title: Clinical and molecular virological differences between fulminant hepatic failures following acute and chronic infection with hepatitis B virus.
abstract: Clinical and molecular biological characteristics were compared between patients who presented with fulminant hepatic failure following acute infection with hepatitis B virus (HBV) and those who developed hepatic failure during they carried HBV. The 11 patients with acute HBV infection had higher levels of alanine aminotransferase (mean +/- SD: 4943 +/- 2867 vs 1157 +/- 678 IU/L, P < 0.01), more often with a single peak (91% vs. 0%, P < 0.001), and lower total bilirubin level (15.3 +/- 4.4 vs 28.1 +/- 14.3 mg/1000 ml, P < 0.01) than the 13 patients with chronic HBV infection. Hepatitis B surface antigen was detected less often (55% vs. 100%, P < 0.05) and viral DNA polymerase less frequently (0% vs. 46%, P < 0.05) in the patients with acute than chronic HBV infection. Hepatitis B e antigen was detected in one (9%) patient with acute infection, less frequently than in six (46%) patients with chronic infection (P < 0.05). Mutations in the precore region was detected in HBV DNA clones from ten (91%) patients with acute infection and only in those from eight (62%) patients with chronic infection. All HBV DNA clones from the five (38%) patients with chronic infection that did not have precore mutations, however, possessed mutations in the core promoter. These results indicate that HBV mutants incapable of translating hepatitis B e antigen would play a major role in fulminant hepatic failure occurring after acute HBV infection. In contrast, HBV variants with core promoter mutations for reducing the transcription of hepatitis B e antigen would play an additional role in fulminant hepatic failure developing during chronic infection.
authors.affiliation: Division of Gastroenterology, Showa University Fujigaoka Hospital, Yokohama, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Yoshiba
authors.forename: K
authors.initials: K
authors.lastname: Sekiyama
authors.forename: H
authors.initials: H
authors.lastname: Okamoto
authors.forename: M
authors.initials: M
authors.lastname: Mayumi
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D001483:Base Sequence; D004252:DNA Mutational Analysis; D004279:DNA, Viral; D005260:Female; D006501:Hepatic Encephalopathy / Q000097:blood / Q000276:immunology / Q000821:virology*; D006509:Hepatitis B / Q000097:blood / Q000150:complications / Q000276:immunology / Q000821:virology*; D006512:Hepatitis B Core Antigens / Q000235:genetics; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000150:complications / Q000276:immunology / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic
chemical_list: D004279:DNA, Viral; D006512:Hepatitis B Core Antigens; D000410:Alanine Transaminase