrogation of blue rubber bleb nevus syndrome.

Methods: Case report

Results: Blue rubber bleb nevus syndrome is an uncommon, but well documented cause of GI blood loss in children. Low flow vascular lesions may occur throughout the GI tract, most commonly in small bowel. There are currently no reports documenting the endosonographic Doppler interrogation of these lesions. We report the case of an eight year old with increasing fatigue and pallor found to have a microcytic anemia (Hgb 6.0 g/dL, MCV 61). The patient reported daily soft brown stools. The patient had a similar episode 18 months prior to this presentation: Hgb was 5.1 with MCV of 54. At that time the child was noted to drink approximately forty ounces of milk a day. The patient was transfused and begun on iron therapy. The child remained completely asymptomatic and was documented to have a hemoglobin of 11.8 g/dL three months prior to this presentation. On evaluation at this presentation stools were guaiac positive. Endoscopy was performed. On upper endoscopy the patient was noted to have two vascular lesions: a ten millimeter lesion on the greater curvature of the stomach and a larger, fifteen millimeter vascular lesion in the second portion of the duodenum. Wireless capsule endoscopy demonstrated six additional lesions throughout the jejunum and ileum. Endoscopic ultrasound was performed to further delineate the nature of the lesions prior to intervention. The gastric lesion was noted to be an intramucosal vascular lesion in the second layer. Doppler interrogation revealed arterial flow to the vascular lesion: an arterial vessel arising in the muscularis (fourth layer) was documented to pass through the third layer and into the intramucosal vascular lesion. After multidisciplinary evaluation, the patient continues on iron. Balloon enteroscopy with endoscopic ablation or endoscopically assisted laparascopic ablation will be considered if anemia becomes intractable.

Conclusion: This is the first report of documentation of flow in blue rubber bleb nevus syndrome.


Thomas Park, MD*, Richard Farmer, MD, MACG, Ashok Shah, MD, MACG. Gastroenterology, University of Rochester, Rochester, NY.

Purpose: We present a patient with cutaneous leukocytoclastic vasculitis during a flare of Crohn's disease, an association that has been reported rarely in the literature.

Methods: N/A

Results: A 30 y/o African-American man with a history of Crohn's colitis for 11 years presented to the emergency room with 2 weeks of bloody loose stools 15-20 times a day and abdominal cramping. He had been taking 60-80 mg of prednisone a day for several days with no benefit. His prednisone dose was increased to 100 mg a day and sent home. His colitis improved over the next two days, with 5-10 slightly bloody and more formed stools a day. He then developed a pruritic, slightly raised, violaceous skin eruption over all his extremities (see image). Plaques were 2-3 cm in size. He returned to the ED, where a punch biopsy was taken. Keflex and Benadryl were started. Lab tests were significant for a white count of 16.2; the remainder of the CBC and chemistries were normal. Anti-streptolysin-O antibody, hepatitis C, ANA, HIV, serum and urine electrophoresis, serum complement, and cryoglobulins were negative. Hepatitis B surface antibody and core antibody were positive. Histologic analysis of the skin lesion revealed leukocytoclastic vasculitis. A colonoscopy several days later revealed moderate colitis from the hepatic flexure to the rectum, with diffuse erythema and a nodular appearance. The right colon and terminal ileum were normal. There were multiple pseudopolyps and punctate ulcers in the descending colon. Random biopsies taken throughout the colon were significant for mild-moderate chronic colitis in the left colon. No granulomas or dysplasia were seen. Over the next several days, his colitis symptoms completely resolved. In addition, the cutaneous lesions over his upper extremities resolved, and his lesions over his lower extremities decreased in size, resolving completely after 2 months.

Conclusion: We present a very rare case of biopsy-proven cutaneous leukocytoclastic vasculitis following an acute flare of Crohn's colitis. This lends further support to the possible important role of circulating immune complexes theorized to be important in inflammatory bowel disease and cutaneous vasculitis.


Ian Wall, DO*, Nison Badalov, MD, Neli Farazmand, RPAC, Muhammad Abdullah, MD, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD, MPH, Pratap Gadangi, MD. Department of Medicine Division of Gastroenterology, Maimonides Medical Center, Brooklyn, NY, Department of Surgery, Coney Island Hospital, Brooklyn, NY.

Purpose: INTRODUCTION: Superficial angiomyxomas (SA) are rare, benign, cutaneous tumors that occur mostly on the trunk, head and neck, or lower limb. We report the first case of a superficial angiomyxoma presenting as an ano-rectal polyp. A 51 year old man presented for screening colonoscopy. A full colonoscopy was performed to the cecum. A polypoid mass was noted on retroflexion arising in the region of the anorectal junction (Fig. 1). An MRI revealed only distal rectal wall thickening. The patient underwent transanal excision of a 1.5 x 2 cm pigmented mass located in the anterior quadrant of the rectum at the level of the dentate line. The mass was excised with a 1 cm circumferential margin and the defect was repaired using an endorectal mucosal flap. Histological evaluation was consistent with a superficial angiomyxoma with a lack of nuclear atypia or mitoses (Fig. 2). Immunohistochemical staining was focally positive for CD34 and negative for S 100, SMA, Desmin, and Fli-1. Postoperatively the patient recovered well. Superficial angiomyxoma (SA) have been reported to occur in the scrotum, buttocks and perineum but have never been described to occur intra-luminally in the rectum. Presumably the stratified squamous epithelium of the dentate line provided the tissue source for this SA lesion. SA consist of nodular mucoid tumors interspersed with small to medium sized vessels and a moderate inflammatory cell infiltrate, specifically neutrophils. Immunohistochemical staining of these lesions are variable, limiting their diagnostic usefulness. SA can occur as a part of a complex described by Carny that consists of spotty pigmentation, myxomas, and endocrine dysfunction. Clinically SA present as painless slow growing cutaneous lesions. The lesions are benign with no reported instances of metastatic disease. SA range in size from 0.5 to 14 cms. Age at presentation is between 20 and 40 years old. They have a high local reoccurrence rate of 33%. Our patient had a follow up examination at four months that revealed no gross lesion and biopsies revealed only granulation tissue. In summary we present the first reported case of a superficial angiomyxoma presenting as an intra-luminal rectal polyp. Superficial angiomyxoma should be added to the differential diagnosis of rectal polyps.


Eileen Wang, BA*, Nirmal Kaur, MD, Richard Saad, MD. University of Michigan Medical Center, Ann Arbor, MI.

Purpose: Anisakiasis is a gastrointestinal infection caused by the Anisakis larvae, a nematode found in undercooked seafood. Although fewer than 10 cases are diagnosed annually in the U.S., the incidence is expected to rise due to the increase in raw fish consumption. There have been few reported cases of duodenal anisakiasis and its complications.

Methods: NA

Results: Case: A 25-year-old previously healthy man presented with 4 days of severe epigastric pain of acute onset 48 hours after eating squid. Physical exam only revealed epigastric tenderness. Laboratory studies were remarkable for a leukocytosis of 11.2 x 10.sup.3 cells/[mu]L, eosinophilia of 7.1%, AST 118 units/L, ALT 124 units/L, alkaline phosphatase 177 units/L, total bilirubin 1.6 mg/dL, serum amylase 120 units/L, and serum lipase 112 units/L. Abdominal CT scan and right upper quadrant ultrasound were unremarkable. Upper endoscopy revealed a 1 cm worm in the second portion of the duodenum. This was extracted with biopsy forceps and morphologically identified as Anisakis simplex. Albendazole therapy was initiated to ensure eradication. Two days later, his pain was resolving and laboratory abnormalities were normalizing.

Conclusion: Clinical presentation of anisakiasis can be variable, including symptoms of abdominal pain, nausea, vomiting, and diarrhea. Patients may develop low-grade fever with mild to moderate leukocytosis. The range of peripheral eosinophilia varies widely. Acute anisakiasis can be overlooked and has been misdiagnosed as acute appendicitis, Crohn's disease, peptic ulcer disease, and gastric cancer. For gastroduodenal anisakiasis, endoscopy continues to be diagnostic and potentially therapeutic. Endoscopic removal results in quicker relief of symptoms and is thought to prevent an allergic reaction and the formation of eosinophilic granulomas. The Anisakis larvae may invade the gastrointestinal wall to the level of the muscularis mucosae and cause edema, eosinophilic infiltration, and a granulomatous reaction. For our patient, the rise in hepatopancreatic enzymes suggests transient extrahepatic biliary obstruction caused by edema at the Sphincter of Oddi from mucosal damage by the Anisakis larvae. Discovery of the Anisakis larva in the second portion of the duodenum and relatively rapid resolution of the laboratory abnormalities help support this hypothesis.


Jonathan Ricker, DO*, Leon Kundrotas, MD. Gastroenterology, Wilford Hall Medical Center, San Antonio, TX.

Purpose: Gastrointestinal Stromal Tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract.

Methods: In 1996 before the advent of c-kit testing, a 71 year old male underwent upper endoscopy. Incidentally, a 1.5-cm submucosal lesion was discovered. The patient was followed annually and 2 years from the inital discovery, the lesion transformed into an ulcerated polypoid lesion. Surgically removed, it was found to be a GIST. On surveillance endoscopy, there was no recurrence, however a large hepatic mass was found on radiographic studies.

Results: GISTs can behave in a wide variety of ways, from completely benign to grossly malignant.

Conclusion: As the behavior of these tumors has yet to be completely understood, they will continue to be the subject of research.


Deepthi Bollineni, MD*, Ujwal Thapa, MD, Vijay Arya, MD, Afaf Abdu, MD, Prem Misra, MD. Department of Pathology, Department of Gastroenterology, Wyckoff Heights Medical Center, Brooklyn, NY.

Purpose: Colon carcinoma usually metastasizes initially to regional lymphatics and later through the bloodstream. Hematogenous metastasis usually includes the liver, lungs and brain. Cutaneous metastasis from abdominal malignancies occurs in less than 5% of the cases. Those arising from adenocarcinomas of the colon and rectum occur in less than 4% of the cases and usually herald widespread disease and a poor prognosis. Here we are presenting a case of subcutaneous metastasis with h/o adenocarcinoma colon with no other distant metastasis. 51 year old african american male h/o colon carcinoma (well differentiated adenocarcinoma, 25 cm obstructing polypoid lesion) s/p sigmoid resection 5 months ago with ongoing chemotherapy (5 Fluorouracil and Leucovorin) every week was admitted for painless mass in the lower abdomen for 2 days. Patient was asymptomatic except for well defined non tender non mobile hard mass that did not change with head elevation or on coughing and straining with no signs of inflammation on palpation. No hepatosplenomegaly or ascitis. All labs including Hb were normal except for carcinoembryonic antigen 30.4 mg/ml. CT of head and chest were normal. CT of abdomen and pelvis showed no metastatic foci in the present admission. Excisional biopsy of the abdominal mass (4.5 cm x 4 cm) showed fibroadipose tissue with metastatic adenocarcinoma favor colon primary. Fascia remained intact and no mesh was required. Development of subcutaneous metastasis from colon cancer is an extremely rare event, usually occurring in the abdomen in the setting of diffusely disseminated disease and commonly carrying a dismal prognosis. In the absence of liver involvement skin metastasis is very uncommon like in this case. Several mechanisms of cutaneous metastasis have proposed including direct extension, hematogenous spread, lymphatic spread along ligaments of embryonic origin and implantation of exfoliated tumor cells. The most common site of cutaneous metastasis from colon cancer is the abdomen. Occurrence in previous scars after tumor resection has been described in 0.6 percent of patients experiencing a recurrence, with only 0.2 percent being diagnosed clinically. We believe that our case is very uncommon in the setting of subcutaneous metastasis after definitive treatment of the primary carcinoma in a short period of time without an underlying distant metastasis. (Images and Microscopy pictures will be provided)


Shannon Chang*, Lisa Casey, MD, Virendra Joshi, MD. Gastroenterology, Tulane University Health Sciences Center, New Orleans, LA.

Purpose: The incidence of pancreatitis in patients with HIV is 35 to 800 times higher than in the general population. Lymphoma involving the pancreas is rare and constitutes only 0.16-0.2% of pancreatic malignancies. Pancreatic involvement with neoplasia in HIV patients is usually silent or subclinical until associated with disseminated disease. We report a rare case of pancreatic Burkitt's lymphoma presenting as symptomatic pancreatitis, diagnosed by endoscopic ultrasound (EUS) and fine-needle aspiration (FNA) before evident on CT scan.

Methods: N/A.

Results: A 34 year old woman with HIV presented with several days of abdominal pain located in the epigastrium and left upper quadrant. The patient denied any nausea, vomiting, or change in bowel movements. She had been admitted in the past with similar episodes. Her current medications included Atripla, iron sulfate, and Bactrim. She denied use of alcohol, tobacco, or illicit drugs. On physical exam, the abdomen was tender to palpation in the epigastrium and left upper quadrant without rebound. Laboratory evaluation was notable for a white blood cell count of 7.3 10.sup.∧3/[mu]L, hemoglobin of 8.4 gm/dL, amylase of 458 U/L, and lipase 1172 U/L. CT showed an enlarged, low-density pancreas consistent with interstitial pancreatitis. No intraadbominal lymphadenopathy was noted. EGD showed thickened gastric mucosa with enlarged rugae and antral nodularity. EUS showed a diffuse, hypoechoic mass (4.3 x 4.5 cm) in the pancreatic head and diffuse hypoechoic architecture of body and tail suggestive of an infiltrative process or interstitial pancreatitis. FNA of the pancreatic mass showed acini with scattered large, atypical lymphocytes with cytoplasmic vacuoles suspicious for a lymphoproliferative process. Immunostains for CMV, HSV, EBV and fungi were negative. A gastric biopsy of the thickened mucosa showed diffuse infiltrate of large cells in the submucosa with no infiltration into the epithelial lining. The pathology was consistent with large B-cell non-Hodgkins lymphoma. FISH was positive for t(8; 14)(q24; q32), which is diagnostic of Burkitt's lymphoma. One month after this diagnosis, CT showed lymphadenopathy in the axilla and the mediastinum.

Conclusion: We report an unusual scenario of recurrent acute pancreatitis as an initial manifestation of Burkitt's lymphoma involving pancreas in an HIV patient. Clinicians need to maintain an increased index of suspicion for a lymphoproliferative process involving the pancreas in HIV patients with recurrent acute pancreatitis. We propose EUS/FNA as a first line diagnostic modality for evaluating recurrent acute pancreatitis in the HIV population. Delay in early accurate diagnosis may lead to high mortality.


Jay Luther, MD*, Alexander Faje, MD, Richard Saad, MD, William Chey, MD. Internal Medicine, University of Michigan Health Systems, Ann Arbor, MI.

Purpose: Sclerosing mesenteritis is a rare inflammatory disorder most commonly affecting the small bowel mesentery. It is generally an idiopathic disorder with variable clinical outcomes. We report a patient with extensive sclerosing mesenteritis secondary to anaplastic lymphoma leading to a fatal outcome. Methods: A 29 year old woman presented with a six month history of diffuse abdominal cramping, jaundice, worsening appetite, and significant weight loss. An exhaustive work-up, including EGD, colonoscopy, bone marrow biopsy, rheumatologic and autoimmune panel, was unremarkable. MRI imaging revealed extensive periduodenal and peripancreatic inflammation as well as portal vein thrombus. Samples obtained from exploratory laparatomy revealed nonspecific inflammatory and fibrotic changes. The patient was eventually transferred to a tertiary care center for further management. Results: After a careful review of her outside records, radiological studies and biopsy specimens, a presumptive diagnosis of sclerosing mesenteritis was made. The patient was initiated on oral steroid treatment with no clear improvement in symptomatology. During the course of hospitalization, the patient developed bacteremia requiring cessation of steroid treatments. Her symptoms progressed rather acutely with fibrotic compression of her vasculature and resultant lactic acidosis and respiratory failure, ultimately leading to death. Autopsy revealed multiple intra-abdominal adhesions involving the visceral organs and peritoneum. A remarkable amount of fibrotic tissue encased the first part of the duodenum as it entered the retroperitoneum, the pancreas, portal vein, and bile duct. Additionally, there was also peri-aortic fibrosis extending from the level of the renal arteries to the bifurcation of the iliac vessels, causing obstruction of bilateral renal vessels, ureters, superior and inferior mesenteric arteries, and inferior vena cava. This extensive fibrosis was eventually identified as secondary to anaplastic lymphoma. Conclusions: This report graphically illustrates that intra-abdominal lymphoma can present in a manner that is clinically identical to sclerosing mesenteritis. Our case suffered a rapidly progressive course with a fatal outcome. These observations emphasize the importance of clinician's awareness of this unusual association.


Bingru Xie, MD, PhD.*, John Sotiriadis, MD, PhD., Kunal Grover, MD, Mark Sterling, MD, Weizheng Wang, MD. Department of Medicine, Division of Gastroenterology and Hepatology, UMDNJ - New Jersey Medical School, Newark, NJ.

Purpose: Henoch-Schonlein purpura (HSP) is a systemic vasculitis characterized by immune complex deposition, usually in the skin and kidney, rarely in the gastrointestinal (GI) tract. It occurs mainly in young children. While the triad of purpura, arthritis, and abdominal pain is the classic presentation of HSP, the manifestation of GI involvement in adults is less defined.

Methods: We report a rare case of massive GI bleeding and diffuse bowel wall thickening caused by mesenteric small vessel vasculitis due to HSP post-MRSA infection.

Results: Patient is a 24 year old male with a medical history of multiple left arm MRSA-abscesses in the past. The patient now presents with severe left lower quadrant abdominal pain, hematemesis, and melena. Computed tomography of the abdomen and pelvis revealed diffuse small bowel wall thickening. Subsequent esophagogastroduodenoscopy (EGD) and push enteroscopy showed acute gastritis and "punched-out" ulcers in the proximal jejunum. The patient developed a diffuse palpable, pruritic, coalescing rash throughout his bilateral lower extremities 6 days after the initial symptoms. Skin biopsy of the rash showed vasculitis consistent with HSP. Plasmapheresis and immunosuppressive therapy with oral prednisone were begun. However, the patient developed recurrent hematemesis and melena. Repeat EGD showed an ulcerated esophageal mucosa with severe inflammation; biopsy demonstrated a neutrophilic vasculitis. Small bowel biopsy showed granulation tissue with a neutrophilic vasculitis with fibrinoid necrosis. The patient was kept on bowel rest with parenteral nutrition and given intravenous methylprednisolone. The hospital course was complicated by alveolar hemorrhage and acute renal failure likely from HSP vasculitis, requiring intubation and hemodialysis. Subsequent kidney biopsy showed vasculitis with acute post infectious glomerular nephritis. Eventually, the patient improved clinically with the resolution of the rash and improvement of pulmonary and renal function to baseline. The patient was tapered off steroids, tolerated oral feeds and was finally discharged home on hospital day 21.

Conclusion: HSP vasculitis with diffuse GI involvement causing massive GI bleeding is rare, but carries a high mortality. This case presentation is that of adult onset HSP developed after MRSA infection in a patient that presented with massive GI bleeding prior to the appearance of typical palpable purpura In an era when MRSA is omnipresent, it should be considered as an important risk factor for developing HSP. Furthermore, early endoscopic intervention and biopsies are vital to diagnosing this rare entity in order to initiate early systemic steroid therapy, especially when the GI hemorrhage is the only initial presentation.


Jason Wilson, MD*, Mark Delegge, MD, FACG. Gastroenterology, Medical University of South Carolina, Charleston, SC.

Purpose: Self-expanding metal stents (SEMS) have been designed to be removed endoscopically. These stents have increasingly been used to treat benign disease, particularly esophageal perforation. The ideal type of stent and the ideal duration of placement for this indication are unknown. We report two cases in which a total of three Alimaxx-E[trademark] (Alveolus, Inc) stents were placed to treat post-dilation esophageal perforations. All three stents fragmented during attempted endoscopic removal.

Methods: Case 1: An 84 year old female presented with dysphagia after radiation treatments (XRT) for breast cancer. At endoscopy an esophageal stricture was seen and dilated with a Savory dilator. The dilation was complicated by a 2 cm mid-esophageal perforation. A covered self-expanding Nitinol stent (Alimaxx-E[trademark], Alveolus, Inc) that is designed for endoscopic removal was placed. The patient initially did well but 12 months later presented with dysphagia and a 20 lb weight loss due to esophageal stenosis around the proximal end of the stent. The stenosis was dilated and stent removal was attempted. The manufacturer guidelines for removal were followed; the purse string was grasped and pulled. The proximal end fragmented and broke away. A rigid endoscope and forceps were used to separate and remove the stent in a piecemeal fashion, and after 4 hours the entire stent was successfully removed. Case 2: A 71 year old male presented with dysphagia after XRT for head and neck cancer. An esophageal stricture developed and was dilated with a Savory dilator, and this was complicated by a 5 cm mid-esophageal perforation. Two Alimaxx-E stents were placed to completely cover the perforation. After 3 months stent removal was attempted. Endoscopic forceps were used to grasp the purse string, and again the proximal end fragmented and broke away. The stent was eventually removed piecemeal using an endoscope and forceps. The second stent was grasped by the purse string and removal resulted in it breaking into two halves. The first half was easily removed, but the second half could not be pulled proximally. The esophagus was accessed through a pre-existing gastrostomy and the stent remnant was pulled into the stomach. The distal end was then grasped with a snare and removed through the mouth. After 5 hours both stents were successfully removed.

Results: It is unclear why all three of these stents fragmented. Gastric acid may have played a role. The manufacturer recommendations were carefully followed. Multiple in vivo studies in humans have demonstrated that Nitinol implants in other body locations do not corrode, even after twelve months.

Conclusion: Based on our experience we recommend caution when placing SEMS for benign esophageal disease.


Kunal Grover, MD*, Bingru Xie, MD, PhD, Weizheng Wang, MD. Department of Medicine, Division of Gastroenterology and Hepatology, UMDNJ - New Jersey Medical School, Newark, NJ.

Purpose: Ischemic gastric necrosis (IGN) is a rare clinical entity with an unknown incidence. Etiologies include atherosclerosis, embolism, infection, corrosive burns, and idiopathic. Most reported cases have had advanced necrosis and required surgical treatment.

Methods: We report a case of epigastric pain and upper GI bleeding caused by IGN due to alcohol ingestion which was managed conservatively.

Results: A 43 year old male with a past medical history of AIDS, hypertension, and chronic alcohol abuse presents to the emergency department with epigastric pain and hematemesis for 1 day. The patient admitted to drinking 10 beers and a 1/3 pint of vodka the previous day. He denied use of any illicit substances or medications for 3 weeks. He had a heart rate of 122, however his blood pressure remained stable. Abdominal examination revealed epigastric tenderness to light and deep palpation, however no rebound or guarding. Laboratory evaluation noted normal basic chemistry, amylase, lipase, coagulation and hepatic panels. The hemoglobin was 9.0 g/dL, platelet count was 53,000 and white blood cell count was 1,900. The patient was started on pantoprazole and octreotide intravenous drips and emergent upper esophagogastroduodenoscopy (EGD) was done. EGD found candida esophagitis and a small Mallory-Weiss tear. Biopsies were obtained from the stomach as the mucosa was noted to be diffusely edematous, erythematous, and friable. Post procedure the patient was placed on IV fluconazole and continued on the pantoprazole drip. Serial blood counts showed a drop in the hemoglobin. Four units of packed red blood cells were transfused with an appropriate response in hemoglobin and vital signs. The patient was started on a clear liquid diet the following day. There were no further episodes of hematemesis and no further transfusions were required. Repeat EGD was done 72 hours after admission noted decreased gastric edema and friability. Pantoprazole drip was changed to twice a day oral dosing and the diet was advanced. Pathology showed ischemic mucosal necrosis of the stomach. There were no viral inclusion bodies, H. pylori or vasculitis noted. The patient was subsequently discharged with planned follow up.

Conclusion: IGN has been scarcely reported in the literature. To our knowledge, this is the first reported case of alcohol induced IGN. EGD and biopsy confirmation are important to help guide therapy. Treatment should include acid suppression with proton pump inhibitor, aggressive hydration and blood transfusion to prevent further ischemia and necrosis. Repeat EGD is warranted to evaluate the severity and response to conservative treatment, and to determine the need for surgical intervention.


