Statins can affect hepatic chemistry by altering lipid metabolism, but this phenomenon can also occur with other lipid-lowering drugs. A Meta-analysis from 13 placebo-controlled trials with a total of 43,275 patients assessed the effects of statins on hepatotoxicity, of which 27,276 received statin therapy. Of these, 5 were pravastatin trials (n=2619), 4 were lovastatin trials (n=16,085), 2 were fluvastatin trials (n=2106), and 2 were simvastatin trials (n=5605). After a median follow-up of 3.6 years, the incidence of liver transaminase levels elevated more than 3 times the upper limit of normal in patients receiving either statin or placebo was 1.14% and 1.05%, respectively (OR=1.26, 0.99-1.62). Analysis of single statins revealed that only fluvastatin significantly increased transaminase levels compared to placebo (1.13% v 0.29%; 3.54, 1.1-11.6). Another Meta-analysis, which assessed the relationship between transaminase levels and LDL-C reduction, pooled data from 23 statin treatment groups of 75,317 patients in 16 randomized controlled trials. 23 statin treatment groups, including lovastatin (5), simvastatin (6), pravastatin (5), fluvastatin (1), and atorvastatin (6), did not find The percentage of LDL-reduction was associated with an increase in transaminases. Analysis of statin doses revealed that a 10% reduction in LDL-C over 100,000 person-years of follow-up was associated with the occurrence of elevated transaminases in high, moderate, and low dose statins of 271, 195, and 114, respectively. this correlation was associated with a particular statin, such that the risk of transaminase abnormalities was four times greater with high dose atorvastatin than with low dose atorvastatin. Meta-analysis of both clinical trials did not show liver failure. Only 30 cases of statin-induced liver failure have been reported in the West between 1987 and 2000. The incidence of liver failure in statin-taking patients was estimated at 1 case per 1 million person-years of use, a figure similar to the entire US population. In patients who developed elevated alanine aminotransferase after statin administration, transaminase levels normalized despite continued administration, perhaps due to reduced hepatic steatosis. In