title: Hepatocyte destruction with enhanced collagen synthesis: characteristic feature of chronic hepatitis C patients on haemodialysis.
abstract: Hepatitis C virus (HCV) infection is frequent among patients with end-stage renal disease on haemodialysis and is considered to be an independent risk factor for mortality in this setting. However, only a few of these patients are treated with anti-hepatitis virus treatment before the development of end-stage renal disease. Recent guidelines recommend identification of patients with good prognoses who are in need of interferon treatment, but we know little of patients who must be treated urgently. Ninety-eight patients on haemodialysis (48 anti-HCV-positive and 50 anti-HCV-negative patients) were enrolled in this study; HCV RNA was detected in 43 anti-HCV-positive patients. Univariate analysis and multivariate regression analysis were applied to identify variables independently associated with persistent HCV infection. Seven variables were proven to be associated with persistent HCV infection. Among them, type IV collagen 7S and N-terminal propeptide of type III procollagen (P-III-P) were defined as independent variables useful in distinguishing HCV RNA-positive patients from HCV RNA-negative patients with 0.91 sensitivity, 0.91 specificity, 0.89 positive predictive value and 0.93 negative predictive value. Our observations suggest that hepatocyte destruction with enhanced liver fibrosis is a characteristic clinical feature of persistent HCV infection. Type IV collagen 7S of ≥ 5 ng/mL and/or P-III-P of ≥ 5 U/mL would be useful markers to identify patients in need of interferon treatment, which supports the idea of the Kidney Disease: Improving Global Outcomes guidelines that a good prognosis in patients with HCV infection on haemodialysis should prompt consideration for IFN treatment when applicable.
authors.affiliation: Department of Gastroenterology and Hepatology, Kochi Medical School, Nankoku, Kochi 783-8505, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ue
authors.forename: N
authors.initials: N
authors.lastname: Ikebe
authors.forename: K
authors.initials: K
authors.lastname: Munekage
authors.forename: T
authors.initials: T
authors.lastname: Ochi
authors.forename: A
authors.initials: A
authors.lastname: Hirose
authors.forename: H
authors.initials: H
authors.lastname: Kataoka
authors.forename: S
authors.initials: S
authors.lastname: Fujimoto
authors.forename: K
authors.initials: K
authors.lastname: Kikuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Okuhara
authors.forename: M
authors.initials: M
authors.lastname: Ono
authors.forename: T
authors.initials: T
authors.lastname: Saibara
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016923:Cell Death; D003094:Collagen / Q000096:biosynthesis*; D005260:Female; D018937:Hepatitis C Antibodies / Q000097:blood; D019698:Hepatitis C, Chronic / Q000150:complications / Q000473:pathology*; D022781:Hepatocytes / Q000502:physiology*; D006801:Humans; D008099:Liver / Q000473:pathology*; D008103:Liver Cirrhosis / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D006435:Renal Dialysis
chemical_list: D018937:Hepatitis C Antibodies; D012367:RNA, Viral; D003094:Collagen