Carlos Romero, MD, MS*, Eduardo Gonzalez, MD, Michelle Rivera, MD, Pablo Costas, MD. Department of Medicine, University of Puerto Rico, San Juan, PR.

Purpose: 55-year-old woman with history of mitral valve replacement on chronic anticoagulation presented with recurrent episodes of melena and anemia since 2003. Extensive workup including a capsule endoscopy failed to reveal the source of bleeding. In mid-2004, a right hemicolectomy was performed after angiography suggested the presence of angiodysplasia in ascending colon. Despite this intervention, she persisted with episodic obscure gastrointestinal bleeding. In early 2008, she was transferred to our institution after presenting with hematochezia. Physical examination on admission revealed hypotension, conjunctival pallor and port-wine stools. Lab workup revealed hemoglobin of 3.8 and over anticoagulation (INR 7.5). After successful resuscitation and reversal of anticoagulation; upper endoscopy, push enteroscopy and colonoscopy failed to identify the source of bleeding. An angiography done at recurrent bleeding identified a possible source of bleeding in the jejunum. An intra-operative enteroscopy revealed a 3-cm mass at the proximal ileum with an associated clot. The lesion was excised and identified histologically as a gastrointestinal stromal tumor (GIST). Patient has done well post-operatively and was able to restart anticoagulation successfully without further gastrointestinal bleeding. The median time for the diagnosis of obscure gastrointestinal bleeding is approximately 2 years. These patients usually undergo repetitive diagnostic test, multiple transfusion and hospitalizations before diagnosis. This patient underwent a capsule endoscopy with no suggestive lesion identified. The final diagnosis was done with intraoperative enteroscopy. Gastrointestinal bleeding is the most common presentation of GISTs. Overt bleeding from over anticoagulation was life threatening in our patient. Intraoperative enteroscopy is a viable option for diagnosis of these lesions with this kind of presentation.


Paul Benson, MD*, Nathan Shores, MD, Joel Bruggen, MD, John Long, MD. Internal Medicine, Wake Forest University, Winston-Salem, NC.

Purpose: Laparoscopic Heller myotomy is an effective surgical therapy for idiopathic achalasia. Unfortunately 5-10% of patients develop recurrent dysphagia or chest pain in the early postoperative period. The most common cause for recurrence is an incomplete myotomy, in which the muscle fibers at the distal end of the myotomy are not completely released. Proper recognition of an incomplete myotomy is poorly described in the literature and the best approach to therapy is unclear.

Methods: A 63 yo female with diabetes and hypertension who presented with dysphagia to solids and liquids and a 40 pound weight loss was diagnosed with achalasia on barium esophogram and manometry. The manometry showed a hypertensive lower esophageal sphincter (LES), incomplete LES relaxation, and aperistalsis with low-amplitude, simultaneous contractions after all wet swallows. She underwent a laparoscopic Heller myotomy with Dor fundoplication which was initially successful. However, she returned one year later with recurrent dysphagia, chest pain and weight loss.

Results: Evaluation with esophogram and endoscopy showed a focal distal stenosis lacking the appearance of a peptic or fibrotic stricture (see Figure). Repeat manometry showed an isolated high-pressure zone (HPZ) with failure of relaxation within the proximal margin of the LES. This HPZ was consistent with intact residual LES fibers from an incomplete myotomy. Thus, pneumatic dilation (PD) was chosen as the therapeutic approach instead of a repeat surgery. The dilation was performed with a 3 cm balloon and was successful - at follow-up 1 and 4 months later she reported resolution of dysphagia and chest pain and had a weight gain of 8 pounds.

Conclusion: This case nicely illustrates what might be observed in a patient with achalasia and recurrent symptoms due to an incomplete myotomy. A focal residual HPZ at the proximal end of the LES was observed on endoscopy, radiology, and manometry. Our case is interesting in that the residual HPZ was located at the proximal rather than distal margin of the LES. The use of PD following incomplete myotomy has been reported in the literature with success rates as high as 80 percent. More studies are needed to improve recognition of an incomplete myotomy and to develop criteria for the selection of patients who would benefit most from PD after failed myotomy.


Amir Agha, MD*, Joseph McKinley, MD, Patrick Brady, MD, Jay Mamel, MD. Department of Gastroenterology, Internal Medicine, University of South Florida, Tampa, FL.

Purpose: A 32 year old male with no significant past medical history presented with a 3 day history of dyspnea, left-sided pleuritic chest pain and 2 weeks of melena. He denied abdominal pain, nausea, vomiting, cough, fevers and hemoptysis. He was on no medications and did not have a family history of GI malignancies. Physical exam revealed prominent sinus tachycardia with a rate in the 120s and significant conjunctival pallor. Initial laboratory studies revealed a hemoglobin of 4.9, mcv 72, hematocrit of 14%, and platelets of 550,000. Initial CXR revealed multiple nodules throughout both lung fields. After volume resuscitation an EGD was performed but was non diagnostic. Capsule endoscopy identified the bleeding source in the proximal jejunum within an area of ulceration and stenosis. Push enteroscopy exposed two large, 2-4 cm ulcerated mass lesions 40 cm distal to the pylorus. Multiple biopsies were obtained and pathological analysis was consistent with metastatic choriocarcinoma. CT scans of the head, chest, abdomen, and pelvis revealed multiple metastatic lesions within the brain, lungs, liver, spleen and bilateral kidneys. The patient was started on aggressive chemotherapy and in the immediate follow up period the patient has done well and has had no recurrence of GI bleeding. Capsule endoscopy has rapidly emerged as an effective, non-invasive modality for detecting obscure GI bleeding. A recent study revealed that capsule endoscopy was able to detect small bowel pathology in 82% of patients with GI bleeding of unknown etiology with prior negative results for colonoscopy, EGD, small bowel series, and even angiography. Specifically, it was able to accurately identify small bowel angiodysplasias, polyps, carcinoid tumors, Crohn's disease and metastatic melanomas. Its potential use for early recognition of small bowel tumors is of the utmost importance. As seen in this case, caspsule endoscopy was able to detect a case of previously undiagnosed metastatic germ cell tumor. Only 5% of germ cell tumors (usually embryonal and choriocarcinoma) involve the GI tract. Jejunal involvement is exceedingly rare as around 95% of cases are found within the duodenum. The majority of cases are metastatic upon initial diagnosis and thus confer a relatively poor prognosis. The major complications include intestinal obstruction, bleeding and perforation.


Pramod Joseph, MD*, Mohamad Erfani, MD, Trikante Rajapaksa, MD, Nejat Kiyici, MD, Hilary Hertan, MD. Our Lady of Mercy Medical Center, Bronx, NY.

Purpose: A 67-year-old man presented to the hospital with anemia, abdominal pain and constipation. The clinical examination was unremarkable, except for minimally guaic positive stool. Initial colonoscopy showed a 3 mm lesion at the splenic flexure. Biopsy showed invasive carcinoma with moderately differentiated gland like structures, unlikely to be a primary colonic adenocarcinoma. Immunohistochemical stains were done that were CK7, CK17 positive and CK 20 negative, suggesting a pancreatobiliary or lung primary lesion. Subsequently the patient had a chest CT which revealed a right upper lobe lung mass. He had no evidence of significant lesions elsewhere. The bronchial biopsy revealed an undifferentiated large cell carcinoma of the lung. The patient underwent chemotherapy. Follow-up colonoscopy,9 months later, was normal. Repeat chest CT showed an increase in the size of the lung mass with a new liver lesion. Metastatic lesions to the colon are rare and can pose diagnostic and management difficulties. The malignancies known to cause secondaries in the colon are stomach, breast, ovary, cervix, kidney, lung, bladder, prostate, and melanoma. The usual presentation is with multiple metastatic deposits, but can present as solitary lesion. Colonic metastases from lung cancer may present clinically or as a finding at colonoscopy. Clinically they present with symptoms of colonic obstruction, lower gastrointestinal bleed (occult or massive), weight loss, anemia, bowel perforation, or gastrointestinal fistula. The usual presentation is after the diagnosis of the primary lesion, but can occur synchronously or before the diagnosis of the primary, as in our patient. The lung cancer with intestinal metastasis has been reported to have poor prognosis. The treatment modalities depend on the nature of presentation and extent of the disease. The colonic lesions complicated by obstruction, bleeding, or perforation has to be treated before the assessment of the lung lesion. Depending on the extent of the disease, the treatment options are a 'curative resection', palliative procedure (resection or stoma), or chemotherapy. The 'curative resection' (resection of the colonic and lung lesions), in selected patients, is reported to have survival advantage. Bronchogenic carcinoma rarely causes synchronous or metachronous metastases in the colon. In those cases, the treatment options are a 'curative resection', palliative procedure, or chemotherapy, depending on the extent and differentiation of the tumor. In selected cases, the 'curative resection' has survival advantage.


Jitendrakumar Patel, MD*, Julio Ventura, MD, Avani Patel, MD. Internal Medicine, Jamaica Hospital Medical Center, Jamaica, NY.

Purpose: The uterine leiomyosarcoma (LMS) is a rare sarcoma arising from the smooth muscle cells found within the myometrium. Smooth muscle is found in most hollow organs and the walls of blood vessels, but LMS most commonly occur in the uterus and gastrointestinal tract. Uterine LMS represent 25-35% of uterine sarcomas and 1% of all uterine malignancies. We present a case of LMS metastasis to the duodenum, which is very rare.

Methods: A 46 y/o Guyanese female was admitted with complaints of weakness, palpitation, dizziness and black stool for 2 weeks. The patient also reported wight lost of about 10 lb after she started passing dark stool. The patient had a significant past surgical history of hysterectomy 3 years prior secondary to uterine leiomyosarcoma, as well as hypertension. She had a family history of diabetes, hypertension and breast cancer on her maternal side.

Results: On physical examination, a cachexic appearance with pale mucosal membrane observed. Abdomen was soft, non-tender, non-distended without evidence of hepatosplenomegaly. A healed surgical scar noted on lower abdomen. Examinations of rest of the systems were normal. Stool guaiac was positive. Laboratory evaluation revealed microcytic anemia. Serum chemistry and liver function tests were normal. Since patient had history of dark stools, a gastroscopy was conducted, which revealed small hiatus hernia and ulcerated mass in the bulb immediately after the pylorus, in the first part of the duodenum. Biopsy was taken and sent for histopathology, which showed atypical spindle cells that were consistent with old biopsy of uterus. Diagnosis of metastatic leiomyosarcoma into the duodenum was made and patient referred to the hemato-oncologist for further therapy.

Conclusion: Diagnosis of uterine LMS carries a poor prognosis due to the high rate of recurrence and metastases. The common sites of metastases of uterine LMS are the lungs, kidney, and liver. LMS can develop anywhere along the gastrointestinal tract, including the stomach, rectum and large and small intestines. Around fifty percent of intestinal LMS cases present in the ileum, the lowest part of the small intestine. Upon review of the literature, this case represents only the third other published report of uterine LMS metastasis to the duodenum.


Martin Moehlen, MD, MPH*, Fredric Regenstein, MD, FACG. Section of Gastroenterology and Hepatology, Internal Medicine, Tulane University School of Medicine, New Orleans, LA.

Purpose: Introduction: Sickle cell hepatopathy is used as a general term to describe liver dysfunction occurring in the sickle cell patient. We describe a patient with hemoglobin SS who presented with fulminant liver failure, successfully treated with plasma exchange.

Methods: Case Report: A 35-year-old woman with a history of SS sickle cell anemia was transferred to our facility with worsening liver failure. Ten days prior to transfer, she was admitted to an outside hospital in sickle cell crisis. While undergoing treatment for her sickle crisis, she developed worsening liver dysfunction and a severe coagulopathy, associated with hepatic encephalopathy. She was transferred for further evaluation and to be considered for possible liver transplantation. She denied a previous history of liver disease. On admission to our facility the patient was somnolent with marked asterixis (Stage 3 hepatic encephalopathy). She was deeply jaundiced with an enlarged, tender liver. Admission labs included: WBC 31,300/mm3, hemoglobin 7.8 g/dl, platelets 250,000/mm3, LDH 524 IU, total bilirubin 52.1 mg/dl, ALT 232 IU, AST 498 IU, PT INR 17.7 (see Table). Urine toxicology was positive for cocaine and negative for acetaminophen. Anti-HCV, HBsAg, anti-HBc IgM, and anti-HAV, IgM were negative. Abdominal ultrasound with Duplex Doppler revealed hepatomegaly, no ascites, normal flow in the portal and hepatic veins.

Results: The patient was admitted to the ICU and treated for hepatic encephalopathy; she was not considered to be a transplant candidate. Exchange transfusion was initiated on hospital day 2 and continued for 4 days. Over the next few days her bilirubin and creatinine continued to rise, while the ALT, AST, PT, and level of encephalopathy improved. She was discharged home on day 12.

Conclusion: Discussion: Our patient presented with fulminant hepatic failure associated with severe sickle cell intrahepatic cholestasis. While concomitant cocaine ingestion may have contributed to the severity of her liver injury, the pattern of injury and clinical course were not consistent with cocaine hepatoxicity. Her dramatic response to exchange transfusion reinforces the success of this treatment in patients with intrahepatic cholestatic sickle cell hepatopathy, including those presenting with fulminant hepatic failure. These patients can be treated in a general medical facility capable of performing exchange transfusions, and are rarely, if ever, liver transplant candidates. Thus, initiation of exchange transfusion should not be delayed while attempting to transfer these patients to liver transplant centers.


Neetu Mahendraker, MD*, Mohammad Siddiqui, MD, MPH, Jyothi Reddy, MD, FACG. Internal Medicine, University Of Illinois at Urbana-Champaign, Urbana, IL.

Purpose: Malignant melanoma of the gastrointestinal mucosa in the absence of cutaneous lesions is very rare. We report an unusual case of primary malignant melanoma of the duodenal mucosa. A 38-year-old diabetic male presented with nausea, bilious vomiting and severe, colicky, epigastric pain for 3 days associated with worsening jaundice for 7 days. Proton pump inhibitors were started 3 months earlier for "heart burn". Review of systems was positive for decreased appetite. Rest of the history was non contributory. Physical exam revealed stable vitals; scleral icterus and epigastric tenderness. Initial laboratory work up was significant for elevated total bilirubin, transaminases and alkaline phosphatase suggestive of obstructive jaundice. Computed Tomography scan of abdomen with contrast showed hepatic hilar lymphadenopathy and biliary obstruction. Endoscopic Retrograde Cholangiopancreatogram revealed ulcerated proximal duodenal mass with common bile duct (CBD) stricture. Pathology confirmed duodenal malignant melanoma with involvement of CBD. Comprehensive physical exam to rule out any cutaneous or retinal melanoma was negative. Extensive imaging with whole body positron emission tomography and magnetic resonance imaging of the brain did not reveal any other foci. Despite being on chemotherapy and radiotherapy patient rapidly deteriorated with extensive metastasis and expired within 8 months of diagnosis. This case illustrates that a high index of suspicion is warranted to diagnose mucosal malignant melanoma in a timely manner which can originate in esoteric locations and progress rapidly with significant mortality.


Lakshminarayan Sooraj T K, MD, MPH*, Melchor Demetria, MD, Bashar Attar, MD PhD. Division of Gastroenterology and Hepatology, Cook County-John H. Stroger Jr. Hospital, Rush University, Chicago, IL.

Purpose: NA

Methods: Introduction: Fibrovascular polyps are exceedingly rare benign esophageal polyps with only about 110 cases of mostly giant fibrovascular polyps reported. We present a case of a small esophageal fibrovascular polyp. Case presentation: A 51-year-old African American referred for EGD for melena showed a smooth, cylindrical pedunculated polyp measuring about 2 x 1 cm with overlying normal esophageal mucosa emanating from the upper esophageal sphincter, resembling a fibrovascular polyp (Fig. 1). Biopsies obtained from the polyp are awaited. On review of records a chest CT scan and ENT evaluations done for globus sensation failed to reveal the upper esophageal polyps, which could have caused his symptoms. Discussion: Fibrovascular polyps are rare benign esophageal intraluminal pedunculated tumors with a 0.03% incidence. While small polyps are hard to diagnose, large polyps can be up to 20 cm in length. Irrespective of polyp size and extent, the peduncle almost always originates from the upper esophagus. While dysphagia is the commonest symptom, the most spectacular presentation is polyp regurgitation into the mouth. Polyp tip may ulcerate and bleed, and very rarely large polyps cause laryngeal obstruction and asphyxia. Diagnosis is usually by EGD or barium swallow, but up to a third of cases go undiagnosed. Very large tumors can be mistaken for intramural tumors, but EGD findings of a peduncle in the upper esophagus and the normal overlying esophageal mucosa helps avoid potential misdiagnosis and over treatment. Histologically the polyps are most commonly fibrovascular, with fibroma, lipoma and fibrolipoma being less common. Treatment for polyps larger than 2 cm, or symptomatic polyps is endoscopic, transcervical or tranthoracic excision. Small, asymptomatic polyps can be conservatively managed. Conclusion: In summary, fibrovascular polyps, though rare, should be considered in cases of unexplained dysphagia, and a thorough endoscopic examination must be made during scope withdrawal to avoid missing small upper esophagus lesions.

Results: NA

Conclusion: NA


Travis Rutland, MD*, Lee Thompson, MD, Jorge Herrera, MD. Department of Surgery, Division of Gastroenterology, University of South Alabama, Mobile, AL.

Purpose: When patients present with several symptoms including extraintestinal problems, a unitary diagnosis is occasionally possible. A 28 year-old white female reported one year of diarrhea with more than 10 watery bowel movements daily. There was mild bilateral lower quadrant abdominal pain without associated or alleviating factors. During the preceding two months, she lost 10 pounds. She denied dysentery, hematochezia, fever, chills or laxative use. She had been receiving potassium supplements for chronic hypokalemia and had several episodes of generalized weakness, followed by "paralysis" that had required hospitalization for the treatment of profound hypokalemia. The evaluation included negative results for stool cultures, stool Clostridium difficile toxin, amoeba serology, sedimentation rate, C reactive peptide level, thyroid stimulating hormone level, serum gastrin level, calcitonin level, tissue transglutaminase IgA, serum protein electrophoresis with quantitative immunoglobulins, urine laxative screen, and complete blood cell count. Metabolic panel was remarkable for serum potassium level of 1.8 and a serum bicarbonate level of 20 in the face of a non-anion gap metabolic acidosis. Colonoscopy with terminal ileum intubation showed no mucosal lesions and random biopsies were normal mucosa. CT scan with thin cuts through the pancreas revealed a 7.3 x 6.9 cm mass in the tail of the pancreas. Vasoactive intestinal peptide level was elevated at 1055 pg/mL. Diarrhea and hypokalemia-associated symptoms abated on octreotide. She underwent a laparoscopic subtotal pancreatectomy, splenectomy and lymph node resection. Light microscopy of the pancreatic mass demonstrated a well-differentiated pancreatic endocrine neoplasm with no extension through the tumor capsule. Associated lymph nodes were negative for malignancy. Immunohistochemical analysis had positive staining for anti-cytokeratin (CAM 5.2), neuron-specific enolase (NSE), and synaptophysin (SYP) in the tumor cells, consistent with a neuroendocrine tumor of the pancreas. This case demonstrates the importance of considering pancreatic neuroendocrine tumors in patients presenting with watery diarrhea and periodic hypokalemia-associated paralysis.





Steve Kucera, MD*, Joseph McKinley, MD, Patrick Brady, MD, FACG, FAGA, H. Worth Boyce, MD, MACG, FACP. University of South Florida, Tampa, FL.

Purpose: 66 yr male with a medical history of ESRD, DM, and PVD requiring femoral-popliteal bypass surgery was admitted with bilateral lower extremity claudication. The diagnostic work-up revealed failure of the bypass grafts; the patient subsequently required bilateral above the knee amputations. His operative course was remarkable for sustained periods of hypotension. On post-op day 3, the patient had multiple episodes of melena with an acute drop in hemoglobin of 2 g without abdominal pain. An upper endoscopy was performed. Esophageal necrosis was present circumferentially immediately below the circopharyngeus and extended to the GEJ (photographs 1 and 2). The remainder of the endoscopy was normal; acute esophageal necrosis was presumed to be the etiology of the bleed. Biopsies revealed necrotic debris with acute inflammatory leukocytic infiltration. The patient was treated conservatively with high dose proton-pump inhibitor therapy and maximization of cardiac output. He recovered without complication. Acute esophageal necrosis, or black esophagus, is a rare endoscopic finding, with only a handful of cases described in the world literature. The incidence has been reported to be 0.0125% to 0.2%, with a predominance of the cases involving men mean age 65. The proposed pathophysiology involves ischemia in a majority of cases; massive gastroesophageal reflux, infection, and caustic ingestion have also been implicated. Associated risk factors have included atherosclerotic vascular disease, diabetes, end stage renal disease, and recent surgery - all of which were common to the patient presented. Treatment is largely supportive with bowel rest, high dose PPI therapy, and optimization of cardiac perfusion. Despite supportive care, mortality rates approach 32%.


Christian Clark, MD*, David Holloman, MD, Robert Stuart, MD, John Lazarchick, MD, David Lewin, MD, Lawrence Comerford, MD. Department of Pathology, Department of Medicine, Medical University of South Carolina, Charleston, SC.

Purpose: Aleukemic monocytic leukemia (extramedullary monocytic tumor) is a rare malignancy that involves immature granulocytes and/or monocytes forming a mass in a location other than medullary bone. This is the first known report of this neoplasm involving the gastrointestinal tract from the stomach to the colon.

Methods: A 54-year old female developed acute diarrhea, abdominal cramping weight loss and was found to have clostridium difficile colitis at her local hospital. She was treated with metronidazole but her symptoms returned. She underwent a colonoscopy with biopsy at her local hospital and was diagnosed with ulcerative colitis. She was treated with prednisone and her symptoms markedly improved. Unfortunately her symptoms recurred upon tapering of the steroids. She was transferred to our institution where an upper endoscopy showed diffuse edema, erythema, and ulceration in the stomach with erythema and edema in the duodenum. Colonoscopy showed pan colitis with erythema, edema, and small shallow ulcerations that also involved the terminal ileum. The mucosa of the upper GI tract and lower GI tract appeared endoscopically similar. Biopsies of the stomach, duodedum, terminal ileum, and colon all showed lymphocytic infiltration with stains showing no clonal populations. The duodenal biopsies showed some villous blunting. Prometheus Celiac serology and stool cultures were negative. She developed a dry cough and CT scan of the chest, abdomen and pelvis revealed small lymphadenopathy, mesenteric vessel engorgement, and lower lobe pulmonary nodules. CT-guided pulmonary nodule biopsy showed fibrosis, non-caseating granumola, and pronounced lymphocytic infiltration. Azathioprine was started and she eventually had clinical improvement in her symptoms. Repeat upper endoscopy however showed worsening gastritis with large 1-2 cm nodules throughout her stomach. Pathology review of gastric, duodenal and colon biopsies showed worsening infiltration by atypical hematolymphoid cells shown to stain positively for CD43 and KP1. Bone marrow biopsy was completed with resulting lymphocytic predominance, non-caseating granuloma. She was diagnosed with aleukemic monocytic neoplasm. Her condition deteriorated rapidly and she died prior to being offered chemotherapy.

Results: N/A

Conclusion: Aleukemic monocytic leukemia is an extremely rare condition during which leukemic cells invade tissue prior to appearance in the bone marrow or peripheral blood. This appears to be the sentinel case of gastrointestinal involvement from the stomach to the colon. Given the rarity of this disorder, treatment has been empirical: radiation to affected tissues and systemic chemotherapy. The prognosis is quite poor.


Carlos Romero, MD*, Eduardo Gonzalez, MD, Victor Carlo, MD. Gastroenterology, University of Puerto Rico, San Juan, PR.

