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Gastric outlet obstruction: An unusual complication of tuberculousgastroduodenitis in two brothersG. Anton Decker, Darrell S. Pardi*. Mayo Clinic and Foundation,Rochester, MN.

Purpose: Involvement of the gastrointestinal tract by Mycobacteriumtuberculosis (MTb) is uncommon, and gastroduodenal tuberculous diseaseis rare. We present two brothers from Somalia with granulomatous gastritisand duodenitis with gastric outlet obstruction (GOO) from MTb.Methods: Case 1: A 20 year old man developed GOO with vomiting andweight loss. EGD showed a duodenal stricture with gastric and duodenalgranulomatous inflammation on biopsy. Acid-fast and fungal stains werenegative. He had no pulmonary symptoms and chest xray was normal.Abdominal CT scan revealed marked retroperitoneal and celiac lymphad-enopathy. Biopsy of these nodes showed necrotizing granulomas, but stainsfor MTb were negative. An MTb skin test (PPD) resulted in 30 mm ofinduration and erythema, and 4 drug MTb therapy was begun. Culture ofthe lymph nodes eventually grew MTb. His symptoms resolved over the 6months of therapy.Results: Case 2: The 29 yo brother of case 1 presented 4 years later withthe same symptoms and findings of GOO. EGD showed duodenal inflam-mation and obstruction, and biopsies revealed gastroduodenal granuloma-tous inflammation with negative MTb and fungal stains. His chest xray andPPD were negative. Abdominal CT showed large necrotic lymph nodes inthe region of the duodenum and pancreas. Biopsy of the nodes showed rareacid-fast organisms and polymerase chain reaction for MTb was positive.He is being treated with a 3 drug regimen with a good symptomaticresponse.Conclusions:MTb is a cause of granulomatous gastritis and duodenitis andcan cause gastric outlet obstruction. Negative stains for acid-fast bacilli, anegative PPD and absence of pulmonary disease do not exclude thediagnosis.

635

Metformin induced hepatotoxicity: A case reportAmeet Parikh, John Michel, Ravishankar Ramamoorthy, SimaVossough*. V.A. Medical Center, East Orange, New Jersey, UnitedStates.

Purpose: Metformin is an oral biguanide that is widely used in thetreatment of type 2 diabetes mellitus. We present a case of metformininduced hepatitis.Case:JB is a 54 year old WM with type 2 diabetes mellitus, hypertensionand obesity. He was treated with glyburide, metformin and fosinopril forseveral years. Due to poor glycemic control, the dose of metformin wasincreased from 1.5 gm daily to 2 gms daily. Two weeks after the increasein dose, the patient developed fatigue, anorexia, nausea and clay coloredstool. He denied the use of alcohol, tobacco or non-prescription medica-tions. Physical exam was unremarkable except for scleral icterus. Labsdrawn at that time showed a five-fold elevation in alkaline phosphatase, anda four-fold elevation in transaminases and total bilirubin (mainly directbilirubin), which is consistent with cholestasis. Serologies including ANA,AMA, anti smooth muscle antibody and hepatitis A, B and C profile werenegative. LDH, ceruloplasmin, serum electrolytes, folate and B12 werenormal. Ultrasound of abdomen demonstrated no evidence of bile ductdilatation or ascites. CT scan of abdomen showed borderline hepatomegaly.Liver biopsy showed portal and parenchymal inflammation (see photo).Copper and iron stains were normal. This appearance was felt to beconsistent with drug induced hepatitis. On withdrawal of metformin andglyburide, transaminases became normal and alkaline phosphatase returnedto baseline in 5–6 weeks. Patient was restarted on glyburide and continuedon fosinopril with no increase in transaminases or in alkaline phosphatase.The temporal association of increase in dose of metformin with the onsetof symptoms, and its resolution with discontinuation of metformin impli-cates it as the cause of hepatitis in this patient. This is further substantiated

by the fact that reintroduction of glyburide and continuation of fosinoprildid not cause elevation of liver chemistries.Conclusion: This represents the third case of metformin induced hepatitisin the worldwide literature. Metformin induced hepatotoxicity appears tobe a rare idiosyncratic reaction associated with intrahepatic cholestasis andelevations in serum transaminases. In the present and previous cases,hepatotoxicity resolved within several weeks following discontinuation ofmetformin.

636

A rare complication of ulcerative colitis: An extensive venousthrombosis of major abdominal vesselsPankaj Patel, Mohammed Barawi, Kavita Kongara, Frank Gress, JamesGrendell*. State University of New York, Stony Brook, New York.

Purpose: Introduction: Patients with inflammatory bowel disease have anincreased risk of thrombotic events that are multifactorial in nature. It couldbe secondary to dehydration, thrombocytosis. Protein C and Protein Sdeficiency, increased Factor VII activity and anticardiolipin Ab levels.Treating thrombotic events during active ulcerative colitis can be trouble-some to clinicians due to higher risk of bleeding.Methods: Case Report: A 52-year-old male with 15 year history of ulcer-ative colitis managed only with Asacol po and Rowasa enema came withexacerbation of his colitis. Despite the initial steroid treatment, he contin-ued to have abdominal cramps and blood diarrhea. CT-scan of the abdomenrevealed an extensive clot formation of portal vein, splenic vein, bothsuperior and inferior mesenteric veins. His hematological workup of plate-let count, PT/PTT, Protein C and Protein S levels, Factor V mutation,anticardiolipin Ab, prothrombin gene mutation and hemocystine levelswere normal. He was started on IV Heparin and IV steroids and onlyrequired one unit of blood without any major bleeding episode. After tendays of hospitalization, he was discharged on Coumadin and 6-MP withquiescent colitis. Six months later he was doing well with no abdominalpain, diarrhea or blood in the stool.Conclusions:Discussion: Thrombotic events are not uncommon in ulcer-ative colitis. Heparin use is not contraindicated if there is no massivebleeding and transfusion can be given as needed. In addition, heparin mayhave a beneficial effect controlling active ulcerative colitis as it has beenreported previously.

637

Thrombocytopenia: An unusual manifestation of acute hepatitis BinfectionPankaj Patel, Jehad Miqdadi*. State University of New York, Buffalo,NY, United States.

Purpose:Hepatitis B is a common infection with an estimated worldwideprevalence of 1 billion individuals. It is estimated that every year more than50 million people are infected with the hepatitis B virus. We report a caseof acute hepatitis B infection presenting with thrombocytopenia. A reviewof the literature reveals only four previously reported cases of thrombocy-topenia secondary to acute hepatitis B infection.Methods: A 24-year-old Hispanic male presented with fatigue, bruisesafter minor trauma, epistaxis and bleeding from the lips and gums. He hadseveral risk factors for hepatitis B including intravenous drug abuse,sharing needles, recent incarceration, tattoos and multiple sexual partners.

On examination he had petichae, bleeding from the gums and buccalmucosa. The trunk and extremities were covered with petichae. The abdo-men was not distended or tender, the liver was palpable just below the rightcostal margin with a smooth border. The spleen was not palpable.Laboratory DataPlt. count 5000/cc, Hb 13.3 g/dl, WBC 6600/ccPT 11.9 s, PTT 29.5s, Albumin 3.5 g/dlBilirubin 2.6 mg/dl, ALP 155 U/LAST 1248 U/L, ALT 3565 U/LHBSAg Positive, HBC IgM Positive

2596 Abstracts AJG – Vol. 95, No. 9, 2000