Interaction of metabolic syndrome, nonalcoholic fatty liver disease and chronic hepatitis C

Abstract

Nonalcoholic fatty liver disease (NAFLD) has become one of the most prevalent liver diseases in the Western world. NAFLD represents a wide spectrum of histologic subgroups, with nonalcoholic steatohepatitis as the most aggressive form. The risk of developing NAFLD is strongly associated with metabolic syndrome and insulin resistance. The pathogenesis of NAFLD is a multiple-hit process resulting from hepatic fat deposition that is related to several conditions, including insulin resistance and central obesity. Additional hits, such as oxidative stress or adipocytokines produced by white adipose tissue, can further enhance liver damage leading to nonalcoholic steatohepatitis or fibrosis. Although NAFLD is often the primary liver disease of metabolic conditions, it can also exacerbate other liver diseases such as hepatitis C (HCV); indeed, more than 50% of patients with HCV have hepatic steatosis. Hepatic steatosis can be related to host factors (e.g., obesity, metabolic syndrome or insulin resistance) or to the genotype of virus (e.g., HCV genotype 3). Increasing evidence suggests that hepatic steatosis, insulin resistance and obesity in the setting of HCV have a negative impact on the efficacy of treatment and hepatic progression of fibrosis.