Purpose: 58 year-old women with history of diabetes mellitus and high blood pressure presented to our clinics with complaints of intermittent dysphagia to solids for four years. She states that since 5 months ago, these episodes have become more frequent, usually occurring less than one second after swallowing with associated regurgitation of intact meals. There was no history of odynophagia, heartburn, vomiting, retrosternal chest pain or weight loss. She denied smoking or alcohol abuse. Physical examination revealed a protuberant mandible and puffy hands. No halithosis or signs of malnourishment were present. A barium swallow showed a stricture of the esophagus at the level of the aortic knob. A subsequent upper endoscopy revealed no mucosal lesion supporting an extraluminal etiology of dysphagia. A right aberrant subclavian artery causing thoracic esophagus compression was identified by CT scan. A diagnosis of acromegaly was entertained by the presence of an elevated insulin-like growth hormone levels and physical exam findings. Further imaging studies identified a pituitary mass and patient is on scheduled for transphenoidal resection. Dysphagia lusoria is a rare disorder in adults. The worsening of dysphagia in this patient led to a diagnosis of acromegaly. Oropharyngeal dysphagia in patients with acromegaly secondary to macroglossia has been previously described. To our knowledge, dysphagia lusoria associated to acromegaly has not been previously reported.


Tiffany Zellman, MD*, Atulkumar Patel, MD, FACP, FACG. Gastroenterology, Internal Medicine, William Beaumont Hospital, Royal Oak, MI.

Purpose: Introduction: Colorectal cancer (CRC) is the second leading cause of cancer-related death in the Western world. Abscess formation occurs in only 0.3-0.4% of colorectal cancer cases. As an initial presenting symptom, it is even more uncommon. This can make early diagnosis challenging. We describe a patient who presented with an abdominal abscess, presumed to have ruptured appendicitis, and at surgery found to have CRC at the site of the abscess. Case Description: A 58 year old white male presented with a one-week history of intermittent, cramping periumbilical abdominal pain with radiation to the right lower quadrant. It was associated with decreased appetite and fever. He later admitted he had suffered a bout of severe right lower quadrant pain several months prior for which he did not seek medical treatment. CT scan of the abdomen and pelvis showed a right lower quadrant abscess, as well as thickening of the wall of the terminal ileum and cecum, suggestive of a perforated appendix. He was placed on parenteral antibiotics and underwent CT-guided drainage of the abscess. During his stay, he remained afebrile. His oral intake and abdominal pain improved. The drain was removed and he was discharged on oral antibiotics. A repeat CT scan one month later showed a mass in the right lower quadrant above the cecum. Colonoscopy was performed, which revealed a large ascending colonic mass. Biopsy was consistent with invasive adenocarcinoma. Subsequently, he underwent right colectomy, followed by chemotherapy. Discussion: Because of the variability in presentation, CRC has been called one of the "great imitators" and can mimic almost any other abdominal disease. Abscess formation as an initial presentation of CRC is exceedingly rare. When this occurs, the patient often presents with atypical findings, making it difficult to accurately diagnose and distinguish it from other disease entities. Delay in diagnosis can significantly affect patient morbidity and mortality. Conclusion: Clinicians should be cognizant that colorectal cancer and abscess formation can occur concomitantly. Colorectal cancer should be considered in the differential diagnosis of a patient who presents with an unexplained abdominal abscess.


Mahmoud Lajin, MD*, Atulkumar Patel, MD, FACP, FACG, Rajul Parikh, MD. Hematology Oncology, Gastroenterology, William Beaumont Hospital, RoyalOak, MI.

Purpose: Introduction: Of the various clinical manifestations of Strongyloides Stercoralis, duodinitis with Mesenteric vein thrombosis has not been reported. We present a case of Strongyloides duodinitis and MV thrombosis, Which was discovered in the work up of unexplained pain, eosinophilia and elevated IgE. Case: A 68 year old female presented with a 2 week history of progressive diffuse abdominal pain. Her past medical history included eosinophilia diagnosed 5 years prior to admission, hypertension, osteoporosis and diverticulosis. There was no history of atopy. She had no allergies. Her medications included Mavik and Premarin. She had never used corticosteroids. She was born in Hungary and emigrated to USA 26 years ago, since then she lived in Michigan with no further travel. She had no risk factors for HIV. Her family history was negative for a clotting disorder. On physical exam her vitals were stable, she had no wheezing, cardiac exam was normal. Her abdominal exam revealed mild diffuse tenderness. Her laboratories showed hypereosinophilia (1200 eosinophils per ml) and a total IgE level of 7200 IU/ml. A CT of the abdomen showed sigmoid diverticulitis, R. sided colitis and MV thrombosis. She was treated with antibiotics and anticoagulation, and a hypercoagulable workup was negative. Stool for occult blood was positive. A follow up CT showed resolution of the diverticulitis and the thrombosis; however she continued to complain of pain. she underwent an upper and lower endoscopy. Biopsies showed intense eosinophilic infiltration, and S. Stercoralis was identified in the duodenal biopsy. Subsequently, serum Strongyloides IgG antibody was positive. Stool studies for parasites were negative. She was treated with Ivermectin, and remains completely asymptomatic. Discussion: This case was unusual in that there was no travel history since she emigrated 26 years ago, and additionally the MV thrombosis was an unexpected finding. It is postulated that she acquired the parasite several decades ago from her native country. Although she had risk factors for thrombosis (her hormonal treatment and diverticulitis). It is unknown if Strongyloides had contributed to the pathogenesis of thrombosis. More importantly, the timely diagnosis of this infection prevented initiating corticosteroids for symptomatic "Idiopathic eosinophilic enteropathy" which could have been fatal. It was fortuitous that the parasite was actually identified in the biopsy. Conclusion: A new possible association of S. Stercoralis duodinitis and Mesenteric vein thrombosis is described. Clinicians should consider S. Stercoralis when evaluating hypereosinophilia of unknown etiology, and consider serologic testing, especially prior to starting corticosteroids.


Peter Pico, MD*, Mohamed Hassan, MD, Bilal Hameed, MD. Gastroenterology and Internal Medicine, University of Minnesota, Minneapolis, MN.

Purpose: Psyllium is one of the most commonly used fiber supplements worldwide. There have been case reports of esophageal and intestinal bezoars mass obstruction from psyllium use. A 60 year old male with no history of dysphagia presented with a globus sensation few minutes after taking his daily psyllium supplement. He was unable to swallow solids or liquids. Endoscopy revealed a material bonded to the surface just distal to the oropharynx continuous to the gastro esophageal junction. The material had glue like gelatinous appearance, circumferentially adherent to the underlying mucosa. The lumen of the esophagus remained patent with no mass obstruction. The patient had immediate resolution of symptoms after the procedure. At follow-up endoscopy, there was complete passage of material. Exam revealed a normal mucosa without strictures, rings or abnormalities of peristalsis. Psyllium and Plantago Ovata. In 1986, the FDA recommended dividing doses of psyllium supplements and addended their report in 2007, listing intestinal obstruction as a side effect of granular forms of psyllium. This modification, however, specifically states that this listing does not apply to psyllium powder. This patient illustrates the first published case report of obstruction by coating of the esophagus from the powdered form of psyllium. Physicians should be aware of psyllium use in patients presenting with obstruction.


Ravi Kurella, MD*, Madhavi Rudraraju, MD, Ravindranauth Sawh, MD, Stan Lightfoot, MD, Syed Rizvi, MD, Richard Harty, MD. Primary Care, VA Medical Center, Oklahoma City, OK, Pathology, Department of gastroenterology, OUHSC, Oklahoma City, OK.

Purpose: Intestinal spirochetosis is a rare and difficult to diagnose disease since it presents with non specific symptoms common to several other diseases. It is usually seen in immunocompromised patients. The most common symptoms reported include watery diarrhea, abdominal pain, altered bowel movements and on occasion rectal bleeding. Colonoscopy and biopsy is the only definite way of diagnosis of this disease. Case Report: We present a case of intestinal spirochetosis in an immunocompetent patient who presented with watery diarrhea. 59 year old male presented to primary care physician with intermittent diarrhea for 4 months time. He also reported rectal bleeding on occasion. Symptoms became worse on eating spicy and greasy foods. He denied any loss of appetite or weight. His other medical problems included gastro esophageal reflux disease and hypertension, both were controlled on medications. Patient was subjected to colonoscopy for diagnostic purposes. On colonoscopy, colon mucosa was found to be normal and routine random biopsies were performed. Histopathology revealed intestinal spirochetes which were found at the brush border of the epithelium. He was treated with metronidazole for a period of 14 days. He became asymptomatic after treatment. A follow up sigmoidoscopy performed 3 months later showed no evidence of spirochetes in the biopsy specimens. Conclusion: Intestinal spirochetosis is a rare cause of watery diarrhea in a immunocompetent patient and should be considered in the differential diagnosis of chronic intermittent diarrhea. Differential diagnosis includes colon cancer, Zollinger-Ellison syndrome, gastric ulcers, infective colitis and irritable bowel syndrome. Colonoscopy and biopsy of the intestinal tissue and staining with Warthin-Starry stain is the gold standard in diagnosis of this disease. Metronidazole for 14 days is the drug of choice for eradication of the disease. Prognosis is favorable with treatment.


Anita Bhushan, MD*, Patrick Kamath, MD. Gastroenterology and Hepatology, Mayo Clinic Rochester, Rochester, MN.

Purpose: Ischemic hepatitis refers to diffuse hepatic injury which results from imbalance between hepatic oxygen supply and demand. Patients with OSA have recurrent episodes of respiratory airflow obstruction secondary to upper airway collapse during sleep. Ischemic hepatitis may, therefore, occur secondary to severe arterial hypoxemia as a result of OSA. We report a case of a patient with class III obesity with acute liver injury secondary to OSA induced hypoxemia.

Methods: A 53 year old Caucasian male with class III obesity and history of OSA was admitted with lower extremity cellulitis. The patient was afebrile, hemodynamically stable with oxygen saturation of 87% on room air. Laboratory studies were significant for elevated liver transaminases with AST 1020, ALT 2202. Total bilirubin was 0.9, direct bilirubin 0.4 and alkaline phosphatase was within normal limits. History did not suggest viral, autoimmune or drug-induced hepatitis. Autoimmune markers and serologies for hepatitis A, B and C were negative. There was no clinical evidence of cardiac failure.

Results: Echocardiogram showed normal left and right systolic function. Right heart catheterization revealed normal pulmonary artery and wedge pressures. Hepatic portal vein gradient was normal. A transjugular liver biopsy was performed. Histopathology showed zone 3 hepatocellular necrosis, and mildly active steatohepatitis without fibrosis. Nocturnal pulse oximetry showed multiple and profound desaturations. The cumulative time spent at saturation <85% was 87%. The patient was started on CPAP and supplemental oxygen to maintain optimal saturation during sleep. Liver enzymes improved over the next few days and eventually completely normalized. On a 3 month follow-up, the patient continues to use CPAP machine with significant improvement in nocturnal pulse oximetry. He has been enrolled in a weight reduction program and is undergoing evaluation for bariatric surgery.

Conclusion: Ischemic hepatitis is a rare manifestation of OSA secondary to severe arterial hypoxemia. This entity should be considered in the differential diagnosis of ischemic liver injury. Institution of correct management strategies and prevention of complications of OSA can result in prevention of a potentially fatal acute liver injury.


Steve Egwuonwu, MD*, Marc Zuckerman, MD, FACG. Gastroenterology, Internal Medicine, Texas Tech University Health Science Center, Elpaso, TX.

Purpose: To describe a case of cytomegalovirus induced colitis, complicated by gastrointestinal bleeding and pancreatitis in a patient with AIDS.

Methods: Cytomegalovirus is a member of the herpesviridae subfamily.

Results: A 51 year old male recently diagnosed with AIDS presents with 3 week history of bloody diarrhea, vomitting, chills and abdominal pain. He was not on any medications for HIV at this time. His abdomen was soft, diffusely tender with diminished bowel sounds. CBC revealed a Hgb of 8% and serum lipase was 806. His CD4 count was 35. An abdominopelvic CT showed increased size of pancreas with peripancreatic fat stranding. Patient was placed on NPO and fluid resuscitation. Stool for C. difficile, ova and parasite came back negative. Three days later he had several episodes of hematochezia and continued with abdominal pain. Patient was transfused with 2 units of PRBC and colonoscopy followed by an EGD was done. Colonoscopy revealed congested mucosa and frank blood in the Sigmoid, descending, transverse and ascending colon. EGD showed blood in the duodenum. Biopsy findings include a positive CMV immunostain, chronic colitis and focal ulcerations in the ascending colon, ileocaecal valve and rectum. Duodenal biopsy was also positive for CMV immunostain and revealed extensive duodenal ulcerations. He was started on Valgancyclovir for CMV infection. Patients abdominal pain and hematochezia resolved. Patient went home on Valgancyclovir and has been stable since discharge.

Conclusion: In AIDS patients with gastrointestinal manifestations, opportunistic infections like cytomegalovirus should be part of the differential.


Elisabeth Kramer, BS*, Homayoon Mahjoob, MD, John Carroll, MD. Medicine, Georgetown University Medical Center, Washington, DC.

Purpose: Introduction: Esophageal Squamous Cell carcinomas (SCCA) and leiomyomas are felt to be readily distinguishable from each other, as they originate from different hisotolgic wall layers, and have classically different appearances on presentation. Typical esophageal SCCA's are easily diagnosed by standard endoscopy, by their obvious mucosal friability and their intraluminal mass effect. Conversely, esophageal leiomyomas originate from the deeper muscular layers of the wall, and have a classic endoscopic appearance of a submucosal appearing lesion, with smooth, intact overlying mucosa without friability. We describe two cases of esophageal SCCA that masqueraded as leiomyomas on presentation by endoscopy, EUS and cross sectional imaging. Case 1: A 61 y/o male with a 30 pack year history of smoking presented with a 3 month history of dysphagia. Chest CT revealed a smooth soft tissue mass arising from the esophagus. EGD confirmed a submucosal appearing lesion, with smooth overlying mucosa. EUS demonstrated the lesion to be a hypoechoic mass with irregular borders arising from the muscularis propria, suggestive of a leiomyoma. FNA was done into the lesion and the cytology revealed poorly differentiate SCCA. Case 2: A 75 y/o female with a history of breast cancer presented with chest tightening and a decreased appetite. EGD showed a submucosal appearing lesion in the mid-esophagus with normal overlying mucosa. EUS showed this to be a hypoechoic mass, contiguous with the muscularis propria, likely representing a leiomyoma. FNA was done into the lesion, revealing poorly differentiated SCCA. Conclusion: A hypoechoic esophageal mass arising from the muscularis propria layer on EUS is pathognomonic of a leiomyoma, and FNA into the mass may not always be done because the EUS appearance is so suggestive. We report two cases of SCCA of the esophagus, which had a very atypical growth pattern, with preservation of the mucosal layer, and extension deep into the esophageal wall muscular layer, resulting in an appearance on endoscopy, EUS and CT that mimicked a leioymoma. This suggests that even with a classic appearance on EUS of a leiomyoma, FNA may be critical to obtain an accurate cytologic diagnosis as SCCA can also present in this manner.


Elisabeth Kramer, BS*, Homayoon Mahjoob, MD, John Carroll, MD. Medicine, Georgetown University Medical Center, Washington, DC.

Purpose: Introduction: In the EUS evaluation of pancreatic masses, portions of the left and right lobes of the liver can be seen in the EUS field of view. Published case series have demonstrated that EUS guided transgastric FNA of liver lesions is safe, with a high diagnostic yield. Providing cytologic confirmation of metastatic liver disease at the time of the initial EUS can prevent the need for additional imaging studies or procedures, such as PET CT or percutaneous liver biopsies. We report a case of a pancreatic mass with a suggestion of metastatic spread to the liver, in which both lesions were confirmed to be adenocarcinoma, by simultaneous FNA of both the pancreatic mass and liver lesion, in one EUS procedure. Case Description: A 71-year-old female presented with epigastric pain radiating to the back, and unexplained weight loss. A CT scan of the abdomen showed a mass in the pancreatic neck, as well as low density liver lesions in both the right and left hepatic lobes. The patient was then sent for an EUS, which confirmed the presence of a hypoechoic density in the pancreatic neck. EUS guided FNA was done into the mass and a cytologic diagnosis was made of adenocarcinoma. During the EUS, the left hepatic lobe was visualized, revealing several localized, rounded heterogenous lesions, the largest being 1 cm. Changing to a new 22 gauge needle, FNA was then performed with three passes through the gastric wall and into the largest liver lesion, again yielding a cytologic diagnosis of adenocarcinoma. There was no evidence of bleeding following the transgastric hepatic FNA, and the patient was discharged home without incident. The findings provided cytologic confirmation of a primary pancreatic cancer with documented metastasis to the liver. Based on the proven liver lesion, the patient was deemed inoperable and referred to a pancreatic oncologist, and started treatment with Gemcitabine chemotherapy. Conclusion: Previously published case series have demonstrated that EUS guided transgastric FNA of liver lesions is safe and can be done at the same time as the initial EUS. This case report adds to our knowledge that liver lesions should be looked for during an EUS of the pancreas, and if found, can be safely sampled by transgastric FNA, precluding the need for any additional studies to verify metastatic disease.


Faisal Malik, MBBS, MD*, Syed Ali, MBBS, MD, Khursheed Haider, MBBS, MD, Ali Abrar, MBBS, MD. Internal Medicine, St. Barnabas Hospital, Bronx, NY.

Purpose: Abstract: An association of GIST with other tumor has been previously reported in literature. However, we report the first case of synchronous occurrence of GIST and bilateral papillary (RCC). 50-year old male admitted with complain of dizziness and passing black stool for last 2 weeks. Physical examination was significant for positive occult blood testing and Lab showed microcytic hypochromic anemia. Both endoscopy and colonoscopy were negative. CT abdomen showed a large mass involving the small bowel along with lesions on both kidney and questionable bone lesion in his pelvis. Barium study findings were suggestive of an intramural mass with predominantly exophytic components. Laproscopic resection of the intestinal mass reveals the tumor size of 8 cm and biopsy confirms the diagnosis of GIST. MRI of the kidney confirmed bilateral kidney lesion and biopsy of the right renal mass confirms the diagnosis of papillary renal cell carcinoma type I low grade. Discussion: GISTs are mesenchymal neoplasms of the gastrointestinal and showed association with multiple malignancies including like gastric, colorectal, hepatocellular adenocarcinoma, carcinoid, gastric lymphoma, and ampulla of vater. Four case report of unilateral papillary renal cell carcinoma synchronous with GIST has been previously reported. The association of GIST with multiple tumors necessitates the investigation of second tumor once it is diagnosed. Though rare but it should be among the differential diagnosis of bleeding per rectum when there is no evident cause.


Sayeeda Jabeen, MD*, Howard Chodash, MD. Gastroenterology, Internal Medicine, Southern Illinois University, Springfield, IL.

Purpose: A 72 year old male presented to the ER with severe RUQ pain, nausea, and vomiting of 1 day duration. Labs showed: ALP 106 U/L, AST 356 U/L, ALT 371 U/L, and total bilirubin 4.7 mg/dl, with direct bilirubin of 3.2 mg/dl. Sonogram was consistent with acute cholecystitis with dilated common hepatic duct. Patient spiked temperature of 38.3 C. Ampicillin/sulbactum was started to treat acute cholecystitis/ cholangitis. MRCP reveled choledocholithiasis. ERCP was done with stone extraction and sphincterotomy. Post ERCP pancreatitis was noted with resolution in 2 days. Liver enzymes continued to elevate with ALP 201 U/L, and total bilirubin of 6.0 mg/dl, which was initially suspected could have been either due to persistent choledocholithiasis or ductal edema secondary to ERCP. Ampicillin/sulbactum was continued. In a couple of days liver enzymes doubled with total bilirubin of 12.4 mg/dl. The patient was stable, except for worsening of jaundice and pruritis. While the other possibilities of increased liver enzymes were being investigated, ampicillin/sulbactum was stopped on day 6. Repeat MRCP showed no evidence of choledocholithiasis. HIDA scan showed no excretion of dye into the biliary ducts. All the biochemical work-up for the other probable cause of liver disease was negative. Liver biopsy revealed acute hepatic obstruction, characterized by marked canalicular cholestasis with portal duct edema and inflammation. Total bilirubin and ALP continued to elevate up to 15.2 mg/dl and 488 U/L respectively, with decreasing AST and ALT. After 3 days of stopping ampicillin/sulbactum, liver enzymes trended down satisfactorily with clinical improvement. Discussion Ampicillin/sulbactum has rarely been associated with hepatic injury. It causes hepatocanicular cholestasis which often resembles extrahepatic obstructive jaundice. This may be due to interfere with hepatocyte secretion of bile constituents, other pigments and dye substances. Withdrawal of offending drug lead to reversal of injury. To our knowledge this is the first case of ampicillin/sulbactum induced acute reversible cholestatic hepatotoxicity, in the setting of choledocholithiasis adding complexity to the diagnosis. Diagnosis was made based on negative MRCP after stone extraction, normal viral marker and antibodies, clinical and biochemical improvement after stopping the offending drug. Conclusion Ampicillin/sulbactum is a widely used antibiotic. It can cause acute reversible cholestasis. Clinician should be aware of this adverse effect. It should be highly suspected during persistent elevation of liver enzymes despite treating the primary cause. The suspected drug should be stopped while work up for other co-existing conditions is in progress.


Kiran Goli, MD*, Chandra Lingisetty, MD, Sandip Ghuge, MD, Shobhana Chaudhari, MD, Susan Williams, MD. Gastroenterology, Internal Medicine, New York Medical College/Metropolitan Hospital Center., New York, NY.

Purpose: Introduction: Double pylorus (DP) is a form of gastro duodenal fistula characterized by presence of an accessory pyloric channel between the distal stomach and duodenal bulb so that the stomach and duodenum are connected by two openings separated by a septum. Endoscopic finding of DP has been increasingly reported. There are no standard guidelines for management of DP. We report a case of acquired DP and discuss the evidence based treatment strategy. Case description: A 69 year old man with past medical history of chronic alcohol abuse was referred to gastroenterology clinic for evaluation of epigastric pain. Esophagogastroduodenoscopy (EGD) revealed mild gastritis involving entire stomach, pre-pyloric ulcer and also showed an accessory pyloric channel leading into duodenal bulb consistent with the DP. Rapid urease test was positive for H. pylori. Eradication therapy for H. pylori and anti-ulcer therapy was started. Patient improved symptomatically. A repeat EGD after 2 months demonstrated completely healed pre-pyloric ulcer, negative rapid urease test and persistence of DP. Patient remained asymptomatic and has not reported any recurrence of symptoms as of his last clinic visit. Discussion: The implications and management of persistent DP in adults is debatable. We reviewed most of the available literature in English through medline and pub med search. Congenital DP is extremely rare. Acquired type is more common and usually arises secondary to peptic ulcer disease and may be associated with H. pylori infection. The widely accepted hypothesis for its pathogenesis is that the penetration of a peptic ulcer either from the antrum or duodenal bulb leads to adhesion formation between the walls of the stomach and duodenum. Further ulceration results in the formation of an accessory pyloric channel. Recurrent ulcers in the accessory pyloric channel and occult bleeding are potential complications which usually respond to conservative management. Although malignant transformation was not reported in the fistulous tract, theoretically it is possible. Management of DP is usually conservative and good response is expected with anti ulcer therapy. Other factors which worsen PUD such as medications, alcohol, smoking, caffeine and stress need to be appropriately addressed. Spontaneous closure of accessory pyloric channel occurs infrequently even after medical therapy. Persistence of DP is usually well tolerated. About 20% of patients develop refractory symptoms and need surgical intervention. Accessory pyloric channel ulcers can be difficult to treat because of bile reflux. More studies needed to determine whether periodic surveillance endoscopy is needed in patients with persisting DP.


Sayeeda Jabeen, MD*, Syed Hashmi, MD, Stuart Torgerson, MD, Mukerji Basanti, MD. Gastroenterology, Internal Medicine, Southern Illinois University, Springfield, IL, Rheumatology, Private practice, Springfield, IL, Internal Medicine, Research, Springfield, IL.

