Associations between serum lipids and hepatitis C antiviral treatment efficacy
Open Access
- 11 June 2010
- journal article
- viral hepatitis
- Published by Ovid Technologies (Wolters Kluwer Health) in Journal of Hepatology
- Vol. 52 (3), 854-863
- https://doi.org/10.1002/hep.23796
Abstract
Approximately one half of patients who undergo antiviral therapy for chronic hepatitis C virus (HCV) genotype 1 infection do not respond to treatment. African Americans (AAs) are less responsive to treatment than Caucasian Americans (CAs), but the reasons for this disparity are largely unknown. Recent studies suggest that serum lipids may be associated with treatment response. The aims of this study were to evaluate baseline and changes in serum lipids during therapy, determine whether serum lipids are associated with virological response, and assess whether these measures explain the racial difference in efficacy. The study participants were from Virahep‐C, a prospective study of treatment‐naïve patients with genotype 1 HCV infection who received peginterferon (PEG‐IN) alfa‐2a plus ribavirin therapy for up to 48 weeks. Fasting serum lipids were analyzed at baseline and during and after therapy in 160 AAs and 170 CAs. A relative risk (RR) model was employed to evaluate characteristics associated with sustained virological response (SVR). Antiviral therapy was associated with changes in serum lipids during and after antiviral therapy, with the changes differing by race and the amount of PEG‐IFN taken. Baseline lipid measures independently associated with higher rates of SVR were lower triglyceride and higher low‐density lipoprotein cholesterol, with an interaction between high‐density lipoprotein cholesterol (HDLc) and gender. Lipid measures did not contribute significantly to an explanation of the racial difference in SVR. Conclusion: Serum lipids are associated with SVR, although these paramaters did not explain the racial difference in treatment response. The results of this study are compatible with proposed biological mechanisms of HCV entry, replication, and secretion, and may underscore new potential therapeutic targets for HCV eradication. (Hepatology 2010)This publication has 43 references indexed in Scilit:
- Baseline cholesterol is associated with the response to antiviral therapy in chronic hepatitis CJournal of Gastroenterology and Hepatology, 2008
- Cellular Determinants of Hepatitis C Virus Assembly, Maturation, Degradation, and SecretionJournal of Virology, 2008
- Serum-Derived Hepatitis C Virus Infection of Primary Human Hepatocytes Is Tetraspanin CD81 DependentJournal of Virology, 2008
- Reliance of Host Cholesterol Metabolic Pathways for the Life Cycle of Hepatitis C VirusPLoS Pathogens, 2007
- Cell surface expression of LDL receptor in chronic hepatitis C: correlation with viral loadAmerican Journal of Physiology-Endocrinology and Metabolism, 2007
- Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteinsProceedings of the National Academy of Sciences of the United States of America, 2007
- Atorvastatin does not exhibit antiviral activity against HCV at conventional doses: A pilot clinical trialJournal of Hepatology, 2007
- Initiation of Hepatitis C Virus Infection Is Dependent on Cholesterol and Cooperativity between CD81 and Scavenger Receptor B Type IJournal of Virology, 2007
- Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)JAMA, 2001
- Histological grading and staging of chronic hepatitisJournal of Hepatology, 1995