was negative for lymphoma. A small bowel study failed to reveal anyabnormality.Conclusion: MALT lymphoma is a distinctive type of B–Cell lymphomathat arises from the Mucosa associated lymphoid tissue in the GI tract, lung,salivary gland and thyroid. In the GI tract MALT lymphomas usually occurin the stomach and rarely in the large intestine. MALT lymphoma of thecolon usually presents as multiple polypoid lesions. They could presentwith tenderness in the right lower quadrant and also as an obstructive lesionif they grow large enough. MALT lymphoma of the colon presenting withchronic lower GI blood loss is rare, but possible. Thus, like adenocarci-noma, MALT lymphoma of the colon should be considered in the differ-ential diagnosis of iron deficiency anemia.

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PORTAL HYPERTENSION DUE TO HEPATOPORTALSCLEROSIS IN A PATIENT WITH HIV INFECTIONEric M. Ward, M.D., Timothy A. Woodward, M.D., Murli Krishna, M.D.and James R. Spivey, M.D.*. Gastroenterology and Hepatology, MayoClinic, Jacksonville, FL and Pathology, Mayo Clinic, Jacksonville, FL.

Purpose: A 51–year–old male with a history of infection with the humanimmunodeficiency virus (HIV) presented for evaluation after an episode ofgastrointestinal bleeding. The patient was taking a number of antiretroviralmedications as well as dapsone. Physical examination revealed hepato-splenomegaly but no ascites or other findings suggestive of chronic liverdisease. Laboratory testing demonstrated anemia and thrombocytopenia buthepatic synthetic function was preserved. Abdominal ultrasonography andcomputed tomography were significant only for enlargement of the spleenand liver. Distal esophageal varices were seen during upper endoscopy.Hepatic venography demonstrated normal hepatic veins. The correctedsinusoidal pressure was 20–25 mm Hg. A transjugular liver biopsy wasperformed, and the pathological findings were consistent with hepatoportalsclerosis.

Hepatoportal sclerosis is a well–recognized cause of noncirrhotic portalhypertension. Pathologically, obliterative changes occur in the portal veinbranches. Sinusoidal dilatation and mononuclear infiltration may be seen.The clinical course is characterized by complications of portal hypertensionwith normal hepatic synthetic function. The cause of the disease is notknown, but a number of toxins and medications have been suggested asetiologic agents. Management of esophageal varices and other complica-tions of portal hypertension with beta–blockade, transjugular intrahepaticportosystemic shunts, or surgically placed portosystemic shunts is thecornerstone of therapy for patients with hepatoportal sclerosis.

A computerized Medline search failed to demonstrate any reportedassociations between HIV infection and hepatoportal sclerosis. Further-more, there have been no published cases of hepatoportal sclerosis occur-ring in patients taking antiretroviral medications or dapsone. Our experi-ence with this patient may represent a previously unrecognized hepaticcomplication of HIV disease, treatment with anti–HIV medications, or theuse of dapsone.

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NON–FULMINANT HEPATITIS A COMPLICATED BY ACUTERENAL FAILUREManzoor Rather, M.D.*, Mahmooda Sayeed, M.D. and ShailenderSingh, M.D. Department of Internal Medicine, Mercy Catholic MedicalCenter, Darby, PA and Department of Endocrinology, Thomas JeffersonUniversity Hospital, Philadelphia, PA.

Purpose: A 60–year–old caucasian male with no significant past medicalhistory was admitted with a 3–day history of fever, malaise and decreasedurinary output. On examination his vitals were normal. He had scleralicterus but no stigmata of chronic liver disease. The rest of the physicalexamination was unremarkable. Labs: CBC, peripheral smear, coagulationprofile and ESR were normal. Biochemistry showed blood urea nitrogen of52 mg/dl and serum creatinine of 4.6 mg/dl. Liver function tests revealed