Purpose: A 32 year old AA female with a 3 year history of SLE presented to the ER with severe abdominal pain, nausea, vomiting, diarrhea, multiple joint and muscle pain. She had been on 20 mg of prednisone bid and azathioprine (taking intermittently) 50 mg for 1 year for ongoing myositis. Her abdomen was diffusely tender. Multiple joints were swollen. A pericardial rub was present with a tachycardia of 108 bpm. She was anemic with a Hg of 10 g/dl, amylase 209 U/L, lipase 245 U/L, liver enzymes showed ALT 206 U/L, AST 545 U/L, ALP 67 U/L, total protein 7.2 g/dl, with a low albumin of 2.5 g/dl, CPK 15258 U/L, troponin 0.35 ng/ml, TGs 285 mg/dl, creatinine 1.2 mg/dl. UA showed proteinuria of 100 mg/dl with granular casts. ANA was positive at 1:320, Anti DNA-DS 240 IU/mL, anti smith 111 U/L and complements were low with C3 41 mg/dl and C4 7 mg/dl. CT and ultrasound of abdomen were normal. EKG was normal and echo showed small pericardial effusion. The patient did not use alcohol nor did she have gallstones. With SLE affecting multiple organ systems, rheumatology and GI diagnosed her to have Lupus pancreatitis along with lupus hepatitis, myositis, pericarditis, myocarditis, and glomerulonephritis. Prednisone was increased to 40 mg po bid and azathioprine started at 25 mg po bid and slowly increased to 75 mg po bid. The abdominal pain became less but did not resolve. She was then given IV solumerdol 1 gm daily for 3 days. There was a dramatic decrease in her abdominal pain, the pancreatic and liver enzymes decreased, pericardial effusion resolved and pulse normalized. She was discharged on azathioprine 75 mg po bid and prednisone 40 mg po bid. Discussion:The prevalence of SLE is 40-150 cases/100,000 population. Lupus pancreatitis is very rare with an annual incidence of 0.4-1.1/1000 lupus patients. Estimated mortality is 18-27%. Most of the data is available in case report form, 78 cases reported to date. Multiple etiological causes may exist: autoimmune pancreatitis, vasculitis, and Anti phospholipid antibody related thrombosis. In a lupus patient, who has otherwise unexplained pancreatitis, lupus pancreatitis should be highly suspected. Majority of patients respond well to high dose steroid and azathioprine. A dramatic decrease in mortality has been noted when treated with both steroids and azathioprine. Conclusion:Our case suggests that the onset of lupus pancreatitis is unrelated to the use of steroid or azathioprine. Steroid or azathioprine clearly did not exacerbate pancreatitis. Treatment with mega dose steroid and azathioprine worked very well in our patient. This suggests that the immunosuppressive effect of these drugs was critical in suppressing the overwhelming inflammation in the pancreas and other organ system.


Grace Noh, MD*, Ankit Kansagra, MD, Harmit Kalia, DO, Weizheng Wang, MD. Department of Gastroenterology, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ.

Purpose: Background: Percutaneous liver biopsy (PLB)-associated hemobilia is a rare complication, with an incidence rate of 0.06%. It results from a needle tract connection of the hepatic artery, portal vein or both to the biliary tree. 90% of cases of hemobilia present with upper gastrointestinal bleeding. Only 30-40% of cases have the Sandblom triad of biliary colic, gastrointestinal bleeding and jaundice. Hemobilia usually occurs 5 days post PLB. With a rapid rate of bleeding, acute upper gastrointestinal bleeding such as melena or hematemesis can be seen. When the rate of bleeding is slow, a clot can be formed in the biliary tree causing obstruction, acute cholecystitis or cholangitis. It is extremely rare for acute pancreatitis to occur in this setting. We report the case of a patient with pancreatitis secondary to a clot produced from a liver biopsy. Case: 43-yr-old Caucasian female initially presented with abnormal liver function tests consistent with cholestatic pattern for several months. Pathology from liver biopsy revealed primary biliary cirrhosis. One week later, patient presented with severe abdominal pain, vomiting, jaundice and melena. Physical exam was remarkable for scleral icterus and right upper quadrant tenderness. Admission labs were significant for hemoglobin of 11.7, direct bilirubin 5.6, amylase 815 and lipase 3162. Abdominal ultrasound revealed a 4.5 cm complex right hepatic lesion with dopplers demonstrating no flow within the lesion, suggestive of a hematoma. The common bile duct was dilated to 15 mm and the gallbladder contained a large amount of blood clot without wall thickening. Angiogram showed a pseudoaneurysm in a branch of the right hepatic artery. This was successfully embolized using coils with hemostasis achieved. A decision was made to wait for possible endoscopic retrograde cholangiopancreatography (ERCP) if patient's symptoms worsened; her pancreatitis resolved after 4 days. Discussion: Pancreatitis secondary to PLB associated hemobilia is a rare entity; a review of the English language literature reveals ten documented cases. We examined the diagnostic tests, mechanisms and treatment options for this disease process. There were a wide range of modalities used for diagnosis. Two recognized mechanisms include pseudoaneurysm and arteriobiliary fistula. It seems PLB with or without ultrasound guidance made no difference in the occurrence of these malformations. Super selective catheter arterial embolization led to better outcomes than those patients receiving sphincterotomy. In those patients who underwent ERCP with sphincterotomy, half of those cases were subsequently complicated by cholecystitis requiring cholecystectomy.


Chandra S Lingisetty, MD*, Smitha Kanak, MD, Kiran Goli, MD, Theodore Lenox, MD, Kyamalya Ismailova, MD, Shobhana Chaudhari, MD, FACP, Jennifer Harley, MD, Susan Williams, MD. Gastroenterology, Medicine, New York Medical College/metropolitan Hospital, New York, NY.

Purpose: Introduction: Gastrointestinal (GI) tract involvement in advanced Human Immunodeficiency Virus (HIV) disease can be due to a variety of infectious and non infectious diseases. Endoscopic finding of gastric nodular lesions are not common in patients with HIV disease. Kaposi's sarcoma (KS) and lymphoma are among the common causes of gastric nodules in patients with advanced HIV disease. Here, we present a rare and probably the first reported case of atypical gastric nodule in a patient with advanced HIV disease. Case description: A 29 year old Honduran male with HIV infection (CD 4 count 16 cells/mm3) was admitted to hospital for chief complaints of cough, intermittent fever and weight loss. Chest X-ray and CT-scan showed diffuse interstitial infiltrates highly suggestive of disseminated tuberculosis (TB) with major differential diagnosis of disseminated fungal infection. Transbronchial lung biopsy was performed to confirm the diagnosis. Patient was referred to gastroenterology service for evaluation of abdominal pain and guaiac test positive stools. Esophagogastroduodenoscopy (EGD) and colonoscopy were performed. EGD revealed normal esophagus, gastroesophageal junction and duodenal folds but showed two erythematous nodules in the body of stomach. Multiple biopsies were taken. Colonoscopy was unremarkable. Although, the initial suspicion was gastric KS, the histopathology examination of both gastric tissue and lung tissue showed typical spherules and granulomas characteristic of Coccidioides immitis. A final diagnosis of disseminated coccidioidomycosis was made. Discussion: Disseminated coccidioidomycosis commonly involves the skin, lungs, joints, soft tissue and meninges. Coccidioidomycosis involving GI tract is extremely rare, either in disseminated disease or in an isolated form. We reviewed most of the available medical literature in English through medline and pub med search. A single case involving small bowel was reported, but the involvement of stomach has not been reported. Cryptococcus, histoplasma and mycobacterium infections can manifest as gastric nodules particularly in immunocompromised patients. Sporadic cases of gastric syphilis, gastric leishmaniasis and cytomegalovirus (CMV) associated pseudo tumors were reported. Non infectious causes of gastric nodules include lymphoid hyperplasia, gastric lymphomas, MALT lymphomas, gastric malignancy, KS, gastric carcinoids, gastric glomus tumour, gastric lipoma and gastric leiomyoma. Conclusion: We conclude that gastric coccidioidomycosis can occur as a part of disseminated infection in patients with advanced HIV disease, and search for more data and evidence is needed to establish its significance in GI symptoms and signs.


Sayeeda Jabeen, MD*, Mei Huang, MD, Syed Hashmi, MD. Gastroenterology, Internal Medicine, Southern Illinois University, Springfield, IL, Internal Medicine, Research, Springfield, IL.

Purpose: The clock begins 0 Hours:An 18 year old female on oral contraceptive pills for 3 months presented with severe generalized abdominal pain, nausea, vomiting and mild dyspnea of 1 week duration. On examination, abdomen was diffusely tender and mildly distended. Initial labs: WBC 10.8 k/cmm, AST 58 U/L, ALT 51 U/L, ALP 130 U/L, Platelets 238 k/ cmm, INR 1.5, Lactic acid 7 mmol/L. 17 Hours:Patient was transferred to a tertiary care center for possible mesenteric ischemia. Labs: WBC 20 k/cmm, AST 77 U/L, ALT 90 U/L, Lactic Acid 16 mmol/L, Bicarbonate 7 mmol/L. CT and ultrasound of the abdomen showed hepatic vein thrombosis. The patient was clinically deteriorating. At this point, given the diagnostic dilemma between acute mesenteric ischemia and BCS, an exploratory laparotomy was done to rule out necrotic bowel; instead laparotomy revealed uniformly firm and enlarged liver with moderate ascites and healthy looking bowel. At this point, finding on CT scan as well as the clinical picture was suggestive of Acute Budd-Chiari Syndrome. Transplant center was contacted. 23 Hours: Labs: AST 6880 U/L, ALT 4444 U/L, Platelets 58 k/cmm, ALP 123 U/L, INR 4.3, total bilirubin 1.7 mg/dl. 35 Hours:TIPS was done for decompression. 47 Hours:Patient transferred to transplant center. LFTs were further elevated with moderate encephalopathy. Patient was found to be heterozygous for factor V Leiden. 71 Hours: Patient underwent liver transplant. Explant specimen showed massive infarction consistent with hepatic veno-occlusive disease. Patient was started on immunosuppressants and anticoagulation. The patient recovered satisfactorily. Discussion Budd-Chiari Syndrome is a rare but potentially life threatening disorder caused by hepatic venous outflow obstruction resulting in congestive liver failure. Hypercoagable states are major etiological factors. BCS can present as acute and fulminant (20%), sub-acute (40%), or chronic (40%). Acute form usually presents with abdominal pain, nausea, vomiting, mild jaundice, intractable ascites, elevated serum AST/ALT (>5 times normal). On contrary, our patient presented with normal liver enzymes and severe lactic acidosis. In such cases, a high index of clinical suspicion is required to make the diagnosis, despite normal liver enzymes. Diagnosis can be confirmed by ultrasound, CT scan, MRI or hepatic venography. Treatment involves anticoagulation, thrombolytic therapy, TIPS, stents and liver transplant. Our case highlights the unusual presentation of acute BCS, rapidity of progression and importance of appropriate diagnosis and treatment. Delaying diagnosis can be catastrophic. We emphasize, the fact early diagnosis and effective treatment in such fulminant cases can be life saving.


Chandra S Lingisetty, MD*, Kiran Goli, MD, Sandip Ghuge, MD, Shobhana Chaudhari, MD, FACP, Susan Williams, MD. Gastroenterology, Medicine, New York Medical College/Metropolitan Hospital, New York, NY.

Purpose: Introduction: Drug Induced Liver Injury (DILI) is caused by a variety of medications and dietary supplements including Chinese herbs. Although Chinese traditional complementary and alternative medicines are a leading cause of DILI in Asian countries, it is increasingly reported in western countries. Numerous case reports of DILI with a variety of herbal products were reported, however DILI with vine essence pills has not been reported. We present a case of DILI with vine essence pills and we propose the causal association as per Roussel Uclaf Causality Assessment Method (RUCAM) score. Case description: A 57 year-old obese female (BMI > 50) with past medical history of osteoarthritis and obstructive sleep apnea was hospitalized with 1 week history of fatigue, myalgias, subjective fever and lethargy. Patient denied recent travel, alcohol intake or use of recreational drugs. Physical examination was remarkable for asterixis and tenderness in the right upper quadrant of the abdomen. Laboratory tests revealed normal blood counts with unusual elevation of transaminases with AST 4040 IU/L, ALT 2220 IU/L, ALKP 122 IU/L, total bilirubin 2.36 mg/dl, direct bilirubin 0.80 mg/dl, and albumin 3.7 gm/dl. Coagulation profile showed elevated PT with INR 2.61. Further work up for hepatitis with iron studies, serum ceruloplasmin, and serologic tests for autoimmune and viral hepatitis (including Epstein-Barr virus, cytomegalovirus and herpes simplex virus) were negative. Abdominal imaging was normal. On further questioning, patient admitted to taking Vine Essence pills, a popular Chinese herbal medication for arthritis. Patient took 2 pills three times daily for 2 months, but she increased the frequency two weeks prior to admission. Patient dramatically improved with supportive treatment. Liver enzymes on 6th day of admission showed AST of 42 IU/L and ALT of 363 IU/L which were normalized within 2 weeks of presentation. The semi-qualitative RUCAM score indicated that a diagnosis of herbal medication induced liver injury was 'probable' with a Score of 7. Discussion: Vine Essence pills were incriminated in our patient by the temporal relationship between the hepatitis onset and clinical response to drug withdrawal, together with the exclusion of any other known hepatotoxic factors. A meticulously calculated RUCAM score strongly supported the diagnosis in our case. Conclusion: More studies and toxicology analyses are needed to establish whether the hepatotoxicity of Vine Essence is due to its ingredients or impurities in the preparation. Physicians should be aware of DILI associated with herbal remedies and a routine inquiry about their use should be made at every patient-physician interaction.


Mukul Arya, MD*, Siddharth Mathur, MD, Niket Sonpal, MD, Yashpal Arya, MD. Wyckoff Heights Medical Center, Brooklyn, NY.

Purpose: Sigmoid volvulus is the most-common form volvulus of the gastrointestinal tract and is responsible for 8% of all intestinal obstructions. Sigmoid volvulus is particularly common in elderly persons and constipated patients; one study of 40 patients showed an average age of 71.6 years. Sigmoidoscopic decompression is advocated, although the rate of recurrence is high, varying between 45 and 90%, and is associated with the need for emergency surgery and a higher mortality. Sigmoidopexy has been shown in the literature to reduce the recurrence of symptoms in up to 75% with one site of adherence; however we advocate two points of fixation on the abdominal wall to effectively reduce the risk of recurrent volvulus as demonstrated by the following case.

Methods: An 84 year old female with a PMH significant for atrial fibrillation, hemiplegia due to prior CVA, peripheral vascular disease, and recurrent sigmoid volvulus presented to the ER with complaints of vague abdominal pain, difficulty moving her bowels, and bloating for the past 3 days. The patient denied any nausea, vomiting or diarrhea, and her routine lab values were within normal limits. Physical exam was remarkable only for distension, with positive bowel sounds and generalized tenderness. Abdominal radiographs were consistent with sigmoid volvulus; however the patient refused surgery and thus was scheduled for proctosigmoidoscopy with placement of 2 percutaneous endoscopic colostomy tubes (PEC). Endoscopic examination revealed a focally dilated segment of sigmoid colon extending 20-45 cm which represented the volvulized segment. Two 20 Fr standard PEG tubes were placed in the sigmoid colon via push technique approximately 10 cm apart. The colon aspects of the tubes were then irrigated with betadine; no immediate complications were noted.

Results: The patient was then discharged and was followed up 2 months later at which time the PEC tubes were removed. APC ablation of the stoma was performed from the colonic aspect prior to endoclip closure. No further episodes of sigmoid volvulus have recurred to date.

Conclusion: In conclusion, we believe the two point fixation method may be superior to single tube placement as has been previously reported. Our case once again establishes endoscopic percutaneous colostomy tube placement as a alternative to surgical therapy in patients with recurrent sigmoid volvulus. We recommend randomized clinical trials to compare the two methods.


Suwebatu Odunsi, MD, MMS*, Patrick Kamath, MD. Mayo Clinic Rochester, Rochester, MN.

Purpose: A 65 year old white male with a history of a heart transplant and tricuspid valve replacement presented with an acute onset of abdominal pain and distention a few hours after taking his first dose of lisinopril.

Methods: He denied any fevers, chills, vomiting, diarrhea or constipation. He had no sick contacts or recent travel. He was on immunosuppression and was recently started on lisinopril. He had pain for three days before presenting to the ER. Physical examination revealed no facial edema, a mildly tender and distended abdomen with shifting dullness and bulging flanks. Laboratory examination was unremarkable with the exception of a serum creatinine of 3 and potassium of 5.8. CT scan showed mesenteric congestion, moderate ascites and multiple dilated loops of small bowel.

Results: An ultrasound revealed a normal liver, patent portal and hepatic vessels. A paracentesis provided some symptomatic relief. The total protein in the ascitic fluid was 4. Colonoscopy showed edema of the terminal ileum and biopsies showed no evidence of lymphoma. C1 esterase inhibitor, C3 and C4 were within normal limits. Based on the temporal association of these symptoms with the use of lisinopril, a diagnosis of ACEI induced intestinal angioedema was made. The lisinopril was discontinued and the patient's signs and symptoms improved over a few days. He was discharged and has had no further complaints on subsequent visits.

Conclusion: Peripheral angioedema is a known side effect of ACEI therapy. ACEI peripheral angioedema has a higher prevalence (1% to 4.8%) in patients with cardiac and renal transplant versus 0.2% in the general population. There have been about 20 case reports of visceral angioedema, but only one has been reported in solid organ (liver) transplant patient. The cause for an increased susceptibility to angioedema in patients who have received solid organ transplants is still unclear but immunosuppression has been postulated as a cause. Recognition of this entity is critical in the diagnosis and management in the appropriate patient. The early recognition can save patients unnecessary procedures and surgery.


Sonia Garg, BS*, Samir Shah, MD, Anthony Mega, MD, Edward Feller, MD. Alpert Medical School of Brown University, Providence, RI, Hematology/Oncology, Division of Gastroenterology, Brown University, Providence, RI.

Purpose: Introduction: Renal cell carcinoma (RCC) is a rare cause of gastrointestinal (GI) bleeding. Similarly, GI bleeding is an unusual complication of this common tumor. We report a patient with RCC and hemodynamically significant GI bleeding due to multiple small bowel metastases. This case report illustrates the importance of diligent intestinal investigation for metastatic disease associated with a serious complication. Case Report: A 63 year old man with known metastatic RCC to the brain and lungs presented with tarry stools and weakness for one week. He also reported increased fatigue and dyspnea on exertion. He denied abdominal complaints. On exam, he was alert and oriented. Blood pressure (sitting) = 135/75 and heart rate = 75 bpm. His abdomen was non-tender with no palpable masses or organomegaly. A rectal exam showed black, tarry stool positive for occult blood. Hemoglobin (Hb) level = 12.1 g/dL, compared to a baseline of 14.0 g/dL. UGI endoscopy revealed a 5 mm periampullary, fleshy excrescence without active bleeding. Biopsy indicated duodenitis with a focus of clear cell carcinoma consistent with the patient's primary tumor. His condition and Hb stabilized; further evaluation was scheduled as an outpatient. Over 1-2 weeks he had persistent fatigue and occult blood positive stools. Vital signs showed postural changes and his Hb dropped to 10.1 g/dL. He was admitted and transfused. Colonscopy with terminal ileum intubation did not demonstrate a potential bleeding site. Small bowel enteroscopy to 160 cm revealed two additional small, fleshy masses at 135 and 105 cm. Biopsies showed poorly differentiated neoplastic cells in the lamina propria. Immunohistochemistry studies were compatible with metastatic RCC. Discussion: GI bleeding due to RCC is most commonly metastatic, but unusually can be due to peritoneal dissemination or direct invasion from a contiguous tumor. The spectrum of GI bleeding include occult blood loss, iron deficiency anemia, hematemesis, melena, and hematochezia. In addition, isolated case reports document GI bleeding as the initial manifestation of subsequently diagnosed RCC. Our patient is unusual because he had multiple, poorly accessible small bowel lesions with a potentially misleading UGI endoscopy. Clinician awareness of the diagnostic difficulties and potential for RCC to metastasize with hemodynamically significant bleeding is important for appropriate resuscitation, evaluation and treatment.


Vinod Kurupath, MD,*, Khurshid Mazumdar, MD, Mahesh Krishnaiah, MD, Sury Anand, MD. Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY.

Purpose: Cytomegalovirus (CMV) infection of the gastrointestinal tract used to be a common and serious complication of the Acquired Immunodeficiency Syndrome. This incidence has decreased substantially since effective therapy has been used in recent years (1). CMV infection of the small bowel accounts for 4% of all CMV infections of the GI tract. CMV enteritis manifests clinically by generalized abdominal pain and diarrhea. Rare reports of ileal perforation secondary to CMV have been reported. We report this unusual presentation of multiple ileal ulcers and massive hemorrhage while on effective anti viral therapy.

Methods: case report A forty one year old male with multi drug resistant HIV/AIDS presented with elevated liver enzymes andhemoccult positive stools. He had a history of CMV colitis and retinitis and was on maintenance ganciclovir and foscarnet with good clinical remission. During the hospital course, he developed massive hematochezia with hemodynamic instability and a steepdrop in the hematocrit. The bleeding was recurrent and massive with significant requirements for transfusion.

Results: Colonoscopy showed blood clots but no evidence of colitis. Terminal ileal intubation showed large punched out ulcers. Biopsies of the ulcers showed findings typical of CMV infection with cytomegalic cells and intracytoplasmic inclusions. A nuclear tagged bleeding scan confirmed the source of bleeding to be from the terminal ileum. During surgery, intraoperative enteroscopy showed punched out ulcers involving 70 cm of the distal ileum. The rest of the small bowel was normal. Biopsies again showed findings typical of CMV infection with cytomegalic cells and intracytoplasmic inclusions. The patient underwent distal ileal resection and was discharged uneventfully.

Conclusion: CMV infections of the GI tract occur in the setting of advanced immunosupression, with CD4 counts less than 50 (4). Gastrointestinal sites of CMV involvement are usually the esophagus and colon with infections of the small bowel accounting for less than 5% of the cases. This case report presents an unusual case with no evidence of CMV colitis but with deep ulcers of the terminal ileum causing severe bleeding and requiring surgery. This patient was on optimal maintenance therapy with Gancyclovir and Foscarnet. Review of the literature has no reported case of isolated ileal CMV infection, who while on effective therapy, had massive bleeding requiring surgical treatment.


Son Nguyen, MD*, David Victor, MD, Stephen Abshire, MD. Internal Medicine, Tulane University, New Orleans, LA.

Purpose: Gastrointestinal involvement of disseminated histoplasmosis is an emerging disease. Signs and symptoms mimic inflammatory bowel disease and malignancy in both immunosuppressed and immunocompetent patients, often leading to misdiagnosis and unnecessary therapies. We report a rare case of rectal histoplasmosis in an immunocompetent patient. Case Report: An 86 year old gentleman from South Louisiana with multiple chronic, but stable, medical problems presented with altered mental status, fatigue and generalized weakness. CT scan and MRI of the brain showed multiple brainstem lesions that were suggestive of metastatic disease and further imaging revealed hepatic and pulmonary lesions. In addition to having hemoccult positive stools and iron deficiency anemia, the patient also had a history of colonic polyps found on colonoscopy performed 5 years prior. The patient denied abdominal pain but endorsed constipation. A repeat colonoscopy was performed to attempt to establish a definitive diagnosis. Findings include a large 4-cm exophytic lesion covering about one-third of the circumference of the wall of the rectum, with multiple necrotic satellite lesions noted in the rectosigmoid colon. Initial gross pathologic impression was primary rectal carcinoma with the satellites respresenting either nodal metastases or possibly a second primary malignancy. However, separate biopsies of the rectal and satellite lesions were obtained for histological and pathological analysis, and the results were consistent with infection by Histoplasmosis capsulatum. The patient was started on a long-term course of an antifungal regimen, and had marked clinical improvements of his initial presenting symptoms. Repeat MRI of the brain demonstrated significant improvement of prior lesions. Furthermore, repeat flexible sigmoidoscopy at 6 months showed near resolution of the satellite lesions with marked diminution in the size of the previous rectal lesion. Discussion: In disseminated histoplasmosis, the gastrointestinal tract, predominately the terminal ileum and colon, is involved 50% of the time. Rectal involvement is atypical and reported cases in the literature are largely seen in AIDS patients. Gastrointestinal histoplasmosis can often present as a large obstructing mass suspicious of a carcinoma or as ulcerating lesions suggestive of Crohn's disease. This case illustrates that histoplasmosis is the great imitator and that the gastroenterologist must have an increased degree of suspicion for this emerging disease, as medical management with antifungal therapy has been shown to significantly decrease the mortality rate by more than 4 fold.


