ROSUVASTATIN AND CHRONIC HEPATITIS C (LETTER TO EDITOR)

摘要

The prospective randomized clinical trial of Malaguarnera and colleagues, published in the current issue of Hepatitis Monthly, investigates the potential role of a commercially available HMG Co-A reductase agent—rosuvastatin (Crestor, Astra Zeneca) —in combination with non-pegylated interferon and ribavirin in the treatment of chronic hepatitis C (HCV). HMG Co-A reductase agents, commonly referred to as statins, are popular agents prescribed throughout the world, for their cholesterol lowering effects in order to reduce the risk of cardiovascular morbidity and mortality. They are well-recognized to improve liver biochemistry in dyslipidemic patients with non-alcoholic fatty liver disease (1); but recent reports have suggested that they may possess an antiviral effect on HCV independent of their lipid lowering activity. In an in vitro study (2), various statin agents were reported to have differing effects on HCV replication in combination with interferon with fluvastatin (Lescol, Novartis) exhibiting the strongest anti-HCV activity, atorvastatin (Lipitor, Pfizer) had moderate activity whereas pravastatin (Pravachol, Bristol Myers Squibb) had no activity. Likewise, the combination of statins—specifically simvistatin and mevastatin—in combination with protease/polymerase inhibitor agents were found to clear HCV replicons from culture (3). It is interesting that this in vitro study also found that pravastatin exhibited no antiviral activity (3). Clinically, the experience of statin agents in the treatment of HCV has not been very well-studied and the reported outcomes have been interesting yet at times conflicting. Fluvastatin monotherapy was reported to produce a modest 1.75 log decrease in HCV viral load in HCV monoinfected patients (4).