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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.

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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.

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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

HBSAb NegativeHAV Ab Total Positive, HCV PositiveHDVAb Negative, HIV NegativeResults: Platelet transfusions, IVIG and solumedrol were administered toincrease the platelet count. A bone marrow biopsy showed increasedmegakaryocytes. Because he was on steroids, Lamivudine was empiricallystarted to suppress viral replication. He was discharged on tapering steroidsand Lamivudine. On follow-up, 3 months after discharge, he had serocon-verted to HbSAg negative and his platelet count AST and ALT werenormal. He was continued on Lamivudine for 3 more months.Conclusions: Acute Hepatitis B infection can cause thrombocytopeniathrough an immune mediated mechanism.

Lamivudine may prevent patients who have acute hepatitis B and are onsteroids from developing chronic hepatitis B.

638

Iatrogenic portal hypertension in a liver transplant patientAnca Pop, M.D., Robert Gold, M.D., Patrick Dean, M.D., HosseinAmiri, M.D., Mark A Levstik, M.D. University of Tennessee Memphis.

Background: Vascular complications after liver transplantation are com-mon. Iatrogenic creation of an arterio-portal fistula is rare and might be amajor factor of morbidity if unrecognized.Case Presentation:Twenty eight year old Caucasian male underwent livertransplantation (OLT) for alpha 1 antitrypsin deficiency. Pre OLT gastro-intestinal bleeding led to creation of a distal side to side spleno renal shunt,followed by the placement of a transjugular intrahepatic porto-systemicshunt (TIPS). The patient continued to experience episodes of varicealbleeding starting 3 weeks post transplant. Endoscopic ligation of esopha-geal varices was initially successful. Five months post transplant patientdeveloped duodenal variceal bulb bleeding refractory to endoscopic ther-apy, requiring emergent TIPS placement. At that time extremely high portalgradient pressures (50–60 mm Hg) were noted. Three months later thepresence of a superior mesenteric artery (SMA) branch to splenic vein (SV)fistula/aneurysm was identified angiographically. Patient underwent twosessions of proximal embolization that were unsuccessful. One year post-transplant he presented with ascites, pleural effusions, poor nutritionalstatus and repeated episodes of spontaneous bacterial peritonitis. Patientwas referred for re-transplantation. The steal syndrome and resultant in-testinal angina contributed to meal avoidance and poor nutritional status.Child Pugh score was 8 due to the presence of encephalopathy and analbumin of 3.3. Liver biopsy showed only central vein and sinusoidalengorgement with normal liver architecture. Abdominal ultrasound notedpatent TIPS. Angiography demonstrated a large SV aneurysm and SMA toSV fistula via the gastroepiploic arteries. Measured portal pressure troughthe TIPS was 78 mm Hg. A new episode of variceal bleeding promptedemergent laparotomy with fistula take down and aneurysm resection. Theaneurysm ruptured intraoperatively. Inflating a previously inserted intraaor-tic balloon for a total of 16.5 minutes interrupted arterial inflow from theaorta (from infradiaphragmatic region below). This allowed the aneurysmrepair. Postoperative evolution was satisfactory with initial portal veinthrombosis and later recanalization. He was discharged home 3 weeks lateron coumadin and previous immunosuppression.Conclusion: Superior mesenteric artery/gastroepiploic artery to splenicvein fistula is exceedingly rare, but creation of iatrogenic fistulas followingsurgical shunting, needs to be included in the differential diagnosis ofpost-transplant portal hypertension. Early recognition and repair mightavoid retransplantation.

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Early diagnosis and treatment of acute hepatitis C (HCV)Richard S. Phillips, M.D., FACG, Perry Hookman, MD, FACG; JamieS. Barkin, MD, MACG. University of Miami, School of Medicine/MountSinai Medical Center, Division of Gastroenterology, Miami, FL.

