title: Interferon decreases hepatocellular carcinogenesis in patients with cirrhosis caused by the hepatitis B virus: a pilot study.
abstract: BACKGROUND
  To elucidate the influence of long term interferon administration on the rate of occurrence of hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV)-related cirrhosis, the authors analyzed 313 consecutive patients with cirrhosis.
  
  
  METHODS
  Of the 313 patients, 94 underwent long term intermittent administration of interferon for > or = 6 months, and the remaining 219 patients received no interferon or other antiviral drug.
  
  
  RESULTS
  Cumulative occurrence rates of HCC in the group treated with interferon and the untreated group were 4.5% and 13.3%, respectively, at the end of 3 years; 7.0% and 19.6%, respectively at the end of 5 years; and 17.0% and 30.8%, respectively, at the end of 10 years. The rate of HCC development in the treated group was significantly lower than that of the untreated group (P = 0.0124). The Cox proportional hazard model revealed that interferon treatment was an independent contributing factor in lowering the rate of carcinogenesis (odds ratio = 0.39; P = 0.031) even after correction by significant covariates in multivariate analysis. The virologic study showed that the role of interferon therapy from the viewpoint of cancer prevention was much more significant in patients with a HBV DNA concentration of > or = 10 milliequivalents.
  
  
  CONCLUSIONS
  Interferon therapy for patients with HBV-related cirrhosis significantly decreased the HCC rate, especially in patients with a larger amount of serum HBV DNA. If interferon is administered properly for a selected group of patients, an effective strategy of cancer prevention can be achieved, even in patients with cirrhosis.
authors.affiliation: Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ikeda
authors.forename: S
authors.initials: S
authors.lastname: Saitoh
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
authors.forename: A
authors.initials: A
authors.lastname: Tsubota
authors.forename: M
authors.initials: M
authors.lastname: Fukuda
authors.forename: I
authors.initials: I
authors.lastname: Koida
authors.forename: Y
authors.initials: Y
authors.lastname: Arase
authors.forename: K
authors.initials: K
authors.lastname: Chayama
authors.forename: N
authors.initials: N
authors.lastname: Murashima
authors.forename: H
authors.initials: H
authors.lastname: Kumada
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000473:pathology / Q000517:prevention & control*; D002471:Cell Transformation, Neoplastic; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D006509:Hepatitis B; D006515:Hepatitis B virus; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000150:complications / Q000628:therapy* / Q000821:virology*; D008113:Liver Neoplasms / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D016898:Interferon-alpha