Background
Direct‐acting antivirals (DAAs) rapidly clear hepatitis C virus (HCV), but the lipid dynamics after DAA treatment remain unknown. Low‐density lipoprotein (LDL) cholesterolemia is the predicting factor for the onset and death of atherosclerotic cardiovascular diseases. Thus, in this study, we examined the frequency and risk of hyper‐LDL cholesterolemia in HCV patients who achieved sustained virologic response (SVR) with DAA treatment.
Methods
A total of 121 patients with HCV genotype 1b, who achieved SVR with DAA treatment, were examined for serum levels of total cholesterol, LDL‐cholesterol (LDL‐C), high‐density lipoprotein, and triglycerides from the start of treatment until 2 years after SVR (SVR‐2y). ΔLDL‐C was defined as the change in LDL‐C levels from treatment initiation to SVR‐2y. Hyper‐LDL cholesterolemia was defined as ≥ 140 mg/dL LDL‐C at SVR‐2y. Stepwise multiple regression analysis was performed to determine whether ΔLDL‐C and hyper‐LDL cholesterolemia are associated with other factors, including viral kinetics.
Results
A total of 63, 3, and 55 patients were administered daclatasvir + asunaprevir, ombitasvir + paritaprevir + ritonavir, and ledipasvir + sofosbuvir, respectively. ΔLDL‐C in patients with the IL28B (rs8099917) TG/GG genotype was significantly higher than in those with IL28B TT (27.3 ± 27.0 and 9.6 ± 27.3 mg/dL; P < 0.001). In addition, IL28B TG/GG was an independent risk factor for hyper‐LDL cholesterolemia (odds ratio: 8.47; P < 0.001).
Conclusions
An IL28B polymorphism is associated with ΔLDL‐C and hyper‐LDL cholesterolemia after achieving SVR. Thus, lipid markers should be carefully monitored in patients who achieve SVR with DAA.