Udayakumar Navaneethan, MD*, Mayar Al Mohajer, MD, Ana Mestanza, MD, Joseph Palascak, MD, Andres Gelrud, MD, MMSc. Internal Medicine, University of Cincinnati Medical Center, Cincinnati, OH.

Purpose: Biliary cast syndrome is an unusual complication of orthotopic liver transplantation (OLT) with serious clinical implications. Biliary cast formation is usually associated with biliary strictures and/or hepatic ischemia. Surgical management is the mainstay of treatment. Endoscopic techniques have been recently described in the successful removal of biliary casts. We report a post OLT patient who underwent successful endoscopic removal of biliary cast using single operator cholangioscopy. Our patient is a 68 year-old male with history of OLT seven months before for hepatitis C induced cirrhosis who came for a follow up visit. He had no complaints and physical exam was normal. He had cholestatic liver enzyme elevation (Alkaline phosphatase 580 IU/L, Total bilirubin 2.3 mg/dl) with normal aminotransferases. Hepatitis C RNA was undetectable. Ultrasound demonstrated normal common bile duct (CBD) diameter with normal Doppler flow. Liver biopsy showed no rejection with suggestion of cholestasis. Endoscopic retrograde cholangiopancreatoscopy (ERCP) was performed and cholangiogram showed multiple linear filling defects in the common hepatic duct (CHD) proximal to the anastomosis with extension into the intrahepatic system. After failure of the balloon to remove the filling defect, a single-operator choledochoscope was passed into the CHD for diagnostic and possible therapeutic purposes. A dark brown tubular structure was seen resembling a cast of the bile duct. Using a basket, the distal aspect of the cast was secured and a 6 cm long cast was successfully removed in a single piece. (Image) Cholangiogram showed improvement with excellent biliary drainage both fluoroscopically and endoscopically. Liver function tests have subsequently normalized and the patient remains normal with a follow period of 10 months without recurrence. In conclusion, Biliary cast syndrome is a rare complication of OLT which should be thought of when patients present with cholestatic liver enzyme elevation usually within the first year of transplant. Single operator cholangioscopy provides a safe means of diagnosing and treating patients with Biliary cast syndrome particularly in cases with intrahepatic duct casts where surgery or percutaneous techniques are often required.

Methods: N/A

Results: N/A

Conclusion: N/A


Maria Hatara, MD*, George Aragon, MD, Marie Borum, MD, EdD, MPH. Division of Gastroenterology and Liver Diseases, Internal Medicine, George Washington University, Washington, DC.

Purpose: We report a rare case of incomplete Carney triad with metastatic Gastrointestinal Stromal Tumor (GIST), extra-adrenal paraganglioma and a rare association with Juvenile Polyposis Syndrome (JPS).

Methods: A 16-year-old female presented with symptoms of dyspnea on exertion and fatigue. Initial evaluation revealed iron-deficiency anemia and she was placed on iron supplementation. When her anemia continued to worsen, a CT scan of the abdomen was obtained, which revealed a large gastric mass. She underwent EGD and biopsies showed a GIST which was eventually resected. The large tumor extended through the gastric wall to involve subserosal fat without lymph node involvement. Immunohistochemistry confirmed the diagnosis of GIST. There were also multiple benign gastric polyps in the gross pathologic specimen, consistent with JPS. Restaging with an EGD, seven years later, showed a benign gastric polyp. However, CT of the abdomen showed a 1.5-cm retroperitoneal mass that was later found to be an extra-adrenal paraganglioma with immunohistochemical staining positive for neuroendocrine markers. A PET scan showed several new hepatic nodules consistent with metastatic GIST. She was started on Gleevec and eventually underwent right adrenalectomy, resection of the right liver lobe and thermal ablation of the liver metastasis.

Results: Carney triad is an extremely rare syndrome, with fewer than 30 cases reported with all three tumors present, and fewer than 100 incomplete cases having two of the three tumor types present. Typically, GISTs and chondromas are encountered in incomplete cases. We describe a case of incomplete Carney triad with two elements of Carney triad: metastatic GIST, extra-adrenal paragangliomas and a rare association with JPS, previously not described in the literature. The third element, a pulmonary chondroma, has yet to be detected. Carney triad predominately affects females in over 80% of cases, with the first tumor appearing in the teenage years. The first tumor identified most often is a gastric GIST. Due to a time lapse of many years between identification of the first tumor and appearance of the second type of tumor, all pediatric GIST cases should be considered as potential Carney triad cases. The prognosis is better compared to GIST alone in adults, with a slow course of progression even after metastasis has occurred. The natural course of disease, although indolent, was associated in many cases with severe morbidity due to multiple resections of pulmonary chondromas and paragangliomas.

Conclusion: The case illustrates the need for early recognition to detect the component tumors at a stage when surgery may be curative. Careful long-term follow-up is needed because of the tendency to develop other malignant tumors.


Vinod Kurupath, MD,*, Lakshmibabu Parsa, MD, Frederick Fallick, MD, Jeremiah Kurz, MD. Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Gastroenterology, St. Barnabas Hospital, Bronx, NY.

Purpose: Mesenteric panniculitis (MP) is a condition of unknown etiology involving idiopathic inflammation and fibrotic process of the mesentery. Below is a rare case of MP associated with cryoglobulenimia.

Methods: case report Fifty-year-old female with history of diabetes mellitus, untreated Hepatitis C and hypothyroidism presented with abdominal pain/fever for one week with severe RUQ tenderness, palpable purpuric lesion consistent with leukocytoclastic vasculitis (LV). Laboratory examinations showed mildly elevated transaminases and alkaline phosphatase.

Results: Computed Tomography (CT) of abdomen showed inflammatory changes suggestive of mesenteritis. Intravenous antibiotics were started for possible diverticulitis/mesenteritis. With no response to antibiotics, and worsening abdominal pain, diagnostic laparoscopy was performed before starting steroids due to untreated hepatitis C and low white cell counts. It showed right upper quadrant phelgmon, cirrhotic liver, inflamed mesentery and adhesions of bowel to abdominal wall. Biopsy showed acute and chronic inflammation and hemorrhage consistent with mesenteric panniculitis. Colonoscopy showed multiple hyperplastic polyps and no signs of colitis. Purpuric rash again showed LV. Cryoglobulins were positive and she had a very low rheumatoid titer. Patient was started on tapering dose of steroids and she showed improvement. She was started on Pegasus and Ribvarin for follow-up in liver clinic. Patient's HIV status and other autoimmune work up were negative.

Conclusion: Most authors accept that mesenteric lipodystrophy, MP and sclerosing mesenteritis are part of the spectrum of one disease - usually one feature predominates, whose etiology remains obscure. Mesenteric panniculitis has been associated with a number of autoimmune conditions, with clinical response to immunomodulatory medications including corticosteroids, azathioprine and cyclophosphamide. Dual-phase abdominal CT is the most sensitive imaging modality for detecting MP. This is the first reported case seen of MP caused secondary to cryoglobulenemia that responded well to steroids and had other features of rare cryoglobulemia manifestations of low rheumatoid factor level with no manifestations and LV. Probable etiology would be vasculitis of the mesenteric vessels.


Amir Butt, MD*, Malvinder Singh, MD, Siddarth Mathur, MD, Niket Sonpal, NA, Sushil Duddempudi, MD, Mukul Arya, MD. Division of Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Division of Gastroenterolgy, Wyckoff Heights Medical Center, Brooklyn, NY.

Purpose: A 71 year-old male present to the emergency room with a chief complaint of epigastric pain for two weeks. He mentioned this was associated with post-prandial, non-bilious vomiting. He described having loose dark stools for the same interval. He denied unintentional weight loss. His past history was significant for a sub-total colectomy for hematochezia more than twenty years ago. Physical exam was remarkable for epigastric tenderness and fullness, with a healed midline scar. Bowel sounds were normal. Gastric lavage was negative. CT of the abdomen with oral contrast revealed a distended stomach with thickening of the distal antrum and pylorus. Upper endoscopy revealed a narrow pylorus with friable and erythematous mucosa. Multiple biopsies were taken from this region. In the duodenum, multiple large sessile and pedunculated polyps were noted. A large polyp was clipped at the pedicle and snared from above. Colonoscopy revealed an intact ileo-rectal anastamosis with polyps similar to the ones found in the duodenum. Biopsies from the pyloric channel revealed moderately differentiated invasive adenocarcinoma. Histology of the polyp revealed tree-like arborization, consistent with a hamartomatous polyp. Peutz-Jeghers Syndrome is a rare autosomal dominant disorder characterized by mucocutaneous pigmentation and harmtomatous polyps throughout the gastrointestinal tract. It is associated with an elevated risk of development of gastrointestinal and extra-intestinal malignancy. During the second and third decades of life, patients may present with abdominal pain, hematochezia and obstruction. Prior to this hospital admission, our patient never had an upper endoscopy. We recommend that patients presenting with hematochezia, despite a negative gastric lavage, should undergo an upper endoscopy to ensure such rare diagnosis are not missed.


Amir Butt, MD*, Shikha Doomra, MD, Frederick Fallick, MD. Division of Gastroenterology, The Brooklyn Hospital Center, Brooklyn, NY, Department of Gastroenterology, St. Barnabas Hospital, Bronx, NY.

Purpose: We report a case of a 21-year-old African male who was referred to the emergency room for noticeable abdominal distention. The patient described it as abdominal 'fullness' without symptoms. He also mentioned having constipation since for the past one month and a change in stool consistency, with stools alternating between diarrhea and constipation. He denied any pain in the abdomen, weight loss, nausea, vomiting, or fever. The patient was not on any medication and denied used of performance enhancing medication. Family history was significant for resection of ovarian teratoma in his mother and niece at ages of 19 and 11 respectively. Physical examination was significant for a soft non-tender distended abdomen. A central mass was palpable with unclear margins. A small lymph node was palpable in the right groin. Laboratory data revealed hemoglobin of 13 gm/dL with a normal MCV. His liver function tests showed mildly elevated transaminases (ALT/AST 56/46). An abdominal CT scan was ordered which revealed a large heterogeneous non-calcified, non-fat containing intra-peritoneal mass occupying the majority of the abdomen with displacement of bowel loops and compression of the recto-sigmoid colon. A small amount of ascities was also noted. Markers for malignancy CEA, CA 19-9, HCG were negative. An MRI of the abdomen revealed the same large midline intra-abdominal mass, which appeared to arise just inferior to the level of the pancreas with maximum dimensions of 16 cm by 8 cm by approximately 15 cm wide. The mass did not involve the abdominal wall or the bladder. Markers for malignancy CEA, CA 19-9, HCG were negative. The mass was subsequently biopsied on day three. Core-needle biopsy revealed small, blue cells with hyperchromatic nuclei and scant cytoplasm. Tissue staining was positive for the marker CD 99, consistent with Ewing's sarcoma. In summary, although rare, Ewing's sarcoma should be a part of the differential diagnosis in patients presenting with an abdominal mass. Furthermore, because of the rarity of this tumor, patients diagnosed with Ewing's sarcoma should be referred to centers that have experience with the disease.


Jitendrakumar Patel, MD*, Kashyapkumar Patel, MD, Kelly Cervellione, MA, Avani Patel, MD. Internal Medicine, Jamaica Hospital Medical Center, Jamaica, NY.

Purpose: Granulomatous appendicitis (GA) is a rare condition occurring in 0.1% to 2% of all appendectomies. Possible etiologies of GA include Crohn's disease (CD), sarcoidosis, foreign body reaction, obstruction caused by fecalith, mucocele or tumor and infectious agents such as mycobacterium, fungi and parasites. Idiopathic granulomatous appendicitis (IGA) is an extremely rare condition with unknown etiology.

Methods: A 29-year-old male presented with complain of right lower quadrant (RLQ) pain for 6 months. In addition, patient had nausea, vomiting, diarrhea, fever and chills.

Results: On abdominal examination, localized tenderness present in the RLQ with positive rebound. On laboratory investigation, patient had leukocytosis with normal hemoglobin, amylase and lipase. Patient was admitted for same episodic complaint 6 months and 4 months prior; perforated appendix with peritonitis was diagnosed at those times, but patient refused surgery. He was treated with oral antibiotics and advised to follow-up in surgery clinic. The patient now presented with same complain. Intravenous antibiotics were started; CT scan revealed phlegmon in RLQ. Patient underwent laparoscopic appendectomy. On laproscopy, there were local chronic inflammatory process with fibrosis and adhesion on the lateral wall, which complicated the procedure. Therefore, open laprotomy was attempted. Appendix and cecum was inflamed so appendectomy was completed along with right hemicolectomy and terminal ileactomy. Biopsy of appendix revealed focal ulceration, mucosal necrosis, transmural acute and chronic inflammation with crypt abscess, and multiple small non-necrotizing granulomas with multinucleated giant cells in lamina propria, submucosa and muscularis mucosa. Stain for fungal, acid fast bacilli and Yersinia organisms were negative. Histopathology of right colon and terminal ileum revealed scattered inflammatory cell infiltrate without evidence of cryptitis, crypt abscess or granuloma. Mesenteric lymph nodes showed benign acute and chronic inflammatory infiltrate. Patient was discharged without further episodes.

Conclusion: IGA is an extremely rare condition with unknown etiology, though it is theorized that it may be associated with recurrent and subacute appendicitis. Recurrent appendicitis produces granulomatous reaction secondary to inflammation. Use of temporary treatment, such as antibiotics, delays the need for appendectomy, but may inclrease chances of developing IGA. IGA was initially thought to be part of the Crohns Disease spectrum, but recent studies show that IGA has different histopathological features than CD and that only 5 to 10% of IGA patients eventually developed CD. IGA should be considered in cases that mimic the illness course described here.


Shivangi Kothari, MD*, Chintan Mody, MD, Robert Spira, MD, Joseph DePasquale, MD. Gastroenterology and Hepatology, St. Joseph's Regional Medical Center, Paterson, NJ, Gastroenterology and Hepatology, Internal Medicine, St. Michael's Medical Center, Newark, NJ.

Purpose: Giant sigmoid diverticulum is a rare air-filled cystic cavity greater than 3-4 cm. Giant pseudodiverticulum of sigmoid colon is one of the two types of sigmoid diverticulum. It is a very rare presentation of diverticular disease. It has a typical radiological and histological finding, which is helpful in making the diagnosis.

Methods: A 72-year old female with hypertension presented with complaints of abdominal distention, decreased appetite and weight loss for 2 weeks. The patient denied fever, abdominal pain, vomiting or constipation. On physical exam abdomen was distended, soft, non tender with presence of normal bowel sounds. Labs revealed leukocytosis of 38.2 with 21% bands, normal liver functions, amylase and lipase. Patient was started on antibiotics and IV fluids. Abdominal CT showed an air fluid level with a large 10 cm dilated loop of sigmoid colon. Patient was presumed to have volvulus and colonoscopy was performed. The scope was advanced into a narrowed area in the recto-sigmoid region and it entered into a large air filled cavity lined by blackish appearing serosa. The cavity lacked the lining by normal colonic mucosa. Upon continuous suctioning of the air in the cavity it completely collapsed resolving abdominal distention. Patient was referred to surgery for possible sigmoid pseudodiverticulum versus colonic perforation. Patient underwent exploratory laparotomy with left hemicolectomy, rectal Hartman's pouch and colostomy. The pathology report showed sigmoid pseudodiverticulum with focal acute and chronic inflammation. Post surgical hospital course was uneventful and patient was discharged.

Results: -

Conclusion: Giant Colonic diverticulum (GCD) was first described by Bonvin and Bonte in 1946. GCD has been divided into Type I and Type II. Type I is a pseudodiverticulum with the cyst wall lacking the smooth muscle and consisting mostly of fibrous tissue and chronic inflammatory cells. Type II is a true diverticulum, congenital in origin with the wall consisting of distinct smooth muscular layer and all the layers of normal bowel wall. Type I and Type II account for 87% and 17% cases respectively. Some of the proposed theories of formation are unidirectional ball valve mechanism, gas forming organisms or differences in the intracolonic and GCD pressure through the communicating ostium. Gender distribution is equal in Type I while Type II has male predominance. The common symptom is the abdominal pain with distension in 70% of the patients. Diagnosis is made with plain abdominal films, abdominal CT scan, and colonoscopy. Treatment is based on the type of GCD, for type I - segmental resection is recommended. For type II, diverticulectomy is suggested. Prognosis is usually good after surgical intervention.


Lakshminarayan Sooraj T K, MD, MPH*, Mary Atten, MD, Bashar Attar, MD, PhD, FACG, Victoria Angelova, MD, Benjamin Go, MD. Gastroenterology and Hepatology, Cook County-John H. Stroger Hospital, Rush University, Chicago, IL.

Purpose: NA

Methods: Introduction: Iron overload occurs in patients with chronic hepatitis C infection (HCV), however it is usually mild. Iron is hepatotoxic, hinders therapeutic response to interferon/ribavirin, and accelerates progression to liver fibrosis while also increasing the risk of hepatocellular carcinoma. Hereditary hemochromatosis, an autosomal recessive disease, independently causes iron overload in the homozygous state. H63D mutation accounts for a minority of hereditary hemochromatosis cases, and does not cause iron overload in the heterozygous carrier state. Here we present a patient with heterozygous H63D mutation and HCV infection with significant iron overload. Case presentation: A 45-year-old female was referred for management of HCV genotype 1 infection. She had normal liver enzymes, coagulation profile, leukocyte count, platelet count, low hemoglobin of 11.8 gm/dl, and hematocrit of 34.1%. She had elevated ferritin of 639.9, and transferrin saturation of 81%. DNA analysis showed heterozygous H63D mutation. Liver biopsy showed mild fibrosis (stage 1-2/6), moderate inflammation (MHAI score 6/18), and increased iron deposition in hepatocytes on iron stain (Grade 3/4). She is currently undergoing therapeutic phlebotomy prior to starting HCV therapy. Discussion: The carrier state for hemochromatosis mutations, though not associated with phenotypic hemochromatosis in otherwise normal individuals, assumes clinical importance when it occurs with HCV infection. These patients develop increased hepatic iron deposition and fibrosis. Significant iron overload in a patient with HCV, such as our patient, should raise suspicion for hemochromatosis mutations. If present these patients may benefit from phlebotomy prior to antiviral therapy.


Mohamad Erfani, MD*, Touraj Zolfaghari, MD, Hilary Hertan, MD, FACG. Gastroenterology, Our Lady of Mercy Medical Center, Bronx, NY.

Purpose: Approximately 120,000 percutanaeus endoscopic gastrostomy (PEG) procedures are performed in U.S. annually. Although PEG placement is generally safe, 16 to 70% complication rate is reported. Minor complications include wound infection, tube dysfunction, gastric outlet obstruction, peristomal leakage, bleeding, cutaneous or gastric ulceration, pneumoperitoneum and temporary ileus. Major complications include necrotizing fasciitis, esophageal or gastric perforation, buried bumper syndrome, and inadvertent PEG removal. Here we present another complication of GT migration into the duodenum. This complication has been under-recognized and rarely reported.

Methods: This is a case series study. Five nursing home patients with PEG who were admitted with obstructive symptoms, elevated serum amylase and lipase and normal liver enzymes were reviewed. In all cases the physical and radiological examination (Fig. 1), revealed migration of the GT into the duodenum. Symptoms were resolved after GT replacement or retraction. Serum amylase and lipase were also normalized within 2 to 3 days. No other causes for acute pancreatitis were identified. In one case the patient was re-admitted several times with migrated GT and similar findings. Pancreatic enzymes were normalized after GT replacement in every occasion.

Results: In all cases, there was evidence of migrated GT balloon compressing periampullary area with increased amylase and lipase, which normalized when the balloon was deflated and moved away from the ampullary region. This condition was associated with balloon-type internal bolster, replaceable GT.

Conclusion: In elderly patients with PEG, abdominal pain, vomiting and hyperamylasemia, a migrated GT to the periampullary region should be looked for and the GT should be repositioned.


Shivangi Kothari, MD*, Chintan Mody, MD, Robert Spira, MD, Joseph DePasquale, MD, Gunwant Guron, MD. Gastroenterology and Hepatology, St. Joseph's Regional Medical Center, Paterson, NJ, Internal Medicine, Gastroenterology, St Michaels Medical Center, Newark, NJ, Oncology, St. Michael's Medical Center, Newark, NJ.

Purpose: Hairy Cell Leukemia (HCL) is a form of chronic lymphoproliferative disorder. Leukemic involvement of the gastrointestinal (GI) tract must be considered in any patient with acute or chronic leukemia who presents with unusual GI symptoms. We report a patient with HCL presenting with fever, abdominal pain and was found to have hairy cell (HC) infiltration on random biopsies of endoscopically normal appearing duodenum.

Methods: Our patient is a 48 year old Hispanic male with history of HCL who presented with fever for two days after one cycle of cladribine (2-CdA). Patient had temperature of 101.4 and right abdominal tenderness with no rebound, guarding or rigidity. Labs showed WBC 0.4, ANC 0.2, Hb 8.9, platelet 23, ALP 137, ALT 42, AST 32. He was started on Imipenem, Vancomycin, Diflucan and Neupogen. Extensive septic work-up was negative. HIDA scan was negative. Bone marrow biopsy done for persistent spiking of high grade fever was negative for any pathogens. Abdominal CT showed circumferential thickening of 2nd and 3rd portion of duodenum. EGD revealed a completely normal esophagus and duodenum. Random biopsies of the duodenum revealed chronic inflammatory infiltrate chiefly composed of atypical lymphocytes and plasma cells. Immunohistochemical stains of paraffin sections of biopsy revealed atypical lymphocytes positive for TRAP (tartrate resistant acid phophatase), consistent with hairy cell leukemic infiltrate of duodenum. Patient's WBC subsequently improved on Neupogen and he was discharged.


Conclusion: Extramedullary involvement of the GI tract with leukemia is very rare and usually involvement of lymphoreticular organs, brain, testes and ovaries is seen. The reported autopsy incidence of GI involvement by leukemia ranges from 5.7% to 13% and reaches upto 20% in cases of acute lymphocytic leukemia. Leukemic involvement of the GI tract can be from mouth to anus with duodenum and distal colon being least commonly affected. Macroscopically, GI tract involvement can assume a variety of forms, including necrosis, hemorrhage, ulceration, inflammation or polypoid lesions. We did not find any case in literature with duodenal infiltration by hairy cell leukemia having a normal endoscopic appearance. Acute presentations may include necrotizing enteritis, perforation and abscesses. Radiographic studies may show thickening of bowel wall or ulcerations. Differential should include any underlying infectious etiology. Recurrent GI symptoms in a patient with known leukemic involvement of the GI tract should raise suspicion for leukemic relapse or progression. If index of suspicion is high, random biopsies should be taken regardless of the gross mucosal appearance, as a normal appearing mucosa does not rule out underlying pathology.


Kumaravel Perumalsamy, MD*, Alejandra Borensztein, MS, Natalia Segal, MS, Kadirawel Iswara, MD, Jianjun Li, MD, Scott Tenner, MD. Maimonides Medical Center, Brooklyn, NY.

Purpose: Colitis Cystica Profunda (CCP) is a rare, benign condition that can often provoke a diagnostic dilemma. CCP was shown in study to be confused with adenocarcinoma in up to 25% of cases. CCP is most commonly found in the distal colon. Isolated right colonic CCP is rare and we report a case of CCP of the right colon referred for further management of colonic polyposis.

