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Gut 2004;53:425-430 doi:10.1136/gut.2003.030353
  • Liver

Benefit of interferon therapy in hepatocellular carcinoma prevention for individual patients with chronic hepatitis C

  1. H Yoshida1,
  2. R Tateishi1,
  3. Y Arakawa2,
  4. M Sata3,
  5. S Fujiyama4,
  6. S Nishiguchi5,
  7. H Ishibashi6,
  8. G Yamada7,
  9. O Yokosuka8,
  10. Y Shiratori1,*,
  11. M Omata1
  1. 1Department of Gastroenterology, University of Tokyo, Tokyo, Japan
  2. 2Third Department of Internal Medicine, Nihon University, Tokyo, Japan
  3. 3Second Department of Internal Medicine, Kurume University, Fukuoka, Japan
  4. 4Third Department of Internal Medicine, Kumamoto University, Kumamoto, Japan
  5. 5Third Department of Internal Medicine, Osaka City University, Osaka, Japan
  6. 6Department of Clinical Research, National Nagasaki Medical Centre, Nagasaki, Japan
  7. 7Centre of Liver Disease, Kawasaki Hospital Kawasaki Medical School, Okayama, Japan
  8. 8First Department of Internal Medicine, Chiba University, Chiba, Japan
  1. Correspondence to:
    Dr H Yoshida
    Department of Gastroenterology, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo 113-8655, Japan; yoshida-2imh.u-tokyo.ac.jp
  • Accepted 20 October 2003

Abstract

Background: An increase in the incidence of hepatocellular carcinoma (HCC) in Japan since the 1980s suggests an imminent outbreak in other countries where viral spread occurred more recently. Interferon therapy for chronic hepatitis C, in general, has been shown to prevent HCC.

Aims: To determine the scale of benefit in individual patients.

Subjects: Histologically proven chronic hepatitis C patients in the Inhibition of Hepatocarcinogenesis by

Interferon Therapy (IHIT) cohort (Ann Intern Med1999;:), as updated in March 2003.

Methods: The lifetime risk for HCC was calculated based on HCC incidence rates, stratified by sex, age, fibrosis stage, and outcome of interferon therapy. The gain in HCC free survival was defined as the difference between expected HCC free survival with sustained virological response and that without.

Results: The gain in HCC free survival was greater when a patient was younger and fibrosis was more advanced. For example, a 30 year old male with F3 fibrosis gained 12.4 years by attaining sustained response while a patient with F1 fibrosis older than 60 years gained less than one year. For a treatment protocol with a given sustained response rate, prior estimation of the gain can be obtained by multiplying the calculated HCC free survival for responders by the response rate.

Conclusions: The gain in HCC free survival may serve as an indicator of the benefit of interferon therapy in terms of HCC prevention and be useful in the consideration of indication and selection of treatment protocol for individual patients.

Footnotes

  • ↵* Present address: Department of Gastroenterology, Hepatology, and Infectious Diseases, Okayama University, Okayama

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