title: The presence of steatosis and elevation of alanine aminotransferase levels are associated with fibrosis progression in chronic hepatitis C with non-response to interferon therapy.
abstract: OBJECTIVE
  Interferon (IFN) therapy leads to regression of hepatic fibrosis in chronic hepatitis C patients who achieve a sustained virologic response (SVR), while the beneficial effect is limited in those who fail to do so. The aim of the present study was to define factors associated with progression of fibrosis in patients who do not achieve a SVR.
  
  
  METHODS
  Fibrosis staging scores were compared between paired liver biopsies before and after IFN in 97 chronic hepatitis C patients who failed therapy. The mean interval between biopsies was 5.9 years. Factors associated with progression of fibrosis were analyzed.
  
  
  RESULTS
  Fibrosis progressed in 23%, remained unchanged in 47% and regressed in 29%. Steatosis and a high average alanine aminotransferase (ALT) between biopsies were independent factors for progression of fibrosis with risk ratios of 5.53 and 4.48, respectively. Incidence and yearly rate of progression of fibrosis was 64% and 0.22+/-0.29 fibrosis units per year in those with both risk factors compared to 8% and -0.04+/-0.17 fibrosis units per year in those negative for both factors.
  
  
  CONCLUSIONS
  Hepatic steatosis and elevated ALT levels are risk factors for progression of fibrosis in chronic hepatitis C patients who fail to achieve a SVR to IFN therapy and therefore may be therapeutic targets to halt the potentially progressive disease.
authors.affiliation: Division of Gastroenterology and Hepatology, Musashino Red Cross Hospital, 1-26-1 Kyonan-cho, Musashino-shi, Tokyo, Japan.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kurosaki
authors.forename: Kotaro
authors.initials: K
authors.lastname: Matsunaga
authors.forename: Itsuko
authors.initials: I
authors.lastname: Hirayama
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Tanaka
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Sato
authors.forename: Nobutoshi
authors.initials: N
authors.lastname: Komatsu
authors.forename: Naoki
authors.initials: N
authors.lastname: Umeda
authors.forename: Takanori
authors.initials: T
authors.lastname: Hosokawa
authors.forename: Ken
authors.initials: K
authors.lastname: Ueda
authors.forename: Kaoru
authors.initials: K
authors.lastname: Tsuchiya
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nakanishi
authors.forename: Jun
authors.initials: J
authors.lastname: Itakura
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Asahina
authors.forename: Shozo
authors.initials: S
authors.lastname: Miyake
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Enomoto
authors.forename: Namiki
authors.initials: N
authors.lastname: Izumi
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood*; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications*; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D007372:Interferons / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000209:etiology*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged
chemical_list: D007372:Interferons; D000410:Alanine Transaminase