Quantitative and qualitative lipid improvement with chronic hepatitis C virus eradication using with direct-acting antivirals.

BACKGROUND AND AIMS Direct-acting antivirals (DAAs) have revolutionized hepatitis C virus (HCV) therapy by providing a high sustained virological response (SVR) rate and subsequent favorable lipid increases. Proprotein convertase subtilisin-kexin like-9 (PCSK9) plays an important role in regulating quantitative lipid levels. This study examined the interactions between quantitative PCSK9 and lipid changes as well as qualitative lipid changes in terms of lectin-like oxidized low-density lipoprotein (LDL) receptor-1 ligand containing apolipoprotein B (LAB) and high-density lipoprotein (HDL)-cholesterol uptake capacity (HDL-CUC). METHODS Patients with chronic HCV infection (N = 231) who achieved an SVR by DAAs without lipid-lowering therapy were included for comparisons of PCSK9, LAB, HDL-CUC, and other clinical indices between pretreatment and SVR12 time points. RESULTS LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) levels were quantitatively increased at SVR12 along with higher PCSK9 (all P < 0.0001). PCSK9 was significantly correlated with LDL-C (r = 0.244, P = 0.0003) and ApoB (r = 0.222, P = 0.0009) at SVR12. Regarding qualitative LDL changes, LAB was significantly decreased and LAB/LDL-C and LAB/ApoB proportions were improved at SVR12 (all P < 0.0001). In terms of qualitative HDL changes, HDL-CUC was significantly ameliorated along with HDL-CUC/HDL-C, HDL-CUC/ApoA1, and HDL-CUC/ApoA2 at SVR12 (all P < 0.0001). CONCLUSIONS HCV eradication by DAAs may produce quantitative lipid profile changes along with PCSK9 production recovery in addition to qualitative lipid improvement, which possibly confers the additional secondary benefits of atherosclerosis improvement and cardiovascular disease event reduction. This article is protected by copyright. All rights reserved.