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Quantitative and qualitative lipid improvement with chronic hepatitis C virus eradication using direct‐acting antivirals
Author(s) -
Joshita Satoru,
Yamashita Yuki,
Okamoto Toru,
Usami Yoko,
Sugiura Ayumi,
Yamazaki Tomoo,
Kakino Akemi,
Ota Masao,
Sawamura Tatsuya,
Umemura Takeji
Publication year - 2021
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.13666
Subject(s) - pcsk9 , apolipoprotein b , cholesterol , lipoprotein , apolipoprotein a1 , hepatitis c virus , medicine , lipid profile , ldl receptor , endocrinology , virology , virus
Aim Direct‐acting antivirals 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 direct‐acting antivirals 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 (LDL) cholesterol and HDL cholesterol levels were quantitatively increased at SVR12, along with higher PCSK9 (all p < 0.0001). PCSK9 was significantly correlated with LDL cholesterol ( r = 0.244, p = 0.0003) and apolipoprotein B ( r = 0.222, p = 0.0009) at SVR12. Regarding qualitative LDL changes, LAB was significantly decreased and LAB/LDL cholesterol and LAB/apolipoprotein B 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 cholesterol, HDL‐CUC/ apolipoprotein A1, and HDL‐CUC/ apolipoprotein A2 at SVR12 (all p < 0.0001). Conclusions HCV eradication by direct‐acting antivirals 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.