Hepatitis C Virus and Statins: Is There a Role?
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : José A. Del Campo & Mohamed Eslam & Manuel Romero-Gَmez
- چاپ و سال / کشور: 2011
Description
Hepatitis C treatment-response rates range from 50%–80% depending on genotype, viral load, fibrosis stage, interleukin 28B (IL28B) polymorphism, and metabolic abnormalities. Lipid metabolism could influence sustainedvirological response (SVR), and raised levels of low-density lipoprotein cholesterol were found in sustained responders. The capacity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors to impede hepatitis C virus (HCV) replicon replication in vitro in a dose-dependent fashion raised hope that this class of medications could serve as an adjunct to standard interferon-based therapy. In cell culture models of HCV infection, antiviral activity of statins was greater for fluvastatin. The mechanisms by which statins interfere with HCVreplication are not completely understood yet. Adding statins to peginterferon plus ribavirin may improve (SVR) in HCV patients, but this method requires further prospective evaluation. However, current data suggest that lipid metabolism may be linked to IL28B polymorphisms, and patients bearing favorable genotype CC (rs12979860) showed higher cholesterol levels and higher (SVR) rates, emerging as a confounding factor in the interaction of statins and SVR. The use of statins raises many questions, and additional trials are needed before we can use statins as adjuvant therapy for HCV
Curr Hepatitis Rep (2011) 10:162–167 DOI 10.1007/s11901-011-0100-8 Published online: 18 June 2011
