The interaction of metabolic factors with HCV infection: Does it matter?

Summary 

Given the pandemic spread of the hepatitis C virus (HCV) infection and the metabolic syndrome (MS), the burden of their interaction is a major public health issue, bound to increase in the near term. A better appreciation of the clinical consequences of the relationship between HCV and MS is needed, not only due to their potential synergism on liver disease severity, but also because of the multifaceted interactions between HCV and glucose and lipid metabolism. HCV infection per se does not carry an increased risk of MS, but is able to perturb glucose homeostasis through several direct and indirect mechanisms, leading to both hepatic and extrahepatic insulin resistance. This translates into accelerated liver disease progression (including the development of hepatocellular carcinoma), reduced response to antivirals and, in susceptible individuals, increased risk of developing full-blown type 2 diabetes. HCV may also cause hepatic steatosis, especially in patients infected with genotype 3, although the clinical impact of viral steatosis is debated. Possibly as a result of HCV-induced insulin resistance, and despite a paradoxically favourable lipid profile, the cardiovascular risk is moderately increased in chronic hepatitis C. In addition, the interaction with the MS further increases the risks of cirrhosis, hepatocellular carcinoma, diabetes, and cardiovascular events. Thus, targeted lifestyle and pharmacological measures are urgently warranted in chronic hepatitis C with metabolic alterations.

Keywords:  Metabolic syndrome , Fatty liver , Hepatitis C virus , Insulin resistance , Liver fibrosis , Interferon alpha

Abbreviations:  BMI, body mass index , EGP, endogenous glucose production , HCC, hepatocellular carcinoma , HCV, hepatitis C virus , HDL, high-density lipoprotein , HOMA-IR, homeostasis model assessment of insulin resistance , IFN, interferon , IMT, intima-media thickness , IR, insulin resistance , JNK, c-Jun N-terminal kinase , MS, metabolic syndrome , NAFLD, non-alcoholic fatty liver disease , NASH, non-alcoholic steatohepatitis , OGIS, oral glucose insulin sensitivity , OGTT, oral glucose tolerance test , PPAR, peroxisome proliferator-activated receptor , PTEN, phosphatase and tensin homolog , QUICKI, quantitative insulin sensitivity check index , SHIP2, SH2-containing phosphoinositide 5-phosphatase 2 , SOCS, suppressor of cytokine signaling , T2D, type 2 diabetes , TG, triglycerides , TNF-α, tumor necrosis factor-α

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