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Case–control study for the identification of virological factors associated with fulminant hepatitis B
Author(s) -
Kusakabe Atsunori,
Tanaka Yasuhito,
Mochida Satoshi,
Nakayama Nobuaki,
Inoue Kazuaki,
Sata Michio,
Isoda Norio,
Kang JongHon,
Sumino Yasukiyo,
Yatsuhashi Hiroshi,
Takikawa Yasuhiro,
Kaneko Shuichi,
Yamada Gotaro,
Karino Yoshiyasu,
Tanaka Eiji,
Kato Junji,
Sakaida Isao,
Izumi Namiki,
Sugauchi Fuminaka,
Nojiri Shunsuke,
Joh Takashi,
Miyakawa Yuzo,
Mizokami Masashi
Publication year - 2009
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2009.00519.x
Subject(s) - medicine , fulminant hepatitis , hepatitis b virus , fulminant , odds ratio , hepatitis b , asymptomatic carrier , asymptomatic , hazard ratio , confidence interval , immunology , virology , gastroenterology , hepatitis , virus
Background: Host and viral factors can promote the development of fulminant hepatitis B (FHB), but there have been no case–control studies for figuring out virological parameters that can distinguish FHB. Methods: In a case–control study, virological factors associated with the development of FHB were sought in 50 patients with FH developed by transient hepatitis B virus (HBV) infection (FH‐T) and 50 with acute self‐limited hepatitis B (AHB) who were matched for sex and age. In addition, 12 patients with FH developed by acute exacerbation (AE) of asymptomatic HBV carrier (ASC) (FH‐C) were also compared with 12 patients without FH by AE of chronic hepatitis B (AE‐C). Results: Higher HBV DNA levels, subgenotype B1/Bj, A1762T/G1764A, G1896A, G1899A and A2339G mutation were significantly more frequent ( P < 0.05), while hepatitis B e‐antigen was less frequent in the FH‐T patients than AHB. In multivariate analysis, G1896A mutation (odds ratio [OR], 13.53; 95% confidence interval [CI], 2.75–66.64), serum HBV DNA more than 5.23 log copies/mL (OR, 5.14; 95% CI, 1.10–24.15) and total bilirubin more than 10.35 mg/mL (OR, 7.81; 95% CI, 1.77–34.51) were independently associated with a fulminant outcome by transient HBV infection. On the other hand, in comparison with the patients between FH‐C and AE‐C groups, there was no significant difference of virological factors associated with the development of FHB. Conclusion: A number of virological factors have been defined that may distinguish FH‐T from AHB in a case–control study. The pathogenic mechanism of FHB between transient HBV infection and AE of ASC would be different.