Steatosis, insulin resistance and fibrosis progression in chronic hepatitis C.
Steatosis is a common histological feature of chronic hepatitis C. Two distinct mechanisms seem to be involved in the pathogenesis of hepatic steatosis in chronic hepatitis C virus (HCV) infection. In HCV genotype 3-infected patients, steatosis is likely viral-induced, and represents a direct cytopathic effect of HCV, whereas in patients infected with other genotypes, host metabolic risk factors for insulin resistance such as obesity, type 2 diabetes and hyperlipidemia play a major role in intracellular lipids accumulation. Interestingly, the outcome of steatosis matches the virological response to treatment in HCV genotype 3-infected patients who have purely virus-induced steatosis but not in patients with metabolic causes of steatosis. Suspected molecular underlying mechanisms include interactions between the HCV core protein and intracellular lipid metabolism pathways as well as induction of insulin resistance. Steatosis is of clinical importance as it appears to be associated with more rapid liver fibrosis progression and impaired response to antiviral therapy. However, whether metabolic and host factors associated with steatosis, steatosis per se or both, may be responsible for this association remains to be clarified. This review is aimed at describing the current knowledge of steatosis, insulin resistance and fibrosis progression in chronic hepatitis C.
Department of Hepatology and Gastroenterology, CHU Bordeaux, Hopital Haut Leveque, Pessac, France. laurent.castera@chu-bordeaux.fr
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D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications / Q000209:etiology*; D019698:Hepatitis C, Chronic / Q000150:complications*; D006801:Humans; D007333:Insulin Resistance; D008103:Liver Cirrhosis / Q000209:etiology*