Abstract
Metabolic derangement is characteristic in patients with hepatitis C virus (HCV) infection. Aside from established liver injury, various extrahepatic metabolic disorders impact the natural history of the disease, clinical outcomes, and the efficacy of antiviral therapy. The presence of steatosis, recently redefined as metabolic-associated fatty liver disease (MAFLD), is a common feature in HCV-infected patients, induced by host and/or viral factors. Most chronic HCV-infected (CHC) patients have mild steatosis within the periportal region of the liver with an estimated prevalence of 40% to 86%. Indeed, this is higher than the 19% to 50% prevalence observed in patients with other chronic liver diseases such as chronic hepatitis B (CHB). The histological manifestations of HCV infection are frequently observed in genotype 3 (G-3), where relative to other genotypes, the prevalence and severity of steatosis is also increased. Steatosis may independently influence the treatment efficacy of either interferon-based or interferon-free antiviral regimens. This review aimed to provide updated evidence of the prevalence and risk factors behind HCV-associated steatosis, as well as explore the impact of steatosis on HCV-related outcomes.
Highlights
Hepatic steatosis refers to the accumulation of intrahepatic fat of at least 5% of liver weight
nonalcoholic fatty liver disease (NAFLD) is primarily associated with metabolic syndrome (MetS), which refers to the co-occurrence of several known risk factors of cardiovascular disease (CVD) and type 2 diabetes (T2D), such as insulin resistance (IR), obesity, atherogenic dyslipidemia, and hypertension [11,12]
This review illustrates a significant relationship between chronic HCV-infected (CHC) infection and hepatic steatosis through a combination of both viral and metabolic factors, further revealing a significant association with both hepatic and extrahepatic manifestations
Summary
Hepatic steatosis refers to the accumulation of intrahepatic fat of at least 5% of liver weight. NAFLD is primarily associated with metabolic syndrome (MetS), which refers to the co-occurrence of several known risk factors of cardiovascular disease (CVD) and type 2 diabetes (T2D), such as insulin resistance (IR), obesity, atherogenic dyslipidemia, and hypertension [11,12] These risk factors have been further identified as underlying risk factors for NAFLD and NASH in 63.6% of hepatitis C virus (HCV)-related cirrhotic livers [13]. In obese patients with NASH, another study discovered that a high degree of steatosis and inflammation were amongst the recognized risk factors for fibrosis [33] While more of this correlation between steatosis and fibrosis has been reported in HCV infections [34,35], there have been contradictory findings where liver fibrosis progression was associated with other risk factors including older age, higher BMI, periportal necroinflammation, and ALT and serum ALT elevations, and less so with steatosis [36,37]. Liver steatosis may be considered a risk factor for inflammation, increased hepatic fibrosis, and liver damage or HCC in CHC patients
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