NON-A, NON-B FULMINANT-HEPATITIS IS ALSO NON-E AND NON-C

Objectives: to define the roles of the hepatitis C and E viruses (HCV and HEV) in non-A, non-B (NANB) fulminant hepatitis. Methods: we utili zed the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase ser a of eight presumed viral NANB and seven nonviral NANB fulminant hepat ic failure (FHF) patients. Results: none of the 15 patients had detect able HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in the ir acute phase sera. Three patients, all with features of autoimmune h epatitis, had raised IgG-HEV antibody titers. Due to the possibility o f serologically undetectable hepatitis B virus (HBV) infection in fulm inant hepatitis patients, we performed polymerase chain reaction ampli fication of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA. Concl usions: we did not find evidence implicating HCV or HEV in presumed vi ral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with antoimmune hepatitis, drug-induced hepatotoxicity, or halothane hepatotoxicity.