Author/Authors :
Shavakhi, Ahmad Department of Gastroenterology and Hepatology, Shahrekord University of Medical Sciences, Isfahan , Minakari, Mohamad Department of Gastroenterology and Hepatology, Shahrekord University of Medical Sciences, Isfahan , Bighamian, Afshin Department of Gastroenterology and Hepatology, Shahrekord University of Medical Sciences, Isfahan , Sadeghian, Sina Department of Gastroenterology and Hepatology, Shahrekord University of Medical Sciences, Isfahan , Shavakhi, Sara Department of Gastroenterology and Hepatology, Shahrekord University of Medical Sciences, Isfahan , Khamisi, Naser Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences , Khodadustan, Mahsa Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences , Talebi, Majid Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences , Ataei, Behrooz Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences
Abstract :
Lipid metabolism is one of the hepatitis C virus (HCV) life cycle steps. Statins can reduce cholesterol level and
fi nally can decrease HCV replication. Th us, we assessed the eff ect of Statins in combination with standard antiviral treatment on
hyperlipidemic genotype I HCV infected patients. Materials and Methods: Th is study was a prospective clinical trial. 40 patients
were selected from those referred to educational and Th erapeutic Centers of Isfahan University of Medical Sciences from 2009
to 2010 with confi rmed HCV viremia. All patients received Peg-interferon-a2a and ribavirin. 20 hyperlipidemic Patients received
20 mg atorvastatin nightly for 3 months and placebo was prescribed for 20 normolipidemic HCV infected patients as a control
group. Liver enzymes and complete blood count were checked monthly and thyroid stimulating hormone was checked every
3 months. We also performed quantitative HCV-ribonucleic acid (RNA) test in 12th week of therapy, at the end of treatment and
6 months after therapy for all samples. Results: We didn’t fi nd any signifi cant diff erences in the mean of HCV-RNA numbers
between statin and placebo groups in 12th week of treatment, in the end of treatment and 6 months after treatment (P > 0.05).
Conclusion: Atorvastatin has no eff ect on the mean of HCV viral load when we added it to standard treatment for hepatitis C
infection. Further studies are necessary to examine the possible antiviral properties of statins and their potential role as adjuncts
to standard HCV therapy.
