title: Anticarcinogenic impact of interferon on patients with chronic hepatitis C: a large-scale long-term study in a single center.
abstract: BACKGROUND
  The anticarcinogenic capacity of interferon (IFN) was assessed in a cohort of Japanese patients with chronic hepatitis C en masse.
  
  
  METHODS
  The rate of hepatocarcinogenesis was analyzed in 2,166 patients with chronic hepatitis C, of whom 1,654 had received IFN therapy while 512 had not.
  
  
  RESULTS
  Crude rates of hepatocarcinogenesis in treated and untreated patients were 2.6 and 4.6% at the end of the 5th year, 5.8 and 12.7% at the 10th year and 13.9 and 23.9% at the 15th year (after completion of IFN therapy for those treated) (p < 0.001). IFN decreased the hazard ratio of carcinogenesis to 0.42 (p < 0.001) in multivariate analysis with adjustments for significant covariates including fibrotic stage, gamma-glutamyl transpeptidase level, gender, platelet count and age. Among the 1,654 patients treated with IFN, 606 (36.6%) achieved persistent loss of hepatitis C virus (HCV) RNA and an additional 266 (16.1%) gained normal levels of alanine aminotransferase without loss of HCV RNA for 6 months or longer after the completion of IFN therapy. Cumulative rates of hepatocarcinogenesis in sustained virological responders and biochemical responders were 1.4 and 2.0% at the end of the 5th year, 1.9 and 3.6% at the 10th year and 1.9 and 7.5% at the 15th year, respectively. The hazard ratio of sustained virological response was 0.10 (p < 0.001), and that of biochemical response was 0.12 (p < 0.001). Normalization of aminotransferase levels after IFN therapy without loss of serum HCV RNA decreased hepatocarcinogenesis.
  
  
  CONCLUSIONS
  IFN significantly decreased the rate of hepatocarcinogenesis in patients with chronic hepatitis C as a whole in Japan, even in those who fail to clear HCV RNA from serum.
authors.affiliation: Department of Gastroenterology, Toranomon Hospital, Toranomon 2-2-2, Minato-ku, Tokyo 105-8470, Japan. ikedakenji@tora.email.ne.jp
authors.forename: Kenji
authors.initials: K
authors.lastname: Ikeda
authors.forename: Yasuji
authors.initials: Y
authors.lastname: Arase
authors.forename: Satoshi
authors.initials: S
authors.lastname: Saitoh
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Someya
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hosaka
authors.forename: Hitomi
authors.initials: H
authors.lastname: Sezaki
authors.forename: Norio
authors.initials: N
authors.lastname: Akuta
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Suzuki
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Kumada
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000209:etiology / Q000517:prevention & control*; D015331:Cohort Studies; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D007370:Interferon Type I / Q000627:therapeutic use*; D016899:Interferon-beta / Q000627:therapeutic use*; D007564:Japan; D008113:Liver Neoplasms / Q000209:etiology / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011994:Recombinant Proteins; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D007370:Interferon Type I; D011994:Recombinant Proteins; D016899:Interferon-beta