serum AST of 2053 U/L, ALT of 1717 U/L, alkaline phosphatase of 222U/L, serum total bilirubin 11.7mg/dl, direct bilirubin 7.8 mg/dl, totalprotein 6.3 gm/dl and serum albumin 2.2 gm/dl. Urinalysis showed cloudyurine with specific gravity of 1.016, pH 5.5, bilirubin 3�, moderate occultblood and 400 mg/dl of protein. Urinary sediment showed 10 RBC/hpf withno casts. Urinary sodium was within normal limits. Serology for hepatitiswas positive for antihepatitis A IgM antibody. Assays for leptospira, CMV,Hepatitis B, hepatitis C and cryoglobulins were negative. Toxicologyscreen and ANA was negative along with normal complement levels (C3,C4). Ultrasonography revealed no abnormality of the kidneys. On thirdadmission day he became anuric with serum creatinine value of 9.9 mg/dland hemodialysis was initiated. He was maintained on hemodialysis for sixweeks with complete recovery of renal function. Unfortunately renal bi-opsy could not be performed since the patient refused for the procedure. Hisliver funtion showed gradual recovery and returned to normal level afterfour weeks.Discussion: Hepatitis A is a mild and self–limiting infection of the liverwith good prognosis. Acute renal failure (ARF) complicating hepatitis A isvery rare. The exact mechanism of ARF in hepatitis A is unclear. Thedifferent mechanisms proposed include, prerenal azotemia leading to acutetubular necrosis, immune complex mediated glomerulonephritis, endotox-ins and hyperbilirubinemia induced renal vasoconstriction and a directcytopathic effect of Hepatitis A virus. The likely mechanism of ARF in ourpatient is glomerular injury suggested by the presence of proteinuria andhematuria.

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FORTUITOUS M2A OBSTRUCTION LEADS TOLOCALIZATION OF UNSUSPECTED VASCULAR STRICTUREDawn M. Sears, M.D., Andres Avots–Avotins, M.D.*, Joseph White,M.D. and Kim Culp, M.D. Gastroenterology, Scott & White MemorialHospital, Temple, TX.

Purpose: M2A capsule endoscopy allows visualization of the entire smallbowel without a scope. The ability to diagnose small bowel pathology hasbeen limited to modalities such as Sonde enteroscopy, push enteroscopyand small bowel radiography. The ability to deploy the capsule down theentire bowel and transmit images externally is truly a new frontier withuntold possibilities. The following case demonstrates the limits of theformerly standard techniques of small bowel evaluation.

A 64–year–old previously healthy Caucasian female was hospitalizedfor anemia with a hemoglobin of 6.9 and an MCV of 75. She denied signsor symptoms of gastrointestinal blood loss. After transfusion, she under-went colonoscopy, esophagogastroduodenoscopy, CT of abdomen andpelvis, and a small bowel follow through. All of these studies wereunrevealing. She was discharged home on iron, rebeprazole, HRT andaspirin. At follow up, her hemoglobin increased to 12.7, she had positiveanti–gliadin antibodies, while her anti–reticulin and anti–endomysial an-tibodies were negative. EGD with small bowel biopsies and enteroscopy to100 cm were performed and both were found to be normal. M2A capsuleendoscopy was performed. The images from the study revealed an ery-thematous narrowing seen at 1 hour and 24 minutes after ingestion. Thecapsule appeared to remain at this stricture until study conclusion 3 hourslater. Since the capsule did not appear to pass into the colon, the patient wasasked to return weekly for fluoroscopic localization of the retained capsule.The patient remained asymptomatic and the capsule location did not changesignificantly. Four weeks after M2A capsule ingestion, she underwentsurgical resection of the stricture and surrounding 2.6 cm of ileum. A subtlepalpable thickening could be appreciated during surgery. Gross evaluationof the resected ileum revealed a raised, slightly ulcerated, polypoidal,circumferential lesion. Histologic inspection showed fibrosis and neuro-vascular bundles. Her post–operative course has been unremarkable andher hemoglobin remains stable.

This patient did not have her small bowel lesion discovered with stan-dard techniques. The inability of the M2A capsule to pass beyond thestricture led to definitive operative localization of the probable cause of her

S128 Abstracts AJG – Vol. 97, No. 9, Suppl., 2002