부산대학교 도서관

Intrahepatic thrombotic events have been postulated to play a key role in the pathogenesis of hepatic fibrosis. Genetic and acquired thrombotic risk factors may therefore contribute to the varying rates of fibrosis progression observed in patients with chronic hepatitis C virus (HCV) infection. The aim of this study was to assess the impact of inherited mutations in factor V and factor II (prothrombin) on hepatic fibrosis progression rates in individuals infected with HCV. Two hundred and ten Irish women infected with HCV genotype 1b, contracted from a single source (HCV-contaminated anti-D immunoglobulin) were genotyped for the factor V Leiden G1691A and prothrombin G20210A polymorphisms, and compared with Irish Caucasoid controls. Index and subsequent liver biopsies were scored (Ishak scoring system) by a single pathologist. Statistical analysis was performed using SPSS. Factor V Leiden and prothrombin G20210A heterozygosity were determined in 3.7% and 1.85%, respectively, of the study population. There was no association between these polymorphisms and fibrotic score on the index biopsy, or degree of change in fibrotic score on subsequent biopsies. The mean fibrotic score for factor V wild type was 1.06 vs 0.71 for the heterozygotes (P = 0.89). The mean change in fibrotic scores between subsequent biopsies was 0.72 for factor V wild type vs 0.50 for heterozygotes (P = 0.68). Similarly, there was no significant difference in fibrotic score for those with the prothrombin G20210A polymorphism (P = 0.936). Alanine aminotransferase levels for factor V wild type were significantly lower than those for the heterozygotes, 45.9 vs 57 (P = 0.032). Factor V Leiden and prothrombin G20210A heterozygosity rates were infrequently detected in this HCV cohort and were similar to rates seen in a Caucasian Irish control population. In this cohort, neither factor V Leiden nor prothrombin G20210A polymorphisms had a significant impact on fibrotic scores or degree of change between subsequent biopsies. These data do not support a key role for thrombotic risk factors in fibrogenesis in HCV-infected patients.