title: Sustained biochemical remission after interferon treatment may closely be related to the end of treatment biochemical response and associated with a lower incidence of hepatocarcinogenesis.
abstract: Clinical background and incidence of hepatocellular carcinoma (HCC) of patients with chronic hepatitis C who obtained biochemical remission without eradication of virus (biochemical response) after interferon (IFN) treatment was retrospectively analyzed for 755 patients. Annual incidence of HCC was significantly lower in the patients with biochemical response and sustained response than that of the patients that did not show these responses. Logistic regression analysis showed that only the normalization of alanine aminotransferase (ALT) value at the end of IFN treatment was a significant factor for biochemical response. Annual incidence of HCC was significantly lower in the patients who obtained normalization of ALT values at the end of treatment than those who did not. Patients who were younger, who had a lower level of activity and fibrosis indices in histology, higher platelet count, and who were given more higher total dose of IFN were more likely to attain normalization of ALT levels at the end of treatment, and this was related to biochemical response. Low incidence of HCC in patients who obtained normalization of ALT values at the end of treatment was likely because they were in the earlier stage of chronic hepatitis. Active treatment of chronic hepatitis C with interferon in the early phase of the disease may bring about a biochemical response in some patients, even if sustained virological response is not obtained.
authors.affiliation: Department of the Internal Medicine III, School of Medicine, Niigata University, 1-754 Asahimachi-Dori, Niigata City, 951-8122.
authors.forename: Kenta
authors.initials: K
authors.lastname: Suzuki
authors.forename: Shogo
authors.initials: S
authors.lastname: Ohkoshi
authors.forename: Masahiko
authors.initials: M
authors.lastname: Yano
authors.forename: Takafumi
authors.initials: T
authors.lastname: Ichida
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Takimoto
authors.forename: Akira
authors.initials: A
authors.lastname: Naitoh
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
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Aoyagi
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology* / Q000517:prevention & control / Q000821:virology; D002471:Cell Transformation, Neoplastic; D005260:Female; D016174:Hepacivirus / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D015994:Incidence; D007372:Interferons / Q000627:therapeutic use*; D008113:Liver Neoplasms / Q000453:epidemiology* / Q000517:prevention & control / Q000821:virology; D008297:Male; D008875:Middle Aged; D012074:Remission Induction; D012189:Retrospective Studies
chemical_list: D000998:Antiviral Agents; D007372:Interferons; D000410:Alanine Transaminase