title: Interferon inhibits progression of liver fibrosis and reduces the risk of hepatocarcinogenesis in patients with chronic hepatitis C: a retrospective multicenter analysis of 652 patients.
abstract: A retrospective multicenter analysis of 652 patients with chronic hepatitis C who have been treated with interferon (IFN) was performed to assess the effects of IFN on the clinical course and development of HCC. During a mean follow-up of 54.8 months, hepatocellular carcinoma (HCC) developed in 7.0% of the patients. The rate was significantly higher in the patients who did not respond to IFN treatment than in those with sustained virological response and those who obtained a normalization of alanine aminotransferase levels despite the presence of HCV RNA (incomplete response) (P < 0.01). Using multivariate Cox's proportional hazard model, alcohol abuse (P < 0.05) and a higher level of fibrosis (P < 0.05) before treatment were the significant background factors associated with HCC development in the patients who did not respond to IFN. Interestingly, a significant increase in the rate of HCC development occurred in patients who had a histological finding of progressive fibrosis (F3). In addition, patients with low histological staging scores were likely to have an incomplete response, even if a sustained virological response was not obtained. IFN produced an improvement in histological activity and fibrosis stage in the second biopsy specimens irrespective of the clinical outcome when compared against untreated subjects.
authors.affiliation: Department of the Internal Medicine III, School of Medicine, Niigata University, Niigata-City, Japan.
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Takimoto
authors.forename: Shogo
authors.initials: S
authors.lastname: Ohkoshi
authors.forename: Takafumi
authors.initials: T
authors.lastname: Ichida
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Takeda
authors.forename: Minoru
authors.initials: M
authors.lastname: Nomoto
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Asakura
authors.forename: Akira
authors.initials: A
authors.lastname: Naito
authors.forename: Shigeki
authors.initials: S
authors.lastname: Mori
authors.forename: Kojiro
authors.initials: K
authors.lastname: Hata
authors.forename: Kentaro
authors.initials: K
authors.lastname: Igarashi
authors.forename: Hidenori
authors.initials: H
authors.lastname: Hara
authors.forename: Hironobu
authors.initials: H
authors.lastname: Ohta
authors.forename: Kenji
authors.initials: K
authors.lastname: Soga
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Watanabe
authors.forename: Tomoteru
authors.initials: T
authors.lastname: Kamimura
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000517:prevention & control*; D005260:Female; D019698:Hepatitis C, Chronic / Q000628:therapy*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D016899:Interferon-beta / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000628:therapy*; D008113:Liver Neoplasms / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies
chemical_list: D016898:Interferon-alpha; D016899:Interferon-beta; D000410:Alanine Transaminase