Original Article
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Oct 28, 2009; 15(40): 5020-5027
Published online Oct 28, 2009. doi: 10.3748/wjg.15.5020
Do statins reduce hepatitis C RNA titers during routine clinical use?
Kimberly A Forde, Connie Law, Rose O’Flynn, David E Kaplan
Kimberly A Forde, David E Kaplan, Research Section, Philadelphia Veterans Administration Medical Center, Philadelphia, PA 19104, United States
Kimberly A Forde, David E Kaplan, Department of Medicine, Division of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, United States
Connie Law, Rose O’Flynn, Department of Pharmacy, Philadelphia Veterans Administration Medical Center, Philadelphia, PA 19104, United States
Author contributions: Law C, O’Flynn R and Kaplan DE designed the research; Law C and O’Flynn R performed the research; Forde KA and Kaplan DE analyzed the data; Forde KA and Kaplan DE wrote the paper.
Supported by The Veterans Health Administration Research Career Development Award (DEK)
Correspondence to: Dr. David E Kaplan, Research Section, Philadelphia Veterans Administration Medical Center, Research A402A, 3900 Woodland Avenue, Philadelphia, PA 19104, United States. dakaplan@mail.med.upenn.edu
Telephone: +1-215-8235800-6729 Fax: +1-215-8234289
Received: August 20, 2009
Revised: September 9, 2009
Accepted: September 16, 2009
Published online: October 28, 2009

AIM: To compare hepatitis C virus (HCV) titers in patients with chronic hepatitis C with and without exposure to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins).

METHODS: Medical records were reviewed for 6463 patients with documented HCV infection at a single center between March 2004 and September 2006. Patients with confirmed viremia and meeting inclusion criteria were assigned to one of three groups: Group A (n = 50), dyslipidemic patients with statin usage during HCV RNA polymerase chain reaction (PCR) determination; Group B (n = 49), dyslipidemic patients with prior or future statin usage but not at the time of HCV RNA PCR determination; and Group C (n = 102), patients without statin usage during the study period. The primary analysis explored the effect of statin therapy on HCV viremia. Secondary analyses assessed class effect, dose response, and effect of other lipid-lowering therapies on HCV viral titers.

RESULTS: Median HCV RNA titers did not significantly differ among the three groups (Group A: 4 550 000 IU/mL, Group B: 2 850 000 IU/mL, Group C: 3 055 000 IU/mL). For those subjects with longitudinal assessment of HCV viremia prior to and while on statins, there were no significant differences between pre- and post-HCV viral titers. Additionally, no differences in HCV titers were observed at any dose level of the most prescribed statin, simvastatin. However, hypertriglyceridemia independently correlated with HCV titers, and niacin exposure was associated with significantly lower viral titers (P < 0.05).

CONCLUSION: There was no apparent effect of statins on HCV viral replication in this analysis. Further investigation is warranted to explore the possible antiviral properties of triglyceride-lowering agents and their potential role as adjuncts to standard HCV therapy.

Keywords: Hepatitis C, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, Statins, Geranylgeranyl, Prenylation