Methods: 50 year-old woman with no prior PMHx underwent screening colonoscopy. She was found to have multiple sessile growths in the right colon. She was referred for further mangement of right colonic polyposis. During repeat Colonoscopy numerous sessile and polyploid lesions with smooth and tense mucosal surface consistent with submucosal cystic lesions seen in the right colon. These lesions were mainly grouped together in clusters and measured between 0.5 cm and 1 cm in diameter. On needle inspection, these lesions were found to have a liquid, mucinous content and the cystic structures collapsed.

Results: CCP is characterized by the presence of mucin-filled cysts confined to the submucosa most frequently seen in the distal colon. CCP is most often seen in the 3rd and 4th decades of life and has equal predilection for men and women. It is often found in association with solitary rectal ulcers and rectal prolapse as well as defecation disorders. CCP has also been seen in patients with chronic inflammation or trauma such as Crohn's disease, ulcerative colitis and radiation colitis. While several theories have been proposed, it is believed that trauma or chronic inflammation most likely leads to the production of these cysts. The cysts can appear as ulcerated (57%), polyploidy (25%), or flat (18%). The majority of lesions are found in the distal colon, often between 5 and 12 cm from the anal margin on the anterior wall. However, the cysts can be found through the colon and even, rarely, in the small intestine and the stomach. It can also have a segmental distribution or, least frequently, it can present as pancolitis. The lesions seen in CCP have often been mistaken for adenomatous polyps and even adenocarcinoma. Histopathologic analysis can demonstrate mucin pools with flattened epithelial lining within the submucosa. In patients with minimal symptoms, conservative treatment is indicated. The treatment is aimed at reducing straining during defecation by retraining habits, as well as high fiber diets and bulk laxatives. These measures have been demonstrated to cause complete regression within a 6-12 month period in various studies. When rectal prolapse is the cause, surgical correction is indicated to correct the problem.

Conclusion: Isolated right colon CCP is rare and should be considered in the differential diagnosis of multiple polyposis syndrome.


Shivangi Kothari, MD*, Chintan Mody, MD, Robert Spira, MD, Joseph DePasquale, MD. Gastroenterology and Hepatology, St. Joseph's Regional Medical Center, Paterson, NJ, Internal Medicine, Gastroenterology, St. Michael's Medical Center, Newark, NJ.

Purpose: Malignant melanoma is one of the most common malignancies to metastasize to the gastrointestinal (GI) tract. Metastases to GI tract can present at time of primary diagnosis or decades later as first sign of recurrence. Metastatic melanoma to GI tract is found during diagnostic workup in 1%-4% of patients with cutaneous primary and up to 60% of melanoma patients in autopsy.

Methods: Our patient is a 45 year old white male with history of primary non-pigmented urinary bladder melanoma who presented with complaint of dyspepsia for 2 months. Patient had received full course of chemotherapy with Tamodar for 5 months with good response. He denied any nausea, vomiting, dysphagia or bleeding. He had no primary skin lesion found on extensive detailed physical exam. Whole body PET scan showed markedly thickened stomach walls with multiple omental lesions in the perigastric region. Upper endoscopy revealed two large, non-pigmented ulcerating masses in body of stomach on the greater curvature. These masses had "volcano appearance" with heaped up edges and central crater. Multiple biopsies were taken which were consistent with non pigmented metastatic melanoma confirmed by immunohistochemical stains. Patient was subsequently started on carboplatin and has had mild improvement in symptoms.


Conclusion: Gastrointestinal invasion by melanoma is a rare condition and is often associated with invasion of other visceral organs. The endoscopic classification of the gastric metastases comprises three main types: (a) melanotic nodules, often ulcerated at the tip; most common (b) submucosal mass, melanotic or not, elevated and ulcerated at apex; typical aspect of "bull's eye" lesion and (c) mass lesions with varying incidence of necrosis and melanosis. Gastric metastases may appear even as a simple ulcer. Majority of gastric metastases are reported to occur in body and fundus, most often on the greater curvature. Most frequent sites of melanoma metastases include small bowel, stomach, colon, and anorectum in decreasing order. Symptoms may include abdominal pain, dysphagia, small bowel obstruction and GI bleed. Diagnosis requires careful inspection of mucosa and biopsy with special immunohistochemical stains. Management may include surgical resection, chemotherapy, immunotherapy, observation, or enrollment in clinical trials. Surgery seems to be of limited value and should be performed in carefully selected patients and in patients with complications. Prognosis is poor, with median survival time in patients presenting with GI invasion being less than 1 year. Endoscopic "Volcano ulcers" in the stomach have been reported in many secondary neoplasms of the stomach and their presence should always raise suspicion for an underlying malignancy.


Bilal Hameed, MD*, Saqib Razzaque, MD, Ahmad Abdulkarim, MD, Nadeem Chaudhary, MD. Gastroenterology, University of Minnesota, Minneapolis, MN, Gastroenterology, Regions Hospital, St. Paul, MN.

Purpose: Common sites of metastasis for the breast cancer are bones, lungs, central nervous system and liver. Colon is the rarest site of metastasis for breast cancer. 84 year old female with history of stage III infiltrating lobular carcinoma of the breast presented with abdominal discomfort and diarrhea. Extensive work up was negative. Colonoscopy showed three polyps (2-6 mm) in the cecum and ascending colon and about 10 mm polyp at the hepatic flexure. No masses or other lesions seen on colonoscopy. Pathology of hepatic flexure polyp showed sessile serrated adenoma and cells positive for CKAE1/AE3 and ER positive staining consistent with metastatic lobular carcinoma. Similarly biopsy specimen from ascending and cecum showed tubular adenoma and metastatic carcinoma of breast (confirmed with CKAE1/AE3 and ER positive staining, PR and CD68 was negative). Histological comparison was also done from her breast cancer which revealed similar tumor. Patient is currently on systemic chemotherapy (faslodex) and doing well. There are about <30 cases in the literature of breast cancer with metastasis to colon in alive individuals. Most of these tumors were lobular carcinoma. Our patient is unique as there is no other case report of breast cancer with metastasis to colon polyps in an alive patient. Diagnosis of colon metastasis from breast is difficult because of non specific symptoms, variable imaging presentations and its rarity. Patients with history of breast cancer presenting with abdominal pain, diarrhea or obstruction should be examined for possible colon metastasis.


Nelson Lim, MD*, Mia Perez, MD, Donald Rankin, MD, Michael Lim, BS, Manoj Shah, MD. Department of Pediatric Gastroenterology, Department of Pathology, Department of Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA.

Purpose: To report this rare finding.

Methods: Case: A 15 y/o Caucasian male presents with fever of unknown origin. He has a h/o cardiac transplant in 1992 for Hypoplastic left heart syndrome. His cough symptoms did not improve with a course of azithromycin. The patient had a four-week visit with relatives in Michigan and Illinois approximately 3 months prior to the appearance of these symptoms. He now develops nausea, some vomiting, and slightly increased loose stool while hospitalized. A test for urine Histoplasma Ag was positive. A chest CT and sputum cultures showed no evidence of a fungal infection. An EGD showed several several duodenal bulb erosions. During colonoscopy, there was extensive erythema seen with superficial to deep ulcerations scattered from the cecum to sigmoid colon. Multiple pseudopolyps and inflammatory nodules were seen in the cecum. Biopsies were taken throughout which were significant for non-necrotizing granulomas. Giemsa and PAS special stains were also positive for numerous intracellular small yeast forms with focal narrow-based budding and rare hyphal forms. Duodenal biopsies were similar. These were morphologically consistent with Histoplasma capsulatum.

Results: Histoplasma Capsulatum is a dimorphic fungus and found worldwide.1 In North America it is endemic in the major river valleys (Mississippi and Ohio) of the southern and central United States.2 Once the acute infection is spread hematogenously from the lungs to other organs it is generally classified as systemic. In addition to this, findings of positive blood cultures, or positive urine or serum Histoplasma antigens changes its classification to disseminated.2 Most infections are self-limited, but 1 in 2000 infections result in progressive dissemination especially in immunocompromised hosts.4 The symptoms of disseminated histoplasmosis include fever, malaise, anorexia, and weight loss. The gastrointestinal tract is commonly involved (70-90%) during disseminated infection as determined by autopsy studies.4,8 The colon is usually the most involved organ of the gastrointestinal tract followed by the small bowel. Serious gastrointestinal complications include malabsorption from severe diarrhea, ulcerations, strictures, bowel obstruction, gastrointestinal hemorrhage and perforations.7,8

Conclusion: Our case is a unique example of an immunosuppressed patient with recent travel to an endemic area which may have predisposed the duodenum and colon to a Histoplasma Capsulatum infection. Laboratory evidence of dissemination warrants endoscopic exam even when asymptomatic because the gastrointestinal tract is commonly involved. Prompt diagnosis and treatment may reduce the incidence of serious gastrointestinal complications.


Nissrin Ezmerli, MD*, Naveen Gupta, MD, Nadim Haddad, MD. Georgetown University Hospital, Washington, DC.

Purpose: Squamous cell cancer of the esophagus (ESCC) has been decreasing in incidence in the United States (U.S.) however 5 year mortality remains high with survival ranging from 10 to 13 percent. Multiple risk factors have been identified including geographic (highest in China), dietary/lifestyle (alcohol, smoking, and betel nut ingestion) and other risk factors (achalasia and lye ingestion). The role of viral infections has been evaluated and remains controversial. In particular the role of human papilloma virus (HPV)(subtypes 16 and 18) has received the most scrutiny. Prior studies have been questioned as they have been performed in high risk geographical areas. In low risk areas such as the U.S. retrospective pathology reviews reveal no association between the virus and cancer. However, in high risk areas (China), there is appears to be a 6-fold increase risk of ESCC in patients with HPV-16 seropositivity. There also remains a question as to whether this represents a causative factor or a facilitative factor to the development of ESCC. To our best knowledge, outside of pathology reviews, there has been only one case report in North America of an HPV associated ESCC. We present a case of a 48 year old Caucasian female with an HPV-16 associated ESCC. A 48 year old Caucasian female presented for upper endoscopy for evaluation of progressive dysphagia over 2 week duration. Endoscopy revealed an area of salmon colored mucosa with two associated white plaques at 20 cm from the incisors. Biopsies revealed severe dyplasia bordering on squamous cell cancer in situ with koilocytic atypia. PCR revealed the presence of HPV-16. Follow up endoscopy and endoscopic ultrasound revealed intact esophageal wall layers and endoscopy with Lugol staining revealed no further lesions. Endoscopic mucosal resection was performed with final pathology of clear margins with carcinoma in situ without evidence of invasive malignancy. To our knowledge this represent the second reported cause of HPV associated ESCC. The current standard for further HPV evaluation is based on histiologic findings including koilocytosis, giant or multi-nucleated cells, dyskeratosis, hyperkeratosis and acanthosis. Considering the remaining question for an association, the growing body of evidence of the involvement of HPV in the pathogenesis of neoplasia and the availability of vaccination against oncogenic strains of HPV, perhaps further evaluation into the utility for routine testing for the virus is indicated.


Homayoon Mahjoob, MD*, John Carroll, MD, Reena Jha, MD, Elisabeth Kramer, BS, Firas Al-Kawas, MD. Medicine, Georgetown University Medical Center, Washington, DC.

Purpose: Introduction: Ansa Pancreatica is a type of pancreatic ductal variation. The significance of this type of pancreatic duct anomaly and its relationship to the development of pancreatitis is unclear. Case Report: We report the case of a 51-year-old male who presented with 10 episodes of acute pancreatitis and a 30 Lb weight loss over the course of a year. CT scan and MRI findings were consistent with acute pancreatitis. An ERCP was performed, revealing a loop of the pancreatic duct in the head with a branch that directed towards the minor papilla consistent with Ansa Pancreatica. A prophylactic 5F 3 cm stent was placed into the pancreatic duct via major papilla. Sphincterotomy was not performed. EUS revealed a tortuous pancreatic duct with a circular course, located in the pancreatic head. The duct was of normal caliber, at 1.7 mm. Acute inflammatory changes were noted in the parenchyma of the tail of the pancreas. The patient was discharged and shortly after readmitted with another episode of pancreatitis. ERCP was again performed and the pancreatic duct was cannulated and anomaly of pancreatic duct was identified. Despite multiple attempts, it was not possible to cannulate the minor papilla to establish its patency. Pancreatic sphincterotomy was performed via the major papilla. A prophylactic 4 F 3 cm single pig tail stent was placed into the pancreatic duct, and a sphincterotomy was extended over the stent. The patient has been asymptomatic for last six months and gained 20 lbs after discharge. Conclusion: It is presumed that the drainage of pancreatic juice can be impaired by Ansa Pancreatica ductal variation. Such patients are vulnerable to the development of pancreatitis. Pancreatic sphincterotomy via major papilla and/or minor papilla may be considered as a treatment modality in symptomatic patients with this type of anomaly.


Lia Kaufman, BS*, Jennifer Dorfmeister, MD, Sherri Yong, MD, Khondker Islam, MD. Loyola University Medical Center, Maywood, IL.

Purpose: This is a 75 year old male with history of adenocarcinoma of the sigmoid colon status post resection and chemotherapy. Four years after diagnosis the patient was found to be anemic with a hemoglobin of 4.9 gm/dL, and a negative stool guaiac. Subsequent EGD and colonoscopy failed to reveal a clear source of bleeding. Capsule endoscopy (CE) was then performed. Four days after ingestion of the capsule, the patient developed abdominal pain and emesis. A KUB confirmed a retained capsule. The patient refused surgical intervention and decided to follow-up weekly with serial x-rays. KUB at nine weeks showed no change in capsule position. The patient consented to have laparoscopic exploration which revealed a circumferential jejunal mass at the site of capsule retention with extensive lymphadenopathy and carcinomatosis. Subsequent pathology confirmed the jejunal mass as metastatic adenocarcinoma, consistent with a colonic primary. Discussion The most common locations for colorectal adenocarcinoma metastasis include the regional lymph nodes followed by the liver and lung. Primary colorectal cancer metastasis to the small bowel is an unusual occurrence; it has been mentioned in case reports but definitive numbers describing its incidence is lacking. Capsule retention is an infrequent but significant complication of CE. The average reported incidence of capsule retention is 1-3%. Although those patients who are asymptomatic can be managed medically at first, up to 95% of them eventually require surgical intervention. The most common causes of retained capsule include Crohn's disease, NSAID-induced enteropathy or stricture and less commonly malignant tumors. CE can detect small bowel neoplasms that are often missed by traditional examinations. In our patient the CE images did not reveal the pathology likely to be responsible for his chronic anemia. CE was ultimately successful in its diagnostic aim in the manifestation of its one major complication, retention. It was the retention of the capsule that alerted the presence of pathology in our patient. This observation has been made before, acknowledging CE's role in identifying new obstructing lesions when retention has occurred and prompting interventions that otherwise would not have been considered. Conclusion Retention of the capsule endoscope is relatively rare, and most likely represents small bowel pathology. It is difficult to predict in which patients retention will occur. In a patient with a history of intestinal malignancy and surgical resection, a presentation of new iron deficiency anemia may represent recurrence of malignancy or metastatic disease.


Sarah DeNucci, MD*, Omar Hyder, MD, Daniel Quirk, MD, MPH. Internal Medicine, Warren Alpert Medical School of Brown University, Providence, RI.

Purpose: A glucagonoma, a glucagon secreting tumor of the pancreas, can be a devastating diagnosis resulting in metastasis and thromboemoblism. Typical presentation includes dermatitis, diabetes and weight loss. Prior GI diagnosis and non-specific symptoms may delay identification and treatment. To alert clinicians to its spectrum and potential for misdiagnosis, we report a case of glucagonoma presenting as isolated diarrhea in a patient with irritable bowel syndrome (IBS) and diverticulosis. Case Report: A 50 y.o. Male with known IBS, diverticulosis and remote parathyroidectomy presents with alternating diarrhea and constipation for several months. Physical exam: Unremarkable. Chem-7, CBC, LFT, Amylase, Lipase, INR: within normal limits (wnl). Infectious stool workup: negative. Colonoscopy: Diverticular disease in the left colon, no masses, no polyps. Initial CT scan: normal pancreas, known diverticulosis. History of likely hyperparathyroidism raised concern of islet cell tumor. Octreotide scan was scheduled but patient did not follow through. Patient returns one year later with worsened symptoms. Repeat CT scan: 10 mm hypodensity of pancreatic tail. Octreotide Scan: increased uptake in pancreatic tail. CEA 19-9, Gastrin, Chromogranin A, pancreatic polypeptide, somatostatin, VIP, 5HIAA: wnl. Insulin = 28 uIU/mL. Glucagon = 76 pg/mL. Endoscopic US: 1.1 x 1.5 cm round, isoechoic pancreatic tail mass. Patient underwent distal pancreatectomy and splenectomy. Surgical pathology revealed a well-differentiated pancreatic neuroendocrine tumor, positive for glucagon by immunohistochemistry. Discussion: Glucagonoma is a functional pancreatic endocrine tumor (PET) of low incidence, commonly associated with a triad of migratory necrolytic dermatitis, glucose intolerance, and weight loss. Nonspecific symptoms such as anemia, diarrhea, and thromboembolism may also occur. Consistent with other functional PET, symptoms are secondary to hormone-excess, and rarely caused by anatomical effects of the tumor itself, i.e. abdominal pain. Typical work-up is positive for increased plasma glucagon levels and corresponding CT findings, most often in the pancreatic tail. Surgical resection is curative; however disease is frequently metastatic at presentation. Our patient lacked typical features of presentation and only complained of chronic diarrhea. Gastrointestinal complaints in patients with known IBS are often attributed to their pre-existing diagnosis. Especially in patients with IBS and prior endocrine disease, rare but fatal causes of chronic diarrhea, such as glucagonoma, must not be excluded.


Ronald Concha, MD*, Ali Azarm, MD, Adam Goodman, MD, Frank Gress, MD. Gastroenterology and Hepatology, SUNY Downstate Medical Center, Brooklyn, NY.

Purpose: To report a unique case of abdominal aortitis associated with Crohn's disease. Case: A 47 year old African Caribbean female with a history of colonic Crohn's disease and uveitis (diagnosed 3 years earlier) was admitted for increased bowel movements (up to10 stools/day), abdominal pain, and fever (39[degrees]C). Physical examination was normal except for fever. Leukocyte count was normal (10,700 x 10.sup.9/L) and ESR was elevated (74 mm/1st hr). The remaining hematologic parameters were normal. Empirical antibiotic treatment was initially started while awaiting for blood, urine, and stool cultures results, which were all negative. An abdominal CT scan ruled out intra-abdominal abscess but showed an increased wall thickness of the abdominal aorta up to 1 cm in the thickest region (Fig. 1). This thickness extended inferior to the celiac axis to the suprarenal aorta. ANA, anti DS-DNA, AMA, and ASMA were negative. Serology for syphilis was also negative. IV Methylprednisolone was started for suspected autoimmune aortitis. Patient improved clinically and was discharged on escalating doses of azathioprine and prednisone tapering doses. A control CT scan confirmed the normalization of the aorta wall thickness. Discussion: Crohn's disease is considered to be a systemic disease since it is often associated with extra intestinal manifestations. Takayasu Arteritis is an extremely unusual extra-intestinal manifestation of Crohn's disease. In the literature only 21 cases of this unusual association have been reported. The diagnosis of aortitis is based on the occurrence of compatible clinical manifestations together with an imaging study demonstrating vascular wall abnormalities or compatible histologic changes in biopsies. When histology is not available, blood cultures and serology for syphilis must be performed in order to exclude bacterial and fungal infectious aortitis. The development of granulomas and granulomatous vasculitis seen in both Crohn's disease and Takayasu arteritis may suggest a common physiopathologic mechanism.


Tetsuhiro Yoshino, MD*, Shigenari Hozawa, MD, Tokuhiro Kimura, MD, Masahiro Jinzaki, MD, Yuji Yamada, MD, Yoshiyuki Yamagishi, MD, Hideaki Kanamori, MD, Yasunori Okada, MD, Toshifumi Hibi, MD. Department of Radiology, Department of Pathology, Division of Gastroenterology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.

Purpose: Immunohistological and electron microscopic examinations at autopsy were performed to confirm a diagnosis of a patient, who was clinically diagnosed as poorly differentiated adenocarcinoma by percutaneous biopsy of thickening part of peritoneum.

Methods: Enhanced CT scan showed distended stomach and rectum, broad intestinal wall thickening, thickening peritoneum, enlarged mesenteric lymph nodes, small amount of ascites, mild hydronephrosis and thrombosis of innominate and jugular vein. The echo-guided biopsy of the thickening part in the peritoneum was performed, and the lesion was diagnosed as poorly-differentiated adenocarcinoma. However, immunohistological analysis and additional imaging studies could not determine a primary lesion. At autopsy, immunohistochemical studies were performed using primary antibodies for pancytokeratin, epithelial membrane antigen, carcinoembryonic antigen, CA125, neuron-specific enolase, calretinin, D2-40, WT1, cytokeratin 7, cytokeratin 20, BerEP4, LeuM1, CA19-9, chromogranin, synaptophysin, and thyroglobulin. Electron microscopic examination was further performed.

Results: Histological examination revealed invasive growth of neoplastic cuboidal or columnar cells with eccentric nuclei forming papillary and glandular structures. Psammoma bodies were found. These microscopic features were highly reminiscent of ovarian/peritoneal serous adenocarcinoma of women. Tumor invasion was observed in subcutaneous tissue of the abdominal wall. The tumor also invaded the right ureter, resulting in hydronephrosis of the right kidney. No tumor was found in paratesticular regions. Metastasis of the tumor was found in lymph nodes (mesenteric, paraaortic, and paratracheal), left adrenal gland, and bilateral lungs. The lungs showed marked lymphangitis carcinomatosa and tumor emboli in the pulmonary artery branches. Venous thrombi containing metastatic tumor cells filled the lumina of the left jugular vein and left renal vein. No primary tumor was found in the visceral organs. The tumor cells were positive for pancytokeratin, EMA, monoclonal CEA, CA125, and NSE. They were negative for calretinin, D2-40, WT1, cytokeratin 7, cytokeratin 20, BerEP4, LeuM1 (CD15), CA19-9, chromogranin, synaptophysin, and thyroglobulin. In electron microscopic examination of the tumor cells, no apparent microvillus was found, although a small number of irregular short cytoplasmic processes were observed. Bundles of intermediate filaments were not seen in these cells. These findings indicated that the tumor was papillary serous adenocarcinoma of the peritoneum in a man. The diagnosis of peritoneal malignant mesothelioma was unlikely.

Conclusion: This report is the third case of PSCP in male.


Lea Ann Chen, MD*, Elliot Ellis, MD, Hyosun Han, MD, Sita Chokhavatia, MD. Division of Gastroenterology, Department of Medicine, Mount Sinai Hospital, New York, NY.

Purpose: A 54 year old man with diabetes, hypertension, hyperlipidemia, and hypothyroidism presented for evaluation of a painless right neck mass incidentally noticed during shaving. A carcinoid tumor of unknown primary, presenting as a left neck mass, had been treated twelve years ago with radiation and chemotherapy at an outside hospital. A recurrence ten years later was successfully treated, and CT scan after chemotherapy showed no residual tumor. The patient denied diarrhea, palpitations, skin changes, shortness of breath, wheezing, or weight loss. On examination, a non-tender 3 cm by 3 cm mass in the right cervical region and right submandibular lymphadenopathy were palpated. Surgical scars were noted on the left neck consistent with previous carcinoid resection. Labs, including chromogranin A level, were normal. A PET scan showed increased uptake in the right cervical region and the rectosigmoid area, and an octreotide scan did not show any increased uptake. Colonoscopy to the terminal ileum and an upper endoscopy to the third portion of the duodenum revealed normal mucosa, and no submucosal lesions were seen. Carcinoid tumors are rare neuroendocrine neoplasms with approximately 100,000 cases reported in the U.S. Sixty-four percent of all carcinoids originate in the GI tract and twenty eight percent first develop in the lungs or bronchi. Isolated primary cervical carcinoid is exceedingly rare and may be due to a primary in the foregut or rectum. Our patient had 2 recurrences of cervical carcinoid with no diagnosed primary site, suggesting an as yet undiagnosed pulmonary or GI carcinoid metastasizing to the cervical region. Both GI and non-GI neuroendocrine tumors should be considered in patients presenting with a cervical mass.


Sohail Asfandiyar, MD*, Ann Silverman, MD, FACG, Stuart Gordon, MD, FACG. Gastroenterology and Hepatology, Henry Ford Hospital, Detroit, MI.

Purpose: BACKGROUND: Although celiac disease (CD) is associated with various autoimmune disorders and is a cause of nonspecific liver enzyme abnormalities, this entity is not commonly recognized in the setting of end stage liver disease (ESLD). We report three patients who presented over a 6 month timeframe with ESLD for transplant evaluation who were all found to have untreated or refractory CD. CASE REPORTS: Patient A: A 60 year old woman with a history of refractory CD presented with ascites unresponsive to medical management; laboratory and imaging studies were consistent with cirrhosis. She was listed for OLT but expired from sepsis prior to transplant. Patient B: A 71 year old man with esophageal varices and a cirrhotic liver and portal hypertension at CT who presented with chronic diarrhea and a 50 lb weight loss. Small biopsy showed subtotal villous atrophy and crypt hyperplasia. His diarrhea resolved on a gluten free diet. He experienced sudden death secondary to myocardial infarction. Patient C: A 41 year old man with a two year history of liver enzyme abnormalities, and previous documentation of steatohepatitis, presented with progressive jaundice and coagulopathy. Physical exam showed stigmata of cirrhosis and a BMI of 41.5. His daughter had documented CD and the patient acknowledged longstanding diarrhea. Additional evaluation showed positive anti-endomysial IgA antibody and small bowel biopsy with total villous atrophy. His is currently listed for OLT. In each case other causes of liver disease, including metabolic, viral, alcohol and autoimmune were excluded. Patient C was presumed to have underlying NASH as the etiology for his cirrhosis, and patients A and B had presumed cryptogenic liver disease. Patients B and C had been previously evaluated by gastroenterologists for their liver disease but the diagnosis of CD was not entertained.

Conclusion: The mechanism of CD mediated liver injury is unexplained. We speculate that longstanding untreated hepatic dysfunction from CD may lead to cirrhosis, or that CD may act as a cofactor in other underlying liver disorders. In the setting of ESLD, especially NASH or cryptogenic, the entity of CD should be considered, including appropriate serologies or small bowel biopsies.


Ketul Patel, MD*, Jiwanjot Chhatwal, MD, Robbie Taha, DO, Nahid Elyas, MD. Internal Medicine, Providence hospital, Southfield, MI.

Purpose: Introduction Approximately 4.1 million Americans have been infected with Hepatitis C virus, of which 3.2 million are chronically infected. However, Hepatitis C is estimated to account for only 20% of all cases of acute viral hepatitis in the United States. A unique case of a patient who was recently diagnosed with Hepatitis C presented to us in the acute state with the additional findings of fulminant liver disease. Case Report A 59 year old African American male with end-stage renal disease on hemodialisis and diabetes mellitus presented with 3 week duration of nausea, vomiting, diarrhea, jaundice, and severe pruritus. He was noted to have right upper and lower quadrant abdominal pain with increased serum aminotranferases. Laboratory studies were significant for HCV RNA by PCR being positive with quantitative HCV RNA of 26,731,000 international units. Serology was negative for Hepatitis A and B. His alpha fetoprotein tumor marker was elevated at 14.0 and ferritin was also elevated at 6,451. During the course of his admission the patient's serum aminotranferases worsened along with further deterioration of his coagulation studies. Due to these abnormal lab studies with the patient's presentation of symptoms a computed temography guided liver biopsy was performed. The final diagnosis of the biopsy was severe active Hepatitis with acute hepatocellular injury which was consistent with acute viral Hepatitis C. The decision was made to transfer the patient to a liver center for a possible transplant. Upon transfer of the patient, follow up serum aminotransferases improved and he was advised for outpatient therapy with interferon. Due to his history of end-stage renal disease he was not a candidate for ribaviron. Discussion Fulminant Hepatitis C is rare and incidence is unknown. The center for disease control estimated that new acute Hepatitis C virus infections in the United States fell from 240,000 cases per year in the 1980's to 19,000 cases per year in 2006. Most cases of acute Hepatitis C are anicteric and asymptomatic. Transfusion associated cases are now less than 1 per 2 million transfused units of blood. Most cases are due to injection drug users. In fulminant hepatitis the fluctuation of aminotransferases is common after an acute infection of Hepatitis C with symptoms such as nausea, malaise, right upper quadrant pain and jaundice in less than 25% of cases. These acute symptoms are apparent in approximately 2-12 weeks. Fulminant hepatic failure is defined as the rapid development of severe acute liver injury with impaired synthetic function and encephalopathy in a person who had a normal or a well compensated liver.


Raymond Duggan, DO*, Timothy Pfanner, MD. Gastroenterology, Texas A&M Health Science Center - Scott & White Memorial Hospital, Temple, TX.

Purpose: We present a case of a 61 y/o male staus post chemoradiation for squamous cell carcinoma of the base of the tongue. He developed a radiation stricture and outside attmepts at dilation resulted in perforation. The patient had a prolonged recovery requiring placement of a PEG tube for nutrition. An esphagopharyngeal stricturoplasty resulted in relief for 2 month but was followed by reocclusion of the stricture. Subsequently a combined GI/ENT/Thoracic/Vascular Surgery procedure was performed. The stricture was punctured from a retrograde approach with an EUS FNA needle and a 0.018 mm biliary guidewire was placed across it. Next an excimer laser from the antegrade end was used to ablate the scar tissue. Ballon dilation was perfomred to 9 mm and a nasogastric feeding tube left in place. Two days later he was dilated to 10 mm. After that a series of dilations began with an initial interval of 3-5 days for the first month. He was dilated weekly for the next 2 months. Then he underwent dilation every 2 weeks for several months until his PEG tube was removed and he was tolerating a regular diet. Over the course of his multitude of dilations he did receive directed Kennalog steroid injections twice. Now he undergoes surveillance EGD every 2 months with dilation of any hint of a stricture.


Daniel Blachman, MD*, Kiron Das, MD, Naomi Schlesinger, MD. Internal Medicine, Robert Wood Johnson University Hospital, New Brunswick, NJ.

Purpose: Our patient is a 44-year-old African American male who has a 30-year history of Hidradenitis Suppurativa (HS) and Acne Conglobata (AC). HS and AC are part of the follicular occlusion (FO) triad (HS, AC and Perifolliculitis Capitis Abscedens et Suffodiens). He has a 10-year history of a spondyloarthropathy. He has clinical and radiological evidence of ankylosis of bilateral sacroiliac joints and cervical spine ankylosis. Recently he developed high fevers and Pyoderma Gangrenosum (PG) on both his lower extremities, which was resistant to local wound care and systemic corticosteroid treatment. Our purpose is to demonstrate a trial of an anti-tumor necrosis factor (TNF) agent for PG resistant to steroid treatment in a patient with associated HS, AC and Spondyloarthropathy.

Methods: Our patient was treated with a retinoid and antibiotics as needed for his AC and HS. An NSAID has been prescribed for his arthritis as well as sulfasalazine for the spondyloarthropathy. He received aggressive physical therapy for his spondyloarthropathy. Therapy with infliximab in a dosage of 5 mg/kg/d I.V. (three doses at 0, 2 and 6 weeks) was started when he presented with the severe bilateral PG on both legs.

Results: A dramatic improvement was seen after treatment with infliximab for pyoderma as well as the HS, AC and the spondyloarthropathy. After the first dose, the pyoderma lesions on both lower extremities improved significantly. Six months later, the patient is in remission from the skin lesions and his spondyloarthropathy is much improved. He continues treatment with Infliximab and Sulfasalazine.

Conclusion: A triad of HS, AC and spondyloarthropathy is a rare syndrome described only in a few case reports in the literature. PG has been associated with Acne Conglobata in rare cases and has been described extensively in Crohn's disease, which the patient developed one year prior to admission. The exact role of anti-tumor-necrosis-factor antibodies in this syndrome is unclear. Further evaluation is needed to assess the role of anti-TNF as a therapeutic choice for this rare syndrome.


Laxmi Thummalakunta, MD, MPH*, Naishadh Raghuwanshi, MD, MBA, Frank Burton, MD, Richa Gupta, MD. Internal Medicine, St. Luke's Hospital, St. Louis, MO, Gasteroenterology, St. Louis University, St. Louis, MO.

Purpose: A 50 year old obese female with a previous history of cholelithiasis status post cholecystectomy presented with complaints of epigastric pain for the past one week. The pain was moderate to severe in intensity and was radiating straight through to her back. It started after consumption of fatty food. It was associated with nausea and vomiting. She also had a 10 pound weight loss in the last 2 months. She did not have jaundice. On initial presentation a clinical diagnosis of acute pancreatitis was made. The patient subsequently underwent two endoscopic retrograde cholangiopancreatographys (ERCPs) at outside hospitals with failed biliary cannulation. An endoscopic ultrasound (EUS) was then performed which showed a small pancreatic lesion. A fine needle aspiration (FNA) was performed and cytology was negative for malignancy. The CBD was successfully cannulated on the third ERCP attempt and the findings revealed a stricture at the distal third of the CBD and a pancreatic duct stricture at neck of ventral pancreatic duct. A biliary stent was then placed. The patient was discharged home but continued to have nausea, vomiting and abdominal pain for the next 6 weeks. The patient suddenly spiked a high fever along with recurrence of the abdominal pain requiring readmission. An ERCP was performed which demonstrated a CBD stricture suspicious for extrinsic compressive effect from pancreas. Possible filling defects vs. air bubbles above stricture were noted. A biliary balloon dilatation of stricture was performed and a biliary stent was placed. A Computed tomography scan of the abdomen revealed the presence of an enlarged pancreatic head without the presence of a definite mass. The laboratory studies including an amylase, lipase and alkaline phosphatase were normal. The abdominal pain did improve, so the patient was discharged with a plan for repeat ERCP and EUS on an outpatient basis. A distal CBD stricture with proximal dilatation was again evident. The EUS again revealed a discrete lesion within the head of the pancreas. The FNA specimen was diagnosed as adenocarcinoma. Given the above findings, the patient was referred for a pancreaticoduodenectomy. The histological analysis revealed lymphoplasmacytic infiltrate surrounding the ducts and lobular with parenchyma fibrosis consistent with autoimmune pancreatitis. During the work up to discern the etiology of her recurrent acute exacerbation of chronic pancreatitis, the antinuclear antibodies (ANA), anti-smooth muscle antibody (ASMA) and IgG4 serologies were normal. Her IgG4 level was 19 mg/dl with the normal range being between 7 and 89 mg/dl. Our specimen was sent for IgG4 immunohistochemical staining by Mayo Clinic which was positive.


Ahmed Morales, MD*, Praveen Nallapareddy, MD, Shivani Jain, DO, Michael Klamut, MD, Sherri Yong, MD, Khondker Islam, MD. Loyola University Medical Center, Maywood, IL.

Purpose: Clinical Presentation A 23 y/o African American female with history of uncontrolled type I Diabetes with gastroparesis, presents with abdominal pain, which is sharp, diffuse and non-radiating. She denies melena, hematochezia, hematemesis, fever or chills. Her pain is controlled with narcotics or NSAID's. Episodes of alternating diarrhea and constipation are associated with nausea and vomiting. She describes intermittent arthralgias, mostly in her knees and has a history of an intermittent rash primarily involving her legs. Her medications include insulin and NSAID's. Her family history is remarkable for her mother having surgery for a "gastrointestinal problem". She smokes 1-2 cigarettes a day and denies alcohol. Work up includes: a. EGD: small ulcerations in the fundus and proximal body. Biopsies revealed non caseating granulomas, h pylori negative. b. Colonoscopy to the terminal ileum: normal mucosa, biopsies of right colon with non caseating granulomas. -CMP, IBD panel normal. Elevated ESR, ACE level pending -inguinal lymph node biopsy in 2005: positive for non caseating granulomas, neg for AFB and fungal organisms. -gastric emptying study in 2005 with 25% emptying at 90 minutes. Discussion Interesting case of a young woman with uncontrolled diabetes and chronic abdominal pain and vomiting with altered bowel habits. The abdominal pain has been presumed to be related to diabetic gastroparesis, but her endoscopic biopsies revealed non caseating granulomas. The differential diagnosis for gastrointestinal granulomas include inflammatory conditions (Crohn's, Sarcoidosis, vasculitis), infectious (TB, histoplasmosis, H. pylori, Whipple's), drug induced or idiopathic. In her case, the clinical picture is suggestive for a diagnosis of sarcoidosis. The gastrointestinal manifestations occur in approximately 0.1-0.9% of patients with sarcoidosis, and are usually related either to peptic ulcer disease or to narrowing of the gastric lumen due to granulomatous inflammation and associated fibrosis of the gastric wall; in the latter case diminished peristalsis often results. Peripheral lymphadenopathy can occur in up to 40% of the patients. The stomach is the organ most commonly involved. Endoscopy may reveal nodular changes, gastritis, thickened mucosa, greater or lesser curvature deformities, or ulcers. Segmental mucosal thickening and nondistensibility that mimics linitis plastica are the most common abnormalities on upper GI series. Conclusion Gastrointestinal sarcoidosis is a rare cause of abdominal pain and gastroparesis. High index of suspicion is necessary for diagnosis which requires multiple gastrointestinal biopsies, particularly for patients that present with multi-systemic symptoms.


Saba Ansari, MD*, Lourdes Merlo, MD, Avani Patel, MD, Asit Mehta, MD. Internal Medicine, Jamaica Hospital Medical Center, Jamaica, NY.

Purpose: Amyloidosis is a syndrome that occurs when there is a deposition of abnormally configured proteins inside human cells. These proteins interrupt the normal functioning of the cells, leading to serious disease process than can affect multiple organ systems and can prove to be fatal if left untreated. The gastrointestinal tract is often affected by this syndrome. The typical features of GI tract involvement include anorexia, malabsorption, weight loss, diarrhea and/or black stools. We present a rare case with isolated involvement of the stomach presenting only as recurrent hematemesis.

Methods: A 58-year-old male with past medical history of nephrolithiasis) and hypertension presented to the emergency room with complaints of vomiting fresh blood 5-6 times associated with belly pain. He denied any other symptoms. Patient had a similar episode 4 years prior and endoscopy showed gastritis. At that time, colonoscopy was completed and was determined to be normal. He was currently taking spironolactone and verapamil hypertension.

Results: On physical exam patient had mucosal pallor, the belly was benign and stool guaic test was negative. Lab tests revealed anemia with microcytoses, leukocytosis and acute/chronic renal insufficiency. He was started on broad spectrum intravenous antibiotics. Endoscopy showed erythematous, nodular and friable gastric mucosa resembling tumor. Biopsy with Congo red staining revealed amyloid deposits. The patient signed out against medical advise and was lost follow-up. Upon discharge he was afebrile and his white cell count was normal. He was discharged on augmentin and prevacid.

Conclusion: The incidence of gastrointestinal amyloidosis is variable depending on the type. Patients with certain disorders, like multiple myeloma, rheumatoid arthritis and chronic renal insufficiency, are at higher risk for developing amyloidosis. Definitive diagnosis can be obtained using biopsy of the affected organ tissue. Rectal biopsy is more sensitive than fat biopsy. Gastrointestinal involvement is associated with high morbidity, but relatively low mortality. Cause of death in patients with gastrointestinal amyloidosis is usually renal failure, restrictive cardiomyopathy or ischemic heart disease. Treatment is usually directed towards the symptomatic management of gastrointestinal symptoms and treating the underlying cause of amyloidosis. As illustrated by the case presented here, amyloidosis should be considered as one of the differential diagnoses in patients presenting with hematemesis.


Nancy Gundersen, MD*, Robert Kraichely, MD. Internal Medicine, Mayo Clinic Rochester, Rochester, MN, Gastroenterology, Mayo Clinic, Rochester, MN.

Purpose: We present the case of a 71 year old female of Japanese descent who presented with five months of chronic, watery diarrhea of up to 20 bowel movements daily. Her diarrhea was large volume without cramping, pain, or fevers, and persisted during the night and despite fasting. She also had a 20 pound weight loss and dehydration requiring eight hospitalizations for intravenous fluid administration and symptom control. Her past medical history was significant for human T-lymphotropic virus type I-associated adult T cell leukemia/lymphoma (HTLV-1 ATLL) diagnosed two years prior to admission. At that time, she also was diagnosed with Strongyloides stercoralis infection via small bowel biopsies. Though the parasite was successfully eradicated with ivermectin, strongyloides recurred four months prior to presentation, requiring further ivermectin treatment in addition to lifelong suppressive therapy. Past history also was remarkable for Clostridium difficile infection detected six months prior to presentation, successfully treated with a combination of oral metronidazole and vancomycin. A 72 hour stool collection confirmed large volume diarrhea of greater than 5000 grams. Investigation of the diarrhea was largely unremarkable, including evaluation of infectious (negative Clostridium difficile and enteric pathogen cultures, hepatitis serologies, strongyloides culture, ova and parasite studies, and small bowel aspirate), neuroendocrine (normal vasoactive intestinal peptide, thyroid studies, pancreatic polypeptide, calcitonin, 24 hour urine collection of 5-HIAA and histamine, gastrin and gastric pH level), anatomic (normal endoscopies, abdominal CT and MRI scans), and autoimmune (normal TTG, ANA, AMA, serum IgG/IgA levels, SPEP and UPEP) causes. She had little improvement with loperamide, octreotide, cholestyramine, or tincture of opium. Duodenal biopsy revealed intraepithelial lymphocytosis and an atypical CD4 positive T cell infiltrate, consistent with HTLV-1/ATLL infiltration of the small bowel. Chemotherapeutic treatment with alemtuzumab was recommended. HTLV-1 infection is endemic in many parts of the world, including southern Japan. It is a risk factor for strongyloides infection, which can present with diarrhea. Any patient with HTLV-1 infection and chronic diarrhea should be evaluated for strongyloides infection. Though there are few examples describing HTLV-1 lymphomatous infiltration of the small bowel, our case demonstrates it does occur. Refractory diarrhea in patients with HTLV-1 lymphoma requires extensive evaluation, and may even be an indication for chemotherapeutic treatment of ATLL, as in this case.


Ronald Concha, MD*, Ayse Aytaman, MD, Mujtaba Butt, MD, Rosemary Wieczorek, MD, Fidelina Desoto-Lapaix, MD, Gerald Fruchter, MD. Gastroenterology and Hepatology, SUNY Downstate Medical Center, Brooklyn, NY, Pathology, Gastroenterology, VA New York Harbor Health Care System, Brooklyn, NY.

Purpose: To support the possible role of H. pylori infection in the development of granulomatous gastritis. Case 1: A 25 year old male with no prior medical history presented with epigastric pain. EGD showed diffuse antral erythema with a beefy red appearance of the mucosa. Representative biopsies revealed severe chronic inflammation with scattered non-caseating granulomas. H. pylori organisms were identified. Stains for acid-fast bacilli and fungi were negative. PPD was negative. ESR was normal. CT chest was negative for hilar adenopathy. Patient was given clarithromycin based triple therapy for 14 days and his epigastric pain resolved. EGD repeated 6 weeks later demonstrated severe antral erythema with a nodular appearance. Biopsies revealed a single non-caseating granuloma, chronic inflammation and no H. pylori seen. Case 2: 64 year old male presented with upper GI bleed. EGD was performed and showed nodular antral mucosa with multiple shallow ulcerated lesions. Biopsies showed marked chronic active gastritis and non-caseating granuloma. H. pylori organisms were identified. Stains for acid-fast bacilli and fungi were negative. CRP, C-ANCA, and ACE-1 levels in serum were normal. CXR was normal. Patient received clarithromycin based triple therapy for 14 days. EGD repeated 6 weeks later revealed complete healing of the antral ulcerations. Biopsies revealed a single non-caseating granuloma, chronic inflammation, and no H. pylori infection seen. Discussion: Isolated granulomatous gastritis (IGG) is a very rare entity. It refers to an idiopathic chronic granulomatous reaction limited to the stomach. The diagnosis of IGG is made by the exclusion of other granulomatous diseases, such as Crohn's disease, sarcoidosis, infections (e.g., tuberculosis, histoplasmosis, syphilis), foreign bodies, malignancy, or vasculitis. Miyamoto et al. recently described a possible association of IGG with H. pylori since the granulomatous gastritis resolved in two patients one year after successful eradication of H. pylori. In our cases we observed clinical improvement with H. pylori eradication. However, incomplete resolution of granulomas was noted, possibly due to the short term endoscopic follow up after H. pylori eradication. The natural history and the optimal therapy of IGG have not been yet established.


Erin Karandish, MD*, Charlene Prather, MD, MPH. Gastroenterology and Hepatology, St. Louis University, St. Louis, MO.

Purpose: A 52 year-old healthy Caucasian female presented with two weeks of abdominal pain, vomiting, and fevers. She had lost 40 pounds over eight months. She denied diarrhea or family history of gastrointestinal disorders. Physical examination revealed a temperature of 38.2 degrees Celsius. Upper abdomen was tender to palpation. There was no peripheral lymphadenopathy. White blood cell count was 24.7 thousand/mL. Hemoglobin was 9.3 g/dL with MCV 78. Albumin was 2.7 g/dL. Computed tomography of the abdomen and pelvis revealed retroperitoneal and mesenteric lymphadenopathy as well as omental thickening. Excisional omental lymph node resection was performed, yielding architectureal effacement, histiocytic infiltrate, and fatty cysts. On flow cytometry, an aberrant B-cell population was identified, but cytogenetic and molecular testing were normal, as was bone marrow biopsy. Upper endoscopy revealed thickened, boggy folds and white plaques in the duodenum. Distal duodenal biopsies showed thickened, clubbed villi and histiocytic infiltration with a positive periodic acid-schiff (PAS) stain. Electron microscopy was performed, allowing the identification of bacillary organisms with a trilamellar wall. Whipple's disease is a systemic disease caused by Tropheryma whipplei, a gram-positive bacillus closely related to Actinobacter. It is more common in men than women. While any system may be affected, it classically presents with weight loss, chronic diarrhea, and migratory arthralgias. Fever, anemia and lymphadenopathy are also common, which may initially lead to efforts toward diagnosing lymphoma. Neurologic involvement may be isolated from other symptoms and can be irreversible, causing higher morbidity and mortality despite treatment. Diagnosis is secured by distal duodenal biopsy, which reveals thickening or clubbing of the villous architecture and histiocytic infiltration. PAS stain is positive, and electron microscopy reveals the bacillus with the typical trilamellar wall. Polymerase chain reaction is confirmatory but not routinely performed. Treatment with antibiotics is imperative, although the ideal regimen and duration has not been clearly established. A two week course of a third-generation cephalosporin followed by one to two years of trimethoprim/sulfamethoxazole has been generally recommended. This case illustrates both classic and unusual features of Whipple's disease and highlights the necessity of having a high index of suspicion for this rare disease, even when faced with common symptoms.

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Deborah Anghesom, MD*, Kendrick Che, DO, Ronald Griffin, MD, Christian Jackson, MD. Division of Gastroenterology, Loma Linda University Medical Center, Loma Linda, CA, Division of Gastroenterology, Loma Linda VA Medical Center, Loma Linda, CA.

