NAFLD and NASH in HCV Infection: Prevalence and Significance in Hepatic and Extrahepatic Manifestations

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.

Non-invasive quantification of liver fibrosis regression following successful treatment of chronic hepatitis C with direct acting antivirals

“…In our study patients with diabetes mellitus had slightly higher baseline liver stiffness, and we found that we can expect to see increasing liver stiffness during the course of the 12 weeks DAA treatment, but this does not hinder the eventual regression in liver fibrosis by 12 weeks post-treatment (p=0.272), which occurs at a similar rate as that seen in patients without diabetes mellitus. The cumulated risk for advanced fibrosis is even higher in patients who, on top of glucose abnormalities, also associate fatty liver disease, a condition which has been reported to have prevalences as high as 55% in patients with HCV infection (19), and in our study was present in 72.7% of patients, albeit only 13.7% presented advanced steatosis. In this context, a personalized medical nutrition regimen becomes a powerful instrument in preventing and/or treating fatty liver disease in patients with HCV infection (20).…”

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

“…These differences are explained by the Many authors consider that, despite the fact that insulin resistance is the common etiological link, the prevalence of MeS in HCV infection is similar to that of the general population (16). Consequently, in a study by Lonardo, the prevalence of MeS in patients with HCV was 4.1%, similar to that of the control group and reduced compared with the prevalence in NAFLD (27.9%) (17).…”

Extrahepaticus manifesztációk idült hepatitis C-vírus-fertőzöttekben

“…Idült C-vírus hepatitisben szenvedő betegekben körülbelül 50%-ban (40-88%) mutatható ki a máj változó mértékű elzsírosodása, amely mintegy 2,5-szerese a más kórokú májbetegségben ész-leltnek (hepatitis B: 26%, autoimmun májbetegség: 17%) [29,30].…”