Most statins are thought to have modest antiviral activity. This may be from a statin’s ability to inhibit viral replication (mostly in vitro evidence). This retrospective study used a VA database of 8,293 HCV patients and aimed to identify predictors of sustained virologic response to Peginterferon + Ribavirin (unknown genotype) via logistic regression analysis. Any patient with HBV or HIV coinfection, HCC or OLTx was excluded.
The usual predictors of SVR were again noted here: race, cirrhosis, baseline viral load <400,000, and diabetes mellitus/insulin resistance. This may be the first study to show an inverse SVR relationship with HbA1C levels. Somewhat notable was the finding that statin use (simvastatin in 89% of cases) was also predictive. The OR for SVR in diabetic patients on a statin was 1.52, and in all patients on a statin was 1.39. As shown in the figure above, having a LDL < 100 is a negative predictor of SVR, but concomitant use of a statin negates this negative effect.
The study has some drawbacks. Genotype was unknown. Body weight was also unknown, and therefore appropriate Ribaviran weight based dosing could not be analyzed. Interestingly, 78% of the diabetic cohort was not on statin therapy, and only 10.8% of the entire cohort was on statin therapy. While I would not advise starting a statin drug specifically as an adjunct to antiviral therapy (until a randomized, prospective study proves beneficial), I would say that we should be less hesitant to use statins in patients with HCV and liver dysfunction when its use is indicated. To see the full article, click on the link below: