Abstract
Background/Aim: The recovery pattern of hepatitis C virus (HCV)-associated metabolic alteration after sustained virological response (SVR) following direct-acting antivirals (DAAs) remains elusive. Methods: A prospective cohort study of chronic HCV-infected (CHC) patients (n = 415) receiving DAAs (n = 365) was conducted. Metabolic profiles were examined in SVR patients (n = 360) every 3–6 months after therapy and compared with those of sex- and age-matched controls (n = 470). Results: At baseline, of 415, 168 (40.5%) had insulin resistance (IR). The following were associated: levels of high-density lipoprotein cholesterol (HDL-C), triglycerides (TGs), HCV RNA, fibrosis-4 score, and interferon-λ3-rs12979860 genotype with total cholesterol (TC) levels; and TG levels and BMI with HOMA-IR. Over a 3-year follow-up, in SVR patients, BMI and TC levels and TG/HDL-C ratios increased from baseline, while HOMA-IR trended downward by 72 weeks after therapy and then increased. The increased HDL-C levels began to decrease after 72 weeks after therapy. TC and HOMA-IR were negatively associated with each other until 24 weeks after therapy. Earlier increases in BMI and decreases in HOMA-IR were noted in SVR patients with than in those without baseline IR. Compared with controls, in the subgroup without baseline IR, SVR patients had increased BMI and HOMA-IR levels. Metabolic profiles were similar between SVR patients and controls in the subgroup with baseline IR. Conclusions: In SVR patients treated with DAAs, the recovery of altered lipid and glucose metabolism was not coupled until 72-week post-therapy, when HOMA-IR reached its nadir. SVR patients with baseline IR recovered from HCV-associated metabolic alterations earlier than those without baseline IR.
Highlights
Levels reflects the fact that severe hepatic fibrosis leads to hypocholesteremia [32], as the liver is the main organ for cholesterol biosynthesis
IFNL3-rs12979860 CC genotype and high total cholesterol (TC) levels [33], while the positive associations of BMI and TG levels with HOMA-insulin resistance (IR) indicated the utility of BMI and TG in identifying insulin action [34]
The increased rates of cirrhosis and genotype 1 (G1) hepatitis C virus (HCV) in chronic HCV-infected (CHC) patients with baseline IR were consistent with the facts that IR is associated with significant hepatic fibrosis [35] and that G1 HCV is associated with increased IR [36]
Summary
Hepatitis C virus (HCV), classified into eight genotypes [1], is a human pathogen that causes acute and chronic liver disease, chronically infecting an estimated 71.1 million individuals worldwide [2]. In addition to hepatic complications that include steatosis, liver cirrhosis, and hepatocellular carcinoma (HCC), HCV infection induces several extrahepatic complications, such as hypolipidemia, insulin resistance (IR), diabetes, and cardiovascular 4.0/). Events [3,4]. HCV infection is considered to cause metabolic alterations instead of being a viral infection. The reversal of HCV-associated metabolic alterations after sustained virological response (SVR) in interferon-based studies has been well demonstrated [3]. HCV-associated diabetes and some cardiovascular events cannot be reversed, even after viral clearance [3]
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