ArticleEJIFCC2026
Metabolic Dysfunction - Associated Fatty Liver Disease (MAFLD), and Lipid-Based Insulin Resistance Markers in Hepatitis C Virus Infection (HCV).
Article in EJIFCC, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
Aim: Hepatitis C Virus (HCV) infection promotes insulin resistance, and metabolic dysfunction-associated fatty liver disease (MAFLD). HCV per se leads to impairment in host lipid metabolism and causes a deranged lipid profile. This study aims to analyze the prevalence of MAFLD and determine the levels of lipid profile parameters, surrogate markers of insulin resistance, liver fibrosis, and steatosis in patients with HCV infection. Methods: This study used data from the Centers for Disease Control - National Health and Nutritional Examination Survey (CDC-NHANES) 2017-2020. Those who tested positive on HCV RNA PCR were included in HCV group (n=89). Propensity score-based age- and gender-matching was done among those tested negative for HCV to select controls (n=89). Homeostatic Model Assessment of Insulin Resistance (HOMAIR), Homeostatic Model Assessment of Beta-cell Function (HOMAB), and the lipid-based insulin resistance markers such as Visceral Adiposity Index (VAI), Lipid Accumulation Product (LAP), Triglyceride-Glucose Index (TyG) were calculated using the standard formulae. Results: Serum triglycerides, total cholesterol and low-density lipoprotein cholesterol were significantly lower in HCV. HOMAIR, HOMAB were similar, and the lipid-based insulin resistance markers such as VAI, LAP and TyG index were significantly lower in HCV. FibroScan showed less steatosis, but increased fibrosis in the HCV patients. The surrogate markers of insulin resistance showed a significant association with the presence of MAFLD. Conclusion: HCV patients showed hypocholesterolemia, hypotriglyceridemia and the levels of lipid-based insulin resistance markers were significantly lower. TyG index showed a strong positive association with the presence of MAFLD. These observations could be due to association between HCV replication and host lipid metabolism.
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41659284PMC12882070What OpenQuestion holds
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