Purpose: A 64-year-old man with diabetes, atrial fibrillation, hypertension, hepatitis C, and stage 5 chronic kidney disease not on dialysis was admitted with a 4 day history of weakness, black tarry stools and supratherapeutic INR on coumadin. His hemoglobin had dropped from 11 to 5.3. His current medications include metoprolol, amlodipine, furosemide, hydralazine, and metolazone for hypertension. He had also been taking ferrous sulfate 325 mg twice daily supplementation for the past two years. EGD revealed a normal appearing esophagus, small plaque-like lesions in the stomach, and multiple black pigmented spots distributed diffusely throughout the entire duodenum. A colonoscopy done the same day was entirely normal. As no active source of bleeding was found, a capsule endoscopy was performed the next day. This revealed multiple black pigmented lesions beginning in the first portion of the duodenum consistent with previous visualization on EGD but extended to the proximal jejunum. Biopsies revealed scattered pigment-laden macrophages within the intestinal villi and lamina propria which showed hemosiderin deposition with a positive Prussian blue stain consistent with pseudomelanosis. Discussion: Pseudomelanosis involving the jejunum had been described 3 times previously in the literature. Banai et al reported a case in 1997 involving the proximal jejunum in a patient with ulcerative colitis. Weinstock et al reported another case in 2003 involving the stomach, duodenum, and jejunum in a woman with chronic kidney disease also on long term ferrous sulfate medication. Moore et al described a case in 2007 involving the jejunum and ileum diagnosed using capsule endoscopy. Mechanisms of iron deposition on the intestinal walls are unknown. There appears to be a strong association with the use of iron supplementation, kidney disease, and hypertensive medications, namely furosemide and hydralazine, and the incidence of pseudomelanosis. Hemosiderin deposition may also be indicative of chronic, long standing gastrointestinal bleeding, seen in our patient as well as others in previous case studies, possibly secondary to vascular ectasias. Our case is the second described using capsule endoscopy and supports the association of oral iron therapy and hemosiderin deposition causing pseudomelanosis of the proximal small bowel.

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Paul Panzarella, MD*. Winthrop University Hospital, Mineola, NY.

Purpose: Gastroesophageal reflux disease (GERD) is a frequently occurring problem in patients with Cerebral Palsy (CP), often diagnosed at an advanced stage. The prevalence is about 50% in those with an IQ <50, with about 70% having endoscopic evidence of reflux esophagitis. Diagnosis may be difficult in CP patients due to atypical presentations such as frequent pulmonary infections, dental erosions, rumination and hematemesis. Though proton-pump inhibitors (PPI's) are effective, a percentage of CP patients do not respond to medical management. Success of Nissen fundoplication in CP patients is often cited in the pediatric literature but limited data is available in the adult population. We present a case of a 26 year old female with CP who presented to our institution with a history of chronic GERD refractory to PPI's. The patient reported worsening regurgitation with intermittent solid food dysphagia, significant nausea, abdominal pain and a 10 lb weight loss over a 3 month period. Upper endoscopy showed a small sliding hiatal hernia but was essentially normal. A BRAVO pH study revealed multiple episodes of acid reflux, while on high dose PPI. Impedance pH monitoring (on BID PPI) revealed 208 reflux events (normal <73) with evidence of proximal reflux as well. A gastric emptying study was normal. An initial esophageal manometry study at an outside institution showed findings suggestive of scleroderma esophagus with a low LES pressure and aperistalsis. However, serologic workup for scleroderma was negative. A manometry study was repeated in our institution, which revealed normal peristalsis and a normal mean LES pressure of 21 mmHg. Due to the refractory GERD and normal repeat manometry study, the patient was referred for laparoscopic Nissan fundoplication. The patient underwent Nissen fundoplication with complete resolution of her chronic reflux symptoms. One year post operatively, she continues to be asymptomatic and has regained her weight. To our knowledge, this is the first case of successful surgical management of GERD in an adult patient with CP and emphasizes the importance of this modality of treatment in patients with GERD refractory to medical management who are otherwise good surgical candidates.

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Neil Sharma, MD*, Vesna Vrcelj, MD, Prasad Kulkarni, MD. Department of Gastroenterology, University of South Florida, Tampa, FL, Department of Pathology, James A Haley Veterans' Administration Hospital, Tampa, FL.

Purpose: Primary melanoma of the esophagus is an extremely rare diagnosis. Bulky esophageal melanomas are even rarer. We report a case of Malignant Melanoma involving the esophagus in a patient with no prior history of the disease who presented with complaints of dysphagia. Case Report: 79 yo male with a history of prostate cancer, CAD with CABG, and CVA comes to the hospital with complaints of progressive solid food dysphagia and weight loss for 2 months. The patient had no history of Melanoma. A heterogeneously hyperpigmented bulky lesion was seen on EGD from 25 cm to 35 cm in the mid esophagus. The mass was friable and involved 2/3 of the lumen. A small, 3 mm, dark, hyperpigmented lesion was also seen in the gastric body. Biopsies confirmed Melanoma on s100 staining at both sites. Pt was note to have metastatic disease to the liver, and multiple lung nodules on staging CT. The primary Internal Medicine team did not note any evidence of Melanoma on skin exam. Eye exam done by Ophthalmology also did not find any evidence of Melanoma. In view of advanced disease, only palliation was sought. A gastric feeding tube was placed by interventional radiology. Pt was started on Temodar by Oncology, and sent with Hospice follow up. Discussion: Primary Esophageal Melanoma of the esophagus is rare diagnosis with less then 250 cases reported in the world literature to date. Esophageal Melanoma is a very aggressive tumor which carries a poor overall prognosis. There is limited data, primarily in the form of case reports, about potential surgical cures for very early stage disease. Treatment is evolving. Once metastatic, the prognosis for the disease is poor and palliative care should be considered.


Neil Sharma, MD*, Jonathan Keshishian, BS, Jean Johnson, MD, Jeffery Kooper, MD, Adel Daas, MD, Donald Amodeo, MD. Department of Gastroenterology, University of South Florida, Tampa, FL, Department of Pathology, Department of Gastroenterology, Internal Medicine, James A Haley Veterans' Administration Hospital, Tampa, FL, School of Medicine, University of South Florida, Tampa, FL.

Purpose: We report a case of anemia initially attributed to arteriovenous malformations and duodenitis. Further evaluation of the friable mucosa with endoscopy and biopsies revealed the true underlying diagnosis to be AL (Lambda) type Amyloidosis. Case Report: A 59 yo male with DM, CAD, and CKD presented to his PCP with a complaint of fatigue. He denied any gastroenterological complaints and was found to have a Hgb of 6.1 (g/dL) and was FOBT positive. On initial EGD, mild gastritis with a 2 or 3 AVMs were noted in the stomach along with a "friable" appearing duodenitis. The colonoscopy showed a few scattered submucosal hemorrhagic vessels. Since these limited findings did not explain the patient's degree of anemia, a capsule endoscopy was performed which showed angioectasias with limited active bleeding in the proximal jejunum and friable mucosa. Enteroscopy with biopsy of the distal duodenum and proximal jejunum was performed. There was significant oozing of the friable mucosa noted post biopsy. The biopsies were positive for Amyloidosis on Congo Red staining showing classic apple green birefringence. Fat pad biopsy was subsequently done and positive as well, with further staining confirming AL type. Renal and bone marrow biopsies were negative for Amyloidosis. The patient was referred to Oncology and was started on oral melphalan with high dose dexamethasone. Discussion: AL type Amyloidosis has an estimated incidence of 1 in 100,000 in Westernized countries, and its diagnosis upon biopsy from the gastrointestinal tract is even rarer. The presentation of acute on chronic anemia with no gastrointestinal complaints makes this case clinically unique.


Kenneth Reed, DO*, Ketul Patel, MD, Serge Sorser, MD, Robbie Taha, DO, Julia Greer, MD. Providence Hospital, Southfield, MI.

Purpose: Introduction Intussusception is a rare disorder in which the intestine prolapses into an immediately adjacent portion of the intestine forming a telescoping effect. This can often lead to obstruction. Intussusception is the most common cause of intestinal obstruction among children and its etiology is often idiopathic, while a small portion of cases are brought on by a viral infection. Intussusception in adults is a rare phenomenon. Most cases of adult intussusception are the result of an underlying organic cause. Case Presentation A 60-year-old African American male with a history of peptic ulcer disease presented to the emergency room complaining of intermittent abdominal pain associated with progressively worsening constipation of two weeks duration, as well as an unintentional 15 pound weight loss over the prior 2 months. Initial work up included computed tomography (CT) of the abdomen, which showed a large left renal mass, diffuse wall thickening in the descending colon associated with intussusception. Note was also made of a probable colonic mass and multiple pulmonary nodules. A colonoscopy was performed and findings were consistent with an intussusception and an obstructive lesion at 60 centimeters. Biopsies of the lesion were obtained and the area was tattooed with India ink. Necrotic tissue fragments and acutely inflamed benign colonic mucosa were identified on histologic examination. The patient underwent exploratory laparotomy with left partial colectomy and primary anastomosis. A left radical nephrectomy was also attempted, but the tumor was deemed unresectable. The pathology obtained from the partial colectomy was consistent with metastatic renal cell carcinoma. Discussion Renal cell carcinoma is rare, accounting for only 3% of all adult malignancies. Approximately 30% of the cases present with metastatic disease, with a 5-year survival of less than 5%. Intussusceptions account for only 3% of obstructions in adults and of these 90% have an identifiable pathologic lead point. The majority of intussusceptions are either enteric or ileocolic cases, with only one third of adult intussusceptions being colocolic or colorectal in nature. Approximately two thirds of colonic cases have a malignant basis compared to one quarter of enteric types. Debate has centered on whether to perform endoscopic reduction before surgical resection. However, recent trends have favored surgical resection without prior reduction in order to prevent tumor seeding.


Bryan Kavanaugh, MD*, Bridget Seymour, MD, Patricia Kozuch, MD. Gastroenterology & Hepatology, Thomas Jefferson University Hospital, Philadelphia, PA.

Purpose: A previously healthy 62-year-old male from Eastern Pennsylvania was admitted to the hospital with 10 weeks of "band-like" upper abdominal pain associated with nausea, constipation, post-prandial bloating, early satiety and a 30-lb weight loss. These symptoms were preceded by an ovoid, non-pruritic, non-vesicular rash on his right gluteus maximus that spontaneously resolved in 2 weeks. A prior extensive workup including upper and lower endoscopy, abdominopelvic CT, and MRI/MRA, small bowel series, and abdominal ultrasound was unrevealing. Supportive medications included tramadol, hydromorphone, colace, polyethylene glycol, and zolpidem. Physical exam on admission was significant for mild epigastric abdominal tenderness. Laboratory testing revealed an elevated ALT of 53 IU/L (normal <45) and CRP of 1.4 mg/dL (normal <0.80). A gastric emptying scan was performed with an emptying half time of 490 minutes (significantly delayed). On hospital day 2, the patient developed a left-sided facial droop. Brain MRI was normal. Lumbar puncture revealed a lymphocytosis, elevated protein, and elevated Lyme IgG titers. Elevated serum Lyme antibody was confirmed by Western blot. The patient was diagnosed with early-disseminated Lyme disease, complicated by cranial nerve VII palsy and gastroparesis. Ceftriaxone was initiated and continued for 4 weeks at home; a gastroparesis diet and metoclopramide were started. At follow-up 3 weeks later, the patient's symptoms were markedly diminished, and he had gained 5 lbs. Two months after discharge, the patient was asymptomatic except for a slight left-sided facial droop; a repeat gastric emptying scan was normal. Gastroparesis is a chronic disorder of delayed gastric emptying without mechanical obstruction. The most common etiologies are diabetes, post-surgical and idiopathic; a subset of the latter category may be associated with post-viral infections. Lyme disease is the most common tick-borne disease in the U.S. and is caused by the spirochete Borrelia burgdorferi, which can elicit a multisystem inflammatory response and is often accompanied by the hallmark rash, erythema migrans. The most common gastrointestinal symptom of Lyme disease is subclinical hepatitis, although dysmotility syndromes including gastroparesis and intestinal pseudo-obstruction have been reported. While the pathogenesis is not completely understood, gastroparesis secondary to Lyme disease may result from an inflammatory neuropathy of the enteric nervous system by direct invasion of B. burgdorferi or an indirect, cell-mediated inflammatory response. This case highlights an unusual presentation of a relatively common (regional) disease.


Nayantara Coelho-Prabhu, MD*, William Sanchez, MD. Gastroenterology, Mayo Clinic Rochester, Rochester, MN.

Purpose: Mirizzi Syndrome is characterized by biliary obstruction caused by a gallstone impacted in the cystic duct or gallbladder neck creating extrinsic compression and inflammation of the common bile duct. XGC is a rare chronic inflammatory condition of the gallbladder that can involve adjacent structures and thereby mimics gallbladder carcinoma.

Methods: N/A

Results: A 68 year old Caucasian male was evaluated due to a two month history of intermittent nausea, abdominal discomfort, elevated transaminases and hyperbilirubinemia. Medical history was significant for recurrent melanomatous skin cancer resections. He had consumed 2 alcoholic drinks per day for 25 years but had no risk factors for viral hepatitides. On initial assessment, serologic studies for viral hepatitis and autoimmune hepatitis were negative. Initial abdominal ultrasonography showed cholelithiasis but was otherwise unrevealing. Upon recurrence of symptoms, cholelithiasis without choledocholithiasis or dilated ducts was seen on repeat ultrasonography. A liver biopsy was performed which revealed portal inflammation, bile ductular proliferation and periportal fibrosis. MRI of the liver with MRCP showed intrahepatic ductal dilation, an extrinsic-appearing stricture of the proximal hepatic duct and irregular enhancement of the gallbladder wall, concerning for malignancy. ERCP confirmed the stricture at the proximal hepatic duct with a thin irregular wall. Brushings obtained were negative for malignant cytology, FISH was positive, and a serum CA19-9 was mildly elevated. The patient then underwent open cholecystectomy. Examination of the gallbladder was negative for malignancy, but instead revealed acute and chronic cholecystitis with cholelithiasis, peri-gallbladder inflammation, fibrosis and abscess formation with xanthogranulomatous inflammation.

Conclusion: We present a case of recurrent cholestatic hepatitis secondary to Mirizzi syndrome associated with xanthogranulomatous cholecystitis. While Mirizzi syndrome is seen in approximately 1% of all cholecystectomies, to our knowledge, only 4 cases associated with XGC have been reported previously in the literature. Because gallbladder carcinoma is a more common cause of Mirizzi syndrome, and XGC can be diagnosed only on pathologic examination of the resected gallbladder, cholecystectomy remains the treatment of choice if this association is suspected.


Brandon Craft, MD*, Marcelo Vela, MD. Digestive Disease Center, Department of Medicine, Medical University of South Carolina, Charleston, SC.

Purpose: Proton pump inhibitors (PPIs) are among the most commonly prescribed medications in the United States and are generally safe with few side effects. We report a case of recurrent symptomatic hypocalcemia associated with PPI use. A 33 year old female with a history of papillary thyroid cancer resection and subsequent diminished PTH activity requiring oral calcium carbonate to maintain normocalcemia presented with postprandial heartburn. She was started on omeprazole/sodium bicarbonate 40 mg once daily for GERD. After one week of therapy she developed cramping, tetany, and perioral numbness and tingling; serum calcium levels revealed a decrease in calcium levels from a baseline 9.0 to 6.5 mg/dL despite her oral calcium supplementation. Upon discontinuation of omeprazole/sodium bicarbonate, her calcium levels normalized and the symptoms of hypocalcemia resolved. Symptoms of GERD persisted and Esomeprazole 20 mg once daily was begun. After one week of therapy, the symptoms of hypocalcemia returned and serum calcium levels decreased to 7.3 mg/dL. Because esomeprazole 20 mg failed to control her heartburn, the dose was increased to 40 mg once per day without an increase in her calcium supplementation. This resulted in yet another episode of symptomatic hypocalcemia and a drop in calcium levels to 6.3 mg/dL. Her calcium supplementation was changed from calcium carbonate to calcium citrate, resulting in normalization of serum calcium levels; however, calcium carbonate caused significant dyspepsia. Eventually the dose of calcium citrate was titrated so that normocalcemia could be acheived with only minimal dyspepsia with esomeprazole 40 mg per day. The acidic environment in the stomach increases calcium solubility by releasing ionized calcium salts from its insoluble forms. Calcium malabsorption secondary to acid suppression by PPI therapy appears to have caused symptomatic hypocalcemia in this patient with parathyroid insufficiency. Gastrectomy and pernicious anemia have been shown to increase the risk of osteopenia and fracture, and recent studies suggest that chronic acid suppression therapy may lead to an increased risk of hip fractures possibly related to decreased calcium absorption. Symptomatic hypocalcemia due to PPIs is rarely seen in patients with normal parathyroid function. The case we report should alert clinicians about this possible complication of PPIs in patients with hypoparathyroidism, and should also be a reminder about the potential for asymptomatic hypocalcemia in other patients. Compared to calcium carbonate, calcium citrate appears to be better absorbed in the setting of pharmacological acid suppression and should be the supplementation of choice in these patients.


Zeeshan Perveze, MD*, Nasser Saffarian, MD, Ayaz Chaudhary, MD, FACG. Gastroenterology, Internal Medicine, Medical College of Georgia, Augusta, GA, Internal Medicine, Trinity Hospital, Minot, ND.

Purpose: Intro: There are numerous reports of acute hemolysis during hemodialysis over the past two decades. Etiology of hemolysis in hemodialysis patients is usually related to problems with dialysate, which include overheating; hypotonicity; contamination with formaldehyde, bleach, chloramine or nitrates from water supply; and copper from copper tubing. Red cell fragmentation can also occur due to pump malocclusion, inappropriate single needle dialysis ie high flow, or collapse of arterial line. Immune factors as with mismatched transfusion, drugs or hemoglobin abnormality can also be the cause for hemolysis. We report kinking of arterial blood line which resulted in acute pancreatitis as a consequence of acute hemolysis in chronic hemodialysis patient. Case: A 79 year old male with history of end stage renal disease was admitted for dialyisis. Right after dialysis, the patient experienced nausea, vomiting and abdominal pain radiating to the back. Labs drawn at dialysis showed hemoglobin of 8.2 g/dl, which dropped from 10.2 g/dl. Other labs included amylase of 1415 U/L, LDH 3965 IU/L, haptoglobin of 64.9 mg/dl and total bilirubin of 6 mg/dl. Electrolytes, PT, PTT, AST, ALT, complement factors, vitamin B-12, folate and ceruloplasmin were within normal range. ANA, serum and urine electrophoresis were negative. Peripheral blood smear revealed target cell, ovalacytes, schistocytes, helmet and tear drop cells. CT scan of abdomen was done which showed pancreatitis. Imaging did not reveal any gallstones and all other etiologies of pancreatitis were ruled out. Workup for paroxysmal nocturnal hemoglobinuria, glucose-6- phosphate dehydrogenase deficiency and autoimmune hemolysis was negative. There was no contamination with formaldehyde, chloramine, nitrates, copper or hypotonicity of the dialysate. Mechanical hemolysis due to kinking of line was presumed to be the cause. The patient was kept NPO, intravenous fluids and pain management was initiated. After replacing a new line there were no further hemolytic episodes. His condition improved during the hospital stay and was discharged home after two weeks. Discussion: Acute hemolysis on hemodialysis has become rare in recent years. This makes it extremely difficult to link hemolysis with acute pancreatitis in patients on hemodialysis unless it is high on the list of differential. In this case, after excluding all known causes of pancreatitis by radiology, serology and drug screening we proposed hemolysis induced by kinked hemodialysis blood line as a cause of acute pancreatitis. By emphasizing such an unusual mechanism of hemolysis leading to acute pancreatitis, we want to highlight the principle of root cause analysis which eventually led us to the etiology.


Shilpa Madadi, MD*, Mark Versland, MD. Department of Medicine, Division of Gastroenterology, University of Connecticut, Farmington, CT, Department of Medicine, Division of Gastroenterology, The Hospital of Central Connecticut, New Britain, CT.

Purpose: Introduction: Cytomegalovirus (CMV), a DNA virus is a member of the herpes virus family. CMV infection may affect all parts of the gastrointestinal tract, most commonly the esophagus and the colon. It is most often seen in immunocompromised patients. Small bowel involvement is rare. We herein present a case of an immunocompetent woman with isolated CMV infection of the small bowel. Case Report: A 65 year old Chinese woman was hospitalized with profuse diarrhea, vomiting, abdominal pain, and fever. Her past history was significant for hypertension, depression, osteoarthritis, hysterectomy and breast cancer 8 yrs ago treated with lumpectomy and radiation. Her medications included Lotrel, Celebrex, Prozac, Neurontin and Xanax. She was a non smoker and denied any drug use. On physical examination, the patient appeared ill. Her temperature was 101[degrees]F, heart rate 142 beats/min and blood pressure 100/72 mmHg. Her abdominal exam was notable for diffuse tenderness with no rebound. Laboratory values on admission were notable for an elevated creatinine but otherwise normal. Her blood and stool cultures were negative. Abdominal computed tomography showed thickening of the mid to distal small bowel. A small bowel follow through showed mucosal edema and ulcerations in the same area. Colonoscopy with intubation of the terminal ileum was normal including random biopsies. HIV test was negative. Her symptoms persisted and she was then taken for laparoscopy where a segment of abnormal small bowel was resected. Histological examination showed atypical cells with intranuclear inclusions. Immunoperoxidase stain for CMV was strongly positive. A high titer of IgM antibodies to CMV confirmed the diagnosis. Antiviral therapy was initiated and the patient recovered. Discussion: CMV infection in immunocompetent individuals is usually asymptomatic, or may produce a mononucleosis-like illness. It generally resolves without treatment. Small bowel involvement is very rare in immunocompetent individuals. A Medline search produced only 7 cases of CMV enteritis in immunocompetent subjects. The ages ranged from 18 to 68 years. Diarrhea was present in all the patients, abdominal pain in 5 cases and fever in 3 cases. Most patients were treated conservatively and symptoms resolved. Four required surgery for intestinal perforation or strictures. The characteristic histological findings of CMV enteritis are cytomegalic inclusion bodies in the endothelial cells of the capillaries. Ganciclovir and foscarnet are the primary treatment agents for clinically significant CMV infection. In conclusion, CMV enteritis is rare in immunocompetent patients but should be considered in the differential diagnosis of acute enteritis.


Ritesh Jha, MD*, Bashar Attar, MD, PhD, Mary Atten, MD. Division of Gastroenterology and Hepatology, Cook County-John H. Stroger Hospital, Rush University, Chicago, IL.

Purpose: Introduction: Ascariasis results in substantial morbidity and mortality worldwide. The diagnosis is usually incidental when the host passes a worm in the stool or vomit. Stool samples for ova and parasites will also demonstrate Ascaris eggs. Ascariasis diagnosed via EGD is an unusual method of diagnosing this disease. We report the case of a patient who presented with vague abdominal pain and was diagnosed with Ascariasis when an adult Ascaris worm was found in the second portion of his duodenum during EGD. Case: A 73 year old Filipino male with a history of vague abdominal pain presented for an elective outpatient EGD. Physical exam was unremarkable. Laboratory tests revealed a white blood cell count of 9,500/[mu]L with 8.0% eosinophils. EGD revealed a single, superficial, erythematous ulcer in the antrum. The patient was started on Protonix 40 mg twice daily and advised to return in 8 weeks for a repeat EGD to evaluate ulcer healing. Upon returning 8 weeks later for a follow-up EGD the patient reported no change in the character of his abdominal pain. Repeat EGD revealed a well healed ulcer in the gastric antrum, and upon entering the second portion of the patient's duodenum an 18 cm worm was identified. The worm was extracted using rat-tooth forceps, placed in formalin, and sent for histopathology. Pathology results confirmed the worm to be Ascaris lumbricoides. The patient was treated with a single dose of albendazole 400 mg. The patient reported complete relief of symptoms upon follow-up 4 weeks later. Discussion: Ascaris lumbricoides is the largest human intestinal nematode and can reach 40 cm in length. Nearly a fourth of the world's population is infected and Ascaris causes 20,000 deaths a year worldwide. The adult worm in the upper small bowel usually causes no symptoms but may cause vague abdominal symptoms in the form of abdominal pain, distension, nausea and occasional diarrhea. This case demonstrates that patients with vague abdominal pain, who are from or have traveled to endemic areas, should be evaluated for parasitic infections, particularly Ascariasis.


Scott Leverage, MD*, Luis Pena, MD. University of Kentucky, Lexington, KY.

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