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Clinical Observation
February 14, 2000

Fulminant Non–A-G Viral Hepatitis Leading to Liver Transplantation

Author Affiliations

From the Liver Institute and Department of Medicine D, Rabin Medical Center, Beilinson Campus, Petah Tiqva, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel (Drs Ben-Ari, Zemel, and Tur-Kaspa); Hepatobiliary Surgery and Liver Transplantation Service, Hôpital Paul Brousse, Villejuif, Paris, France (Drs Samuel and Gigou); and the Liver Unit, Rambam Medical Center, Haifa (Dr Baruch), and the Department of Medicine B, Soroka Medical Center, Beer-Sheva (Dr Sikuler), Israel.

Arch Intern Med. 2000;160(3):388-392. doi:10.1001/archinte.160.3.388
Abstract

Background  All hepatotropic viruses are known to cause fulminant hepatic failure (FHF). However, in 30% to 40% of patients with FHF, the precise cause remains unknown. We aimed to better define this subgroup.

Methods  We evaluated the clinical course and outcome of 7 patients admitted during a 22-month period with fulminant viral hepatitis leading to liver transplantation; none had serologic or molecular evidence of hepatitis A, B, C, D, E, or G viral infection, thus the term non–A-G viral hepatitis. All known etiologies of FHF were excluded.

Results  All patients had prodromal symptoms suggestive of viral causes. Mean age was 30 years. The interval between onset of jaundice and appearance of encephalopathy was 23 days (range, 4-50 days). Five patients had grade III/IV encephalopathy. Serum alanine aminotransferase levels showed a single peak of activity. The duration between first symptoms and liver transplantation was 28 days (range, 12-71 days). Results of histological study of the explanted liver showed submassive (4 patients) or massive (3 patients) hepatocyte necrosis. In all patients, results of polymerase chain reaction analysis did not detect hepatitis B virus DNA, hepatitis C virus RNA, or hepatitis G virus RNA in the explanted liver. After transplantation, 2 patients showed (6 months later) increased liver enzyme levels of undetermined cause, and results of a liver biopsy showed mild lobular hepatitis; 1 patient had lymphoproliferative disorder (Epstein-Barr virus–originated); and 1 patient, aplastic anemia, which is known to be associated with seronegative viral hepatitis. The latter patient died, whereas the other 6 patients are alive (survival rate, 86%).

Conclusions  Our patients with non–A-G viral hepatitis had a severe acute onset with progressive FHF requiring liver transplantation. There is some suggestion of recurrent viral disease after transplantation implicating other unknown viruses in the etiology.

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