slight variations of viral load only detected with sensitive HBV DNAassays. The relative strength of this group is relatively unknown, but couldbe a very important to treatment with new and safe antivirals, given the wellknown risk of hepatocellular carcinoma and progression to cirrhosis, beinggenerally excluded from regular trials because of normal transaminases(ALT).Methods: We prospectively evaluated 148 HBsAg positive patients during54 months. HBV DNA was assessed every 6–9 months by PCR. Histologyand immunohistochemmistry was available in all patients.Results: Positive HBV DNA was detected in 115/148, with normal ALTin 26% (39). All positive DNA with normal ALT were AntiHBe�(HBeAg-). Only 22% of HBsAg � patients had minimal lesions, withvariable degrees of hepatitis and cirrhosis in all others. Only 23% areproperly defined as inactive carriers, as 77% had DNA persistently ortemporarily detected by PCR. Cirrhosis was diagnosed in 12% of inactivecarriers, 8% of normal ALT patients with � DNA, and in 35% of abnormalALT patients.Conclusions: We conclude that beyond the classical candidates for anti-viral treatment (51%), in our population of patients, a significative group(26%) could be enrolled in therapeutic trials if the treatment goal is toerradicate HBV DNA.

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THE NEED OF VACCINATION AGAINST HEPATITIS A INPATIENTS WITH CHRONIC LIVER DISEASE : FACT ORFANCY?Guilherme Macedo, Ph.D.* Susana Lopes, M.D. Fernando Araujo, M.D.Tavarela Veloso, Ph.D. H S Joao, Porto, Portugal.

Purpose: It has been suggested that there is an ongoing change in recentyears, in the prevalence of anti HAV antibody among portuguese popula-tion, particularly related to overall improvement in sanitary conditions,both in urban and rural areas in the last 3 decades. This lower prevalencewould be related with the lower infection rate in children, adolescents andyoung adults.Methods: Given the recommendations for anti HAV vaccination in chronicliver disease patients, we analysed the prevalence of anti HAV antibody in320 patients from the Hepatology out-patient clinic with mean age of 48years (18-75). Seroconversion was assessed at the 7th month (1 month afterbooster dose).Results: Only in 13 patients (4%) with chronic liver disease, the anti HAVwas not detected. Their mean age is 25 (18–40) years old. Anti HAVprevalence was 87% in � 40 years old patients (85/98) and 100% in � 40years old patients (222/222). Their clinical features are presented (5 withHCV chronic hepatitis, 6 with HBV chronic hepatitis, 1 with AlagilleSyndrome and one post liver transplantation for fulminant hepatitis) andtheir seroconversion rate was 100% .Conclusions: We conclude that, even if among out-patient population thereis a lower prevalence of anti HAV antibody, pre vaccination testing ismandatory, and its use is expected to be exceptional in chronic liver diseasepatients older than 40.

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CORRELATION OF SERUM HEPATITIS C VIRUS RNA LOADAND ITS ASSOCIATION WITH ALANINEAMINOTRANSFERASE IN PATIENTS REPORTING TOGASTROENTEROLOGY AND LIVER CLINIC OF HOLYFAMILY, RAWALPINDI, PAKISTANMohammad Umar, F.C.P.S., Faiz Anwar, F.C.P.S.,Hamama Tul Bushra, F.C.P.S.*, Atifa Shoaib, F.C.P.S.,Amir Chohan, M.B.B.S. Rawalpindi Medical College, Rawalpindi,Punjab, Pakistan.

Purpose: Serum Hepatitis C virus RNA load is among the importantfactors in determining the response to anti-viral therapy in chronic HepatitisC patients. This study was conducted to see pattern of viral load in patients

with chronic hepatitis C in local population and its association with alanineAminotransferase.Methods: We have studied viral load in 50 patients. These are divided into4 categories according to age. We also calculated the relationship betweenviral load and alanine Aminotransferase (ALT). Patients were tested forALT and viral load with Amplicor HCV RNA essay for qualitative detec-tion and DNA essay for quantitative estimation.Results: Total patients are 50, with age ranging from 22 to 56 years. Meanage is 38.94 � 8.52 SD. Females are 21 (42%), Males are 29 (58%); agebetween 20 to 30 years are 8 (16%), between 31 to 40 years are 25 (50%),between 41 to 50 are 12 (24%), 5 (10%) have age greater than 50 years.Mean viral load is 20.44 MEq/ml. 19 (38%) patients have viral load lessthan 3 MEq/ml and 31 (62%) patients have greater than 3 MEq/ml. MeanALT is 112 IU/L.Conclusions: Most patients have viral load � 3 MEq/ml (3 million copies/ml). Mean viral load in patients more than 50 years was significantly (p �0.01) higher than other patients. No positive correlation was found betweenALT and HCV RNA viral load (p � 0.05).

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A CASE OF HEPATIC AMYLOIDOSIS WITH A RAPIDLYPROGRESSIVE COURSEGeorgios I. Papachristou, M.D.*, Shelly S. Lo, M.D.,Toby O. Graham, M.D. University of Pittsburgh Medical Center,Pittsburgh, PA.

Background: Amyloidosis is a rare disorder of protein metabolism thatleads to extracellular tissue deposition of insoluble proteinaceous material.Although hepatic involvement is common in systemic amyloidosis, clini-cally significant liver failure is very rare. We report a case of primaryamyloidosis, AL type, with massive hepatomegaly complicated by swiftlyprogressive liver failure.Case: A 58 year-old African American female visited her primary physi-cian with a 10 day history of epigastric fullness and fatigue. She reportedhaving dark urine, pale stools, and pruritus. On examination she had scleralicterus and a vertical liver span of 20 cm. Laboratory findings weresignificant for abnormal liver tests (AST 91 IU/liter , ALP 1887 IU/liter ,total bilirubin 8.9 mg/dl with a direct of 5.2 mg/dl), hypoalbuminemia (1.8g/dl), and mild coagulopathy (INR 1.4). CT scan showed hepatomegalywith diffusely homogenous low attenuated hepatic parenchyma suggestiveof an infiltrative process. Liver biopsy revealed diffuse parenchymal infil-tration by acellular material with hepatocyte compression and loss. Theimmunostain for amyloid protein P was positive. The M spike (IgG kappa)on electrophoresis confirmed a diagnosis of primary amyloidosis, AL type.One month following diagnosis, she developed liver failure, complicatedby S. viridans sepsis, renal and respiratory failure, and expired.Discussion: Primary systemic amyloidosis (AL) is a plasma cell dyscrasiaassociated with a monoclonal protein derived from immunoglobulin lightchain fragments. The liver is commonly involved in all forms of systemicamyloidosis, especially in AL. Hepatomegaly, modest elevations in ALP,and hypoalbuminemia are the most common features. The presence ofhyperbilirubinemia suggests an ominous prognosis and most deaths arerelated to renal or cardiac complications. Treatment of AL focuses onsuppressing the underlying B cell monoclonal proliferative disorder. Treat-ment options include chemotherapy alone, or chemotherapy followed byautologous stem-cell transplantation in patients with a high performancestatus. In individuals with isolated advanced hepatic amyloidosis, ortho-tropic liver transplantation followed by autologous stem-cell transplanta-tion has been recommended. In the above case, a question remains whetherinitiation of chemotherapy or liver transplantation at the time of presenta-tion, would have altered the patient’s rapid downhill course.

S91AJG – September, Suppl., 2003 Abstracts