Role of iron load on fibrogenesis in chronic hepatitis C

BACKGROUND/AIMS: In chronic viral hepatitis, an enhanced iron load is relat ed to lower response to interferon. Furthermore, iron, through the producti on of oxygen radicals, may stimulate hepatocyte necrosis and the activation of cells responsible for synthesis and deposition of extracellular matrix. We investigated the relationship between iron load, evaluated by serum ass ays, and liver fibrogenesis in chronic active viral hepatitis. METHODOLOGY: Serum iron, ferritin, transferrin saturation and serum markers of hepatic fibrogenesis (Laminin and the amino-terminal peptide of procoll agen III -NPIIIP-) were assayed in 102 patients (47 females, 55 males, mean age 42.48 years) affected by chronic hepatitis C virus and in 81 healthy c ontrols (47 males, 34 females). In hepatitis C virus patients (studied befo re a-interferon treatment) a semiquantitative score for portal inflammation , necrosis and fibrosis was applied to liver biopsy. RESULTS: Serum indices of iron load were higher in hepatitis C virus patien ts than in controls, and were higher in cirrhotic than in chronic hepatitis cases. Ferritin and serum iron were positively correlated with NPIIIP and laminin; moreover cases with ferritin levels over the normal limit for sex and age had higher levels of NPIIIP and laminin than cases with normal or p oor iron status. CONCLUSIONS: Our data suggest that even a mild increase of iron load stimul ates hepatic fibrogenesis, probably adding oxygen free radical injury to th e damage of viral infection.