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 utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANB fulminant hepatic failure (FHF) patients. RESULTS: none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitis patients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANB FHF patients and subsequently found no evidence of HBV DNA. CONCLUSIONS: we did not find evidence implicating HCV or HEV in presumed viral NANB FHF or as agents contributing to or causing the liver failure in nonviral NANB FHF patients with autoimmune hepatitis, drug-induced hepatotoxicity, or halothane hepatotoxicity.
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 utilized the polymerase chain reaction to amplify HCV and HEV RNA sequences and assays to detect antibodies to HCV and HEV in the acute phase sera of eight presumed viral NANB and seven nonviral NANBfulminant hepatic failure (FHF) patients. RESULTS: none of the 15 patients had detectable HCV or HEV RNA or elevated HCV and IgM-HEV antibody titers in their acute phase sera. Three patients, all with features of autoimmune hepatitis, had raised IgG-HEV antibody titers. Due to the possibility of serologically undetectable hepatitis B virus (HBV) infection in fulminant hepatitispatients, we performed polymerase chain reaction amplification of HBV genomic DNA in acute phase sera of the presumed viral NANBFHFpatients and subsequently found no evidence of HBV DNA. CONCLUSIONS: we did not find evidence implicating HCV or HEV in presumed viral NANBFHF or as agents contributing to or causing the liver failure in nonviral NANBFHFpatients with autoimmune hepatitis, drug-induced hepatotoxicity, or halothanehepatotoxicity.
Authors: J C Sáiz; M Sans; A Mas; E Olmedo; X Forns; F X López-Labrador; J C Restrepo; J Costa; J M Salmerón; M Guilera; S Ampurdanés; J M Sánchez-Tapias; M T Jiménez de Anta; J Rodés Journal: Gut Date: 1997-11 Impact factor: 23.059