Abstract
The aim of this paper is to review and up to date the prevalence of hepatitis C virus (HCV)-associated non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) and their significance in both accelerating progression of HCV-related liver disease and development of HCV-associated extrahepatic diseases. The reported mean prevalence of HCV-related NAFLD was 55%, whereas NASH was reported in 4%–10% of cases. HCV genotype 3 directly induces fatty liver deposition, namely “viral steatosis” and it is associated with the highest prevalence and degree of severity, whereas, HCV non-3 genotype infection showed lower prevalence of steatosis, which is associated with metabolic factors and insulin resistance. The host’s genetic background predisposes him or her to the development of steatosis. HCV’s impairment of lipid and glucose metabolism causes fatty liver accumulation; this seems to be a viral strategy to optimize its life cycle. Irrespective of insulin resistance, HCV-associated NAFLD, in a degree-dependent manner, contributes towards accelerating the liver fibrosis progression and development of hepatocellular carcinoma by inducing liver inflammation and oxidative stress. Furthermore, NAFLD is associated with the presence of metabolic syndrome, type 2 diabetes, and atherosclerosis. In addition, HCV-related “metabolic steatosis” impairs the response rate to interferon-based treatment, whereas it seems that “viral steatosis” may harm the response rate to new oral direct antiviral agents. In conclusion, a high prevalence of NAFLD occurs in HCV infections, which is, at least in part, induced by the virus, and that NAFLD significantly impacts progression of the liver disease, therapeutic response, and some extrahepatic diseases.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a condition characterized by fatty liver accumulation with a spectrum of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH)
The data demonstrate that hepatic steatosis is a feature of chronic hepatitis C virus (HCV) infections and that liver fatty accumulation seems to be a finalistic condition favoring the persistence and replication of HCV
HCV-associated steatosis influences the development of some extrahepatic manifestations of chronic HCV infection such as diabetes, metabolic syndrome, and atherosclerosis
Summary
Non-alcoholic fatty liver disease (NAFLD) is a condition characterized by fatty liver accumulation with a spectrum of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). Insulin resistance has been reported with high prevalence in chronic hepatitis C infection cases (up to 80%) and it is commonly observed in HCV non-3 genotypes infected patients, whereas it is not a feature of HCV genotype 3 infection [19]. In HCV-infected patients with visceral obesity, it has been reported that there are increased levels of pro-inflammatory cytokines (IL-6 and TNF-α) that inhibit insulin signaling and the secretion of adiponectin, which results in corresponding consequences for the development of liver steatosis and insulin resistance [37]. The latter represents the pathophysiological link between steatosis and the metabolic syndrome. We demonstrated that the TM6SF2, E167K variant, contributes to liver steatosis in chronic hepatitis C [43]
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