The mean survival time of Child Pugh A patients was 14.4 years in the statin group and 7 years in the control group (0.01). of fibrosis. Finally, data from randomized controlled trials also confirmed that the addition of statin prolongs the survival of patients with advanced HCC even more than sorafenib. Statins are a very promising group of drugs especially in patients with liver disease, where therapeutic options can often be limited. Some indications, such as the prevention of re-bleeding from esophageal varices and the palliative treatment of HCC have been proven through randomized controlled trials, while additional indications still need to be confirmed through prospective studies. gene polymorphisms, pre-treatment hepatitis C virus (HCV) viral load, HCV reduction dynamics, the degree of fibrosis, study conducted by Ikeda et al showed that fluvastatin, lovastatin, simvastatin and atorvastatin prevent the replication of HCV RNA, and that this effect is significantly stronger in fluvastatin compared to other statins. studies showed varied results. Forde et al compared three groups of patients with chronic hepatitis C. Group A consisted of patients with dyslipidemia on statin treatment (without specification) for at least 60 d prior to the HCV RNA quantification, group B included dyslipidemic patients without statin, and group C included patients without dyslipidemia and not on statin treatment. The authors did not report significant differences in HCV RNA levels among these three groups of patients. Fluvastatin dosed 80 mg daily led to the reduction of HCV RNA in 50% of patients, with the highest weekly reduction by 1.75 decadic logarithm. The reduction of HCV RNA occurred in the first four weeks of treatment in 82% patients with viral response. However, after the reduction of the dose the HCV RNA increased in 22% of responders in the following 2-5 wk. Another observational study from Romania showed a significant decrease of HCV RNA after treatment with either 40 mg of fluvastatin or 20 mg Aminophylline of lovastatin (mean levels of HCV RNA before treatment 2376074 3427596 IU/mL, and 1321136 1343570 IU/mL after treatment, 0.001).The administration of both statins was associated with significant reduction of proinflammatory signaling by IL6 and TNF-, while the fluvastatin group also had lower IL-8 levels. On the other hand, a study by Sheridan et al did not find significant differences in HCV RNA levels between patients treated with 40-80 mg of fluvastatin (+/- -3-polyunsaturated fatty acids) and controls after 12 wk of treatment. The main limitation of this study is, that it included 35% of patients that had already been diagnosed with cirrhosis and 45% that were non-responders to PEG IFN treatment. Fluvastatin treatment also had a Aminophylline surprisingly negative effect in HCV/HIV coinfected patients, where it led to a mild increase of HCV RNA (HCV RNA before treatment 5.63 0.5 log10 IU/mL 5.84 0.6 log10 IU/mL after treatment, 0.001), compared to no change in HCV RNA in the control group. The effect of other statins on HCV RNA has not been proven in any studies. Simvastatin treatment for three months did not affect HCV RNA levels significantly and neither did the combination of simvastatin with sertralin. Twelve weeks treatment with rosuvastatin titrated to 40 mg daily led to the decrease of HCV RNA higher than one decadic logarithm Aminophylline only in one out of eleven patients. A FLJ34463 meta-analysis showed a relatively small but significant decrease of HCV RNA (0.2 decadic logarithm decrease, 95%CI: 0.09-0.31, 0.001) in patients treated with fluvastatin,but lovastatin, simvastatin, atorvastatin and rosuvastatin had no effect on HCV RNA levels. These results suggest that standard statin therapy does not have a significant effect on the dynamics of HCV RNA viral load, with the possible exception of fluvastatin. Despite the dubious effects of statins on HCV viral load, there is a distinctive antifibrotic effect of this treatment in HCV infected.