title: Type C-chronic hepatitis patients who had autoimmune phenomenon and developed jaundice during interferon therapy.
abstract: Of a total of 2342 patients with type-C chronic hepatitis treated with interferon (IFN) at this hospital, 3 patients developed jaundice during the course of IFN therapy, but all 3 of them exhibited negative conversion of hepatitis C virus (HCV)-RNA following readministration of IFN. All 3 patients were assessed as having "probable autoimmune hepatitis (AIH)" in accordance with the AIH scoring system, indicating association with an "autoimmune phenomenon". Readministration of IFN at a low-dose induced activation of the autoimmune phenomenon, leading to fulminant hepatocellular impairment. As a result, HCV-RNA content dropped dramatically, possibly contributing to the negative conversion of HCV-RNA noted following the readministration of IFN. At present, no adequate therapy has been established for type-C chronic hepatitis with autoimmune manifestations. However, in conclusion, our findings suggested that: IFN should be a frontline regiment: (1). if autoantibody titers are low or patients are rated as having "probable AIH" or lower in accordance with the AIH scoring system, indicating a strong link to chronic hepatitis or (2). if IFN is expected to be efficacious on the basis of genotype of HCV-RNA level; even if there is acute exacerbation of type-C chronic hepatitis, IFN should be re-administered in the HCV-RNA level has dropped subsequently.
authors.affiliation: Department of Gastroenterology, Toranomon Hospital, 2-2-2 Toranomon, Minato-ku, Tokyo 105-8470, Japan.
authors.forename: Hitomi
authors.initials: H
authors.lastname: Sezaki
authors.forename: Yasuji
authors.initials: Y
authors.lastname: Arase
authors.forename: Akihito
authors.initials: A
authors.lastname: Tsubota
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Saitoh
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Suzuki
authors.forename: Norio
authors.initials: N
authors.lastname: Akuta
authors.forename: Takashi
authors.initials: T
authors.lastname: Someya
authors.forename: Kenji
authors.initials: K
authors.lastname: Ikeda
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Kumada
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D001219:Aspartate Aminotransferases / Q000097:blood; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology; D019693:Hepatitis, Autoimmune / Q000097:blood* / Q000276:immunology; D006801:Humans; D016899:Interferon-beta / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D007565:Jaundice / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis
chemical_list: D000998:Antiviral Agents; D012367:RNA, Viral; D016899:Interferon-beta; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase