Subjects had pre and post 48 week treatment biopsies assessed using themodified Knodell score by a single pathologist blinded to clinical findingsand pre/post biopsy status. Inflammatory component scores were comparedbetween biopsies with improved fibrosis and those with no change infibrosis.Results: Average age was 47.6 � 5.20 years. 77.8% were males and 64.4%Caucasian, 11.1% Hispanic and 24.5% other. 82.2% had genotype 1. Of the45 patients, 48.9% had improved fibrosis of 1 point or more, while 31.1%of patients had no change in fibrosis and 20% had worse fibrosis. Overallthere was a significant improvement in HAI from 5.76 � 1.87 to 4.31 �1.94 (P � 0.01) and in Fibrosis from 2.47 � 1.08 to 2.00 � 1.31 (P �0.01). In patients with improvement in fibrosis, this change in HAI wasattributed to a significant improvement in portal inflammation. There wasa linear correlation (r � 0.313, P � 0.05) between improvement in portalinflammation and improvement in fibrosis. Lobular activity improved inboth groups (see table).

Conclusions: Treatment of Non-Responders to Rebetron with PegylatedInterferon Alpha- 2b plus Ribavirin significantly improves HAI and Fibro-sis. The improvement in fibrosis is related to a decrease in portal andlobular inflammation.

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FATAL FULMINANT VARICELLA HEPATITIS PRESENTINGAS ACUTE ABDOMINAL PAINAline Charabaty Pishvaian, M.D., James H. Lewis, M.D.*. GeorgetownUniversity Hospital, Washington, DC.

Purpose: We report the case of a 38-year-old male, on prednisone for anasthma exacerbation, admitted for severe abdominal pain and fever of38.6C. His abdomen was soft, with normal abdominal sounds, non-tenderto palpation but with voluntary guarding; the liver span was 18cm. He hada diffuse eruption of vesicles, pustules and hemorrhagic bullae over thetrunk, neck, face and scalp. The CBC, chemistries, amylase, lipase, bili-rubin and alkaline phosphatase were normal. AST and ALT were 59 IU/Land 125 IU/L respectively. The ultrasound and CTScan of the abdomen,small bowel follow-through, upper GI series and EGD were essentiallynormal. Within 24hours of his admission, the patient developed severeencephalopathy, oliguric renal failure, respiratory failure, distributiveshock and disseminated intravascular coagulopathy. At this time, his lab-oratory values were as follow: AST 14,600 IU/L, ALT 6,540 IU/L, INR 10,creatinine 5, platelets count 44, PTT 62. The patient was started onacyclovir 10mg/kg q8 hours for varicella hepatitis. A biopsy of the skinlesions revealed severe acantholysis, bullous formation in the epidermisand multinucleated giant cells. Direct immunofluorescence and viral cul-ture of the skin tissue were positive for VZV. The patient expired 13 daysafter his presentation despite aggressive resuscitation.

Primary varicella infection rarely affect adults but carries a higherincidence of visceral involvement in this population. There are only fewcase reports in the literature of fulminant varicella hepatitis. Most patientsare immunocompromised and present with abdominal or back pain, acharacteristic skin rash and fever. Fulminant liver failure develops after fewdays of mild elevation of transaminases, followed by multiorgan failure.Diagnosis can be made by serology, serum PCR or skin biopsy. Liverbiopsy or necropsy often reveals hemorrhagic necrosis, eosinophilic Cow-dry type A intranuclear inclusions, intracellular virions and multinucleatedgiant cells. The diagnosis and initiation of treatment of varicella hepatitis

are often delayed or made post-mortem, and most reported cases are fatalwithin 3 to 13 days of presentation. Hence, it’s imperative to considervaricella hepatitis when an immunocompromised patient presents withunexplained abdominal pain whether or not a skin rash accompanies it.

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FULMINANT HEPATIC FAILURE: A RARE PRESENTATIONOF T-CELL LARGE GRANULAR LYMPHOCYTIC LEUKEMIAMuhammad Alam, M.D., Rony Abou-Jawde, M.D., Bo Shen, M.D.*.The Cleveland Clinic Foundation, Cleveland, OH.

Purpose: Large granular lymphocyte (LGL) leukemia is a clonal disease ofthe LGLs with 85% of cases being from a T-cell lineage. It is characterizedby the infiltration of bone marrow (BM), spleen, and liver by LGLs. In 40%of patients, it is associated with other diseases, such as autoimmune andhematologic diseases. One third of patients are asymptomatic at diagnosis.Symptoms are generally mild and nonspecific. Prognosis of LGL leukemiais favorable, with a long survival even if left untreated. We recentlyencountered a case of LGL leukemia presented as fulminant hepatic failure,which has never been reported in literature.Case ReportResults: A 31 year old non-alcoholic Caucasian male with no past medicalhistory presented to the Emergency Department with one week history ofnausea, fever, cough, headache, and myalgia. He was initially treated withazithromycin and Hycodan. On physical examination, he had confusion,jaundice, and asterixis. There was no hepato-splenomegaly or signs ofchronic liver disease. There was family history of non-Hodgkin’s lym-phoma and acute leukemia. Lab tests showed AST 2180, ALT 2619,bilirubin 3.3, albumin 2.8, alkaline phosphatase 89, sodium 131, hemoglo-bin 15.8, WBC 7.6, ferritin 85953, TIBC 240, transferrin saturation 100%,and iron 240. The patient was found to be in coagulopathy with INR 1.8,APTT 39, fibrin clot 500, AT3 assay 65, D-dimer 18630 and platelets of 19.Peripheral smear revealed 46% atypical lymphocytes. Chest X-ray showedbilateral pleural effusions. Liver vascular US was normal. CT abdomen justrevealed mild ascites. BM biopsy was performed, with flow cytometryrevealing large lymphocytes expressing CD 2, 3, 8, 5, 7, 26 and 57 with theabsence of CD 16 and 56. There was also characteristic hemophagocytosis.BM examination confirmed the diagnosis of LGL leukemia. Transjugularliver biopsy demonstrated diffuse infiltration of macrophages and atypicallymphocytes with hemophagocytosis and necrosis. On hospital day 3, hiscondition deteriorated and developed multi-organ failure and expired onday 6.Conclusions: Fulminant hepatic failure (FHF) can result from a widevariety of causes including viral infection and toxins, and rarely malignantinfiltration. In up to 40% of cases, the cause of FHF could not be identified.Treatment depends on early identification and intervention. Critical reviewof blood smears and early performance of bone marrow biopsy may behelpful for the identification of uncommon hemato-oncologic causes ofFHF.

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DAILY IFN ALPHA 2B AND RIBAVIRIN VS PEG IFN ALPHA2B AND RIBAVIRIN. IS THERE A DIFFERENCE?Urooj Ahmed, M.D., Murat Aladag, M.D., Ayaz Chaudhary, M.D.,Harlan Wright, M.D., Bakr Nour, M.D., Ahmet Gurakar, M.D.,Robert R. Schade, M.D., F.A.C.P.*. Medical College of Georgia,Augusta, GA and Nazih Zudhi Transplantation Institute, Oklahoma City,OK.

Purpose: We compared the results of treatment with PEG IFN Alpha 2band Ribavirin to the results of a historical group that received daily 3MUof IFN Alpha 2b and Ribavirin to determine if there was any difference inshort and durable virologic response between these treatments.Methods: We compared the results of two separate trials. The first trialcompleted in 1999 employed daily IFN Alpha 2b 3MU per day andRibavirin in a group of 25 non-cirrhotic patients(Daily IFN group). The

S104 Abstracts AJG – Vol. 98, No. 9, Suppl., 2003