Liver steatosis and dyslipidemia after HCV eradication by direct acting antiviral agents are synergistic risks of atherosclerosis

PLoS One. 2018 Dec 21;13(12):e0209615. doi: 10.1371/journal.pone.0209615. eCollection 2018.

Abstract

Aim: We comprehensively analyzed how hepatitis C virus (HCV) eradication by interferon (IFN)-free direct-acting-antiviral-agents (DAAs) affects liver steatosis and atherogenic risk.

Methods: Patients treated with IFN-free-DAAs who underwent transient elastography before and at 24-weeks post-treatment, including controlled attenuation parameter (CAP), and achieved sustained viral response (SVR) were enrolled. The association between changes in liver steatosis, lipid-metabolism, and genetic and clinical factors was analyzed.

Results: A total of 117 patients were included. The mean CAP and low-density lipoprotein cholesterol (LDL-C) levels were significantly elevated at SVR24. However, baseline LDL-C and CAP values were significantly negatively correlated with changes in these values after HCV eradication, indicating that in patients with high baseline values, the values generally decreased after HCV eradication. Mean small-dense LDL-C (sdLDL-C), which has greater atherogenic potential, was significantly elevated only in patients with both dyslipidemia (LDL-C >140 mg/dL) and liver steatosis (CAP >248 dB/m) at SVR24. Those patients had significant higher baseline BMI, LDL-C, and total-cholesterol levels.

Conclusions: Generally, successful HCV eradication by IFN-free-DAAs decreases CAP and LDL-C in patients with high baseline values. However, elevated LDL-C was accompanied with elevated sdLDL-C only in patients with liver steatosis and dyslipidemia at SVR24; therefore, those patients may require closer monitoring.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antiviral Agents / adverse effects
  • Atherosclerosis / chemically induced
  • Atherosclerosis / epidemiology
  • Atherosclerosis / metabolism*
  • Atherosclerosis / virology
  • Cholesterol, LDL / metabolism
  • Dyslipidemias / chemically induced
  • Dyslipidemias / epidemiology
  • Dyslipidemias / metabolism*
  • Dyslipidemias / virology
  • Fatty Liver / chemically induced
  • Fatty Liver / epidemiology
  • Fatty Liver / metabolism*
  • Fatty Liver / virology
  • Female
  • Hepacivirus / drug effects
  • Hepacivirus / pathogenicity
  • Hepatitis C, Chronic / complications
  • Hepatitis C, Chronic / drug therapy*
  • Hepatitis C, Chronic / epidemiology
  • Hepatitis C, Chronic / virology
  • Humans
  • Lipid Metabolism / drug effects
  • Liver / drug effects
  • Liver / metabolism
  • Liver / virology
  • Male
  • Middle Aged
  • Ribavirin / adverse effects
  • Risk Factors
  • Sustained Virologic Response

Substances

  • Antiviral Agents
  • Cholesterol, LDL
  • Ribavirin

Grant support

Goki Suda received the following fundings: The Japan Agency for Medical Research and Development (AMED), Grant Number 16fk0210102h0001, 17fk0210106h0501, URL https://www.amed.go.jp/; and Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant number 16K09334, URL https://www.jsps.go.jp/. Naoya Skamoto received funding from the Japan Agency for Medical Research and Development (AMED). Grant number is 17fk0210102h0001. URL is https://www.amed.go.jp/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.