ABSTRACT
Insulin resistance [IR] is one of the extrahepatic complications that occur in chronic hepatitis C virus infection [HCV], and is claimed as one of the fibrogenic factors which cause more rapid fibrosis progression. We examined the effect of HCV infection on insulin resistance states, and the possible link between IR, tumor necrosis factor-alpha [TNF-alpha] activation and development of hepatic fibrosis. Thirty patients with chronic hepatitis C infection divided into 2 groups according to presence or absence of fibrosis, 15 apparently healthy volunteer and 15 patients with hepatic fibrosis due to causes other than HCV were studied. Laboratory assessment of liver functions, fasting glucose, insulin levels, homeostasis model assessment of insulin resistance [HOMA-IR] and soluble tumor necrosis factor receptors 2 [sTNFR2] were done. HOMA-IR and sTNFR2 levels were significantly increased in patients with chronic HCV without fibrosis as compared with healthy control [p<0.01, p<0.001, respectively], and in patients with HCV induced fibrosis compared to HCV patients without fibrosis [p<0.001], and non HCV fibrosis [p<0.001, p< 0.05, respectively]. HOMA-IR was significantly correlated with sTNFR2 and fibrosis stage [p< 0.001]. IR was associated with increased risk of developing hepatic fibrosis in chronic HCV infection [OR 8.0, 95% CI 1.5-42]. Insulin resistance can be induced by chronic HCV infection per se and is correlated to fibrosis stages. Its fibrogenic role may be mediated by TNF-alpha activation