Hepatitis C virus eradication by direct‐acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low‐density lipoprotein cholesterolemia without an increase in body weight

Author:

Tokuchi Yoshimasa1,Suda Goki1ORCID,Kawagishi Naoki1ORCID,Ohara Masatsugu1,Kohya Risako1,Sasaki Takashi1,Yoda Tomoka1,Maehara Osamu2,Ohnishi Shunsuke2,Kubo Akinori1,Yoshida Sonoe1,Fu Qingjie1,Yang Zijian1,Hosoda Shunichi1,Kitagataya Takashi1,Suzuki Kazuharu1,Nakai Masato1,Sho Takuya1,Natsuizaka Mitsuteru1,Ogawa Koji1ORCID,Sakamoto Naoya1

Affiliation:

1. Department of Gastroenterology and Hepatology Hokkaido University Graduate School of Medicine Sapporo Japan

2. Laboratory of Molecular and Cellular Medicine Faculty of Pharmaceutical Sciences Hokkaido University Sapporo Japan

Abstract

AbstractAimHepatitis C virus (HCV) infection has been reported to cause liver steatosis. Thus, eradicating HCV with direct‐acting antivirals (DAAs) is expected to reduce liver steatosis. We aimed to clarify long‐term changes in the prevalence of fatty liver and hyper‐low‐density lipoprotein (LDL) cholesterolemia and their associations in patients who achieve successful HCV eradication using DAAs.MethodsThis retrospective study included patients with HCV who achieved sustained virologic response after interferon‐free DAA and analyzed the changes in the prevalence of fatty liver diagnosed with controlled attenuation parameter (CAP), hyper‐LDL cholesterolemia, and their relationships at baseline (n = 100) and 24 weeks (SVR24, n = 100), 96 weeks (SVR96, n = 100), and 144 weeks (SVR144, n = 90) after DAA.ResultsIn 100 participants, the prevalence of fatty liver (19% vs. 32%, p = 0.0349) and hyper‐LDL cholesterolemia (6% vs. 15%, p = 0.0379) significantly increased without changes in body weight at SVR96. Median total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and small‐dense‐LDL (sdLDL) levels and CAP values were significantly greater at SVR24, SVR96, and SVR144 than at baseline. Baseline CAP values and changes in CAP values were significantly negatively correlated at every observation point: r = −0.5305, p < 0.0001 at SVR24; r = −0.3617, p = 0.0005 at SVR96; and r = −0.4735, p < 0.0001 at SVR144. A similar relationship was observed in cholesterol levels. Unlike at baseline, CAP values were significantly positively correlated with LDL‐C and sdLDL‐C levels at all observation points after DAAs.ConclusionsDirect‐acting antivirals may cause an increased prevalence of fatty liver accompanying hyper‐LDL cholesterolemia without increased body weight. As post‐SVR liver steatosis could cause HCC, careful follow‐up may be required.

Funder

Japan Agency for Medical Research and Development

Publisher

Wiley

Subject

Infectious Diseases,Hepatology

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