Clinical and molecular virological differences between fulminant hepatic failures following acute and chronic infection with hepatitis B virus

✍ Scribed by Inoue, Kazuaki; Yoshiba, Makoto; Sekiyama, Kazuhiko; Okamoto, Hiroaki; Mayumi, Makoto

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 116 KB
• Volume: 55
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/(sici)1096-9071(199805)55:1<35::aid-jmv7>3.0.co;2-p

✦ Synopsis

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 levels (15.3 ± 4.4 vs. 28.1 ± 14.3 mg/100 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.