title: Risk factors for development of hepatocellular carcinoma in patients with chronic hepatitis C after sustained response to interferon.
abstract: BACKGROUND
  Interferon (IFN) is expected to prevent the progression of hepatitis C virus infection to cirrhosis and the development of hepatocellular carcinoma (HCC), but there have been several reports of the development of HCC after a sustained response to IFN. Our aim was to elucidate the incidence and clinical features of, and risk factors for, HCC in sustained responders to IFN, taken for the treatment of chronic hepatitis C.
  
  
  METHODS
  We designed a retrospective cohort study conducted at 16 major Hospitals. The subjects were a total of 1056 patients showing sustained responses, 29 of whom developed HCC.
  
  
  RESULTS
  The incidence of HCC per 100 person-years was 0.56 (95% confidence interval, 0.35-0.76) in sustained responders. By the Cox proportional hazard model, we found that older age, higher serum aspartate aminotransferase level, and lower platelet count before IFN therapy were independent risk factors associated with the development of HCC. A risk index of HCC development, based on the coefficients of these risk factors, was used to classify patients into three groups, with low, intermediate, and high risk. The incidence rates of HCC for these three groups were 0.11, 0.44, and 1.98 per 100 person-years, respectively. The median period to the development of HCC was 4.6 years (range, 1.4-9.0 years), and there were no other specific clinical features of the HCC that developed in these patients.
  
  
  CONCLUSIONS
  This study suggests that the risk of development of HCC is not completely eliminated in sustained responders to IFN. These findings may be useful in determining a follow-up strategy after a sustained response to IFN.
authors.affiliation: Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
authors.forename: Masafumi
authors.initials: M
authors.lastname: Ikeda
authors.forename: Shigetoshi
authors.initials: S
authors.lastname: Fujiyama
authors.forename: Motohiko
authors.initials: M
authors.lastname: Tanaka
authors.forename: Michio
authors.initials: M
authors.lastname: Sata
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Ide
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yatsuhashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Watanabe
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology* / Q000517:prevention & control; D002648:Child; D018450:Disease Progression; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D007372:Interferons / Q000627:therapeutic use*; D008113:Liver Neoplasms / Q000453:epidemiology* / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010976:Platelet Count; D012074:Remission Induction; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors
chemical_list: D000998:Antiviral Agents; D007372:Interferons; D001219:Aspartate Aminotransferases