Abstract
Background & Aims: IL28B polymorphisms have been associated with both treatment induced and spontaneous clearance of hepatitis C virus (HCV). We previously found that LDL cholesterol levels were higher in chronic hepatitis C (CHC) patients with the CC genotype at the rs12979860 polymorphism, located proximal to the IL28 gene. Here we analyzed the association of steatosis with IL28B genotype in treatment naïve patients with CHC. Methods: Two independent cohorts of 145 genotype 1 infected patients from an antifibrotic study and 180 genotype 1 patients from Duke were analyzed for the presence and severity of steatosis in relation to the rs12979860 polymorphism at the IL28B locus. TaqMan assay based genotyping classified three groups CC, CT, and TT. Results: CC genotype was associated with a lower prevalence of steatosis. In the antifibrotic study, steatosis was found in 47.6% (50/105) of IL28B non-CC vs. 22.5% (9/40; p = 0.008) in CC patients. Similarly, steatosis was found in 67.4% (89/132) of non-CC patients compared to only 39.6% (19/48; p = 0.001) of CC patients in the Duke cohort. Conclusions: IL28B CC genotype is associated with less pronounced disturbances of lipid metabolism, as reflected both in serum lipoprotein levels and hepatic steatosis, in HCV infection. © 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 1195-1200 |
| Number of pages | 6 |
| Journal | Journal of Hepatology |
| Volume | 55 |
| Issue number | 6 |
| Online published | 14 Apr 2011 |
| DOIs | |
| Publication status | Published - Dec 2011 |
| Externally published | Yes |
Funding
Alexander Thompson and Paul J. Clark also received funding support from the Richard B. Boebel Family Fund, the National Health and Medical Research Council of Australia, the Gastroenterology Society of Australia and the Royal Australasian College of Physicians. This study was funded in part by a generous grant from the David H. Murdock Institute for Business and Culture via the M.U.R.D.O.C.K. Study and award 1 UL 1 RR024128-01 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) and NIH Roadmap for Medical Research, and its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. We would like to thank all the study participants who contributed their biospecimens and data to the Duke Hepatology Clinic Database and Biorepository and acknowledge Diane Uzarski , Crystal Cates , Chris Delionbach and Melissa Austin for continued maintenance of this valuable resource. We would also like to thank collaborators Drs. Arlene Hughes and Michael Mosteller at GlaxoSmithKline for facilitating the sharing of the farglitazar clinical trial data and providing valuable feedback on the manuscript. This study was funded in large part by a generous grant from the David H Murdock Institute for Business and Culture via the M.U.R.D.O.C.K. Study and NIH CTSA award 1 UL 1 RR024128-01 to Duke University ( Dr. Robert Califf, Principal Investigator ). Drs. Thompson and Clark received funding support from the Duke Clinical Research Institute , a generous research gift from the Richard B . Boebel Family Fund , the National Health and Medical Research Council of Australia and the Gastroenterology Society of Australia .
Research Keywords
- Chronic hepatitis C
- Genetic
- IL28B
- Lipids
- Steatosis