Acute Hepatitis C (HCV) infection is rarely identified, though it is one ofthe most important causes of chronic liver disease in the U.S.Purpose: The purpose of this case study is to report the pitfall of acuteHepatitis C diagnosis and to show the effectiveness of treatment to preventthe development of chronic liver disease.Case Report: A 46-year old man, whose girlfriend had chronic HCV,presented with an acute onset of jaundice following a one-week prodromeof constitutional symptoms. Initial laboratory tests revealed ALT 1500 U/L(nl 0–42), AST 3715 U/L (nl 0–48) and total bilirubin 1.9 mg/dl, whichpeaked to 4.5 mg/dl (nl 0–1.3). Hepatitis A, B and C serology, monospotscreen and autoimmune markers including antinuclear antibody, smoothmuscle antibody and liver-kidney microsome antibody, were negative.CBC, platelet count, prothrombin time and thyroid profile were normal. AnHCV RNA quantitative level by PCR was 240,000 copies/ml genotype 3a,similar to his infected sexual partner. A repeat anti-HCV by EIA waspositive one month later. He was begun on alpha interferon 3 MU daily plusRibavirin 1200 mg daily, which after two months, he arbitrarily increasedhis dose of interferon to 5 MU daily which he continued for an additionalfour months. Liver enzymes normalized. At the end of this 6-month periodof treatment, HCV RNA ultra qualitative PCR assay was negative.Discussion:Despite the high sensitivity of screening assays, false negativeanti-HCV by EIA is likely to occur early in the course of acute HepatitisC—the so-called window period. As was seen in this case, early detectionof HCV RNA by PCR is an important tool for confirming the suspecteddiagnosis of acute HCV infection, as it can be detected as early as 1 to 2weeks after exposure, well before anti-HCV EIA becomes positive. Thusearly detection of acute HCV often requires HCV RNA by PCR. Combi-nation therapy with interferon and Ribavirin should be initiated as soon asthe diagnosis of acute HCV is made, as it may be effective in decreasingthe incidence of chronic infection and the chronic carrier state that usuallyoccurs in more than 80% of HCV patients. Further studies are necessary todetermine the optimum dose and duration of interferon therapy in acuteHCV.

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EUS assisted endoscopic removal of a large Brunner’s glandadenomaB.J. Pollack, S. Kessler, J. Birk, J.C. Anderson. University Hospital,Division of Gastroenterology, State University of New York at StonyBrook, Stony Brook, New York.

Brunner’s Gland Adenomas are rare lesions that are usually located in theduodenal bulb. We present a case of a huge Brunner’s gland adenoma thatwas safely removed by endoscopic polypectomy in a piecemeal fashion,after assessment of the lesion by EUS (endoscopic ultrasonography).Case Report: A 39-year-old man presented with melena and vomiting.Physical examination was unremarkable except for mild orthostaticchanges. Upper endoscopy revealed a huge pedunculated polyp extendingfrom the anterior wall of the bulb. There were several small ulcers withinthe bulb and second portion that appeared to be secondary to irritation fromthe large polyp. An EUS revealed 2 different tissue types: the base had thecharacteristics of a lipoma while the upper portions of the polyp appearedmore akin to a typical pedunculated polyp. Snare polypectomy was at-tempted with end-viewing and side-viewing endoscopes, but was unsuc-cessful. The polyp was then pulled back into the stomach and endoscopicelectrosurgical polypectomy was performed utilizing an end-viewing en-doscope. The snare was placed around the upper-half of the polyp and usingunblended (coagulation) current the polyp tip was transected. The snarecould then be placed over the base, and using blended current, the remain-ing half was removed. At microscopy, the polyp consisted of a mixedepithelial and soft tissue lesion with a well-circumscribed nodule of Brun-ner’s glands distinct from a lipomatous base. The resected specimen was3.5 cm3 3.5 cm3 2.8 cm. The patient was discharged the following dayand remains well 10 months after resection.Discussion:Brunner’s gland adenomas are extremely rare tumors. Endo-scopic snare resection has been described in 12 prior case reports. Extreme

2597AJG – September, 2000 Abstracts