Steatosis and chronic hepatitis C infection: mechanisms and significance.

The co-existence of chronic hepatitis C and hepatic steatosis is well known, occurring in roughly 50% of patients infected with the hepatitis C virus. Recent interest has focused on the pathophysiologic mechanisms explaining the genesis of hepatic steatosis in the setting of chronic hepatitis C. Data suggest that both viral and host metabolic factors are involved in this process. Additionally, it has become evident that the efficacy of current antiviral therapy is decreased in the setting of co-existent steatosis or steatohepatitis, predominantly in genotype non-3 patients. Several potential explanations for this have been proposed and include underlying viral resistance and host-mediated insulin resistance, enhanced fibrosis, altered immune responses, and decreased bioavailability of interferon-based therapy. This review focuses on our current understanding of the mechanisms for steatosis development in the setting of chronic hepatitis C infection and the proposed mechanisms for the observed decreased efficacy of current antiviral therapy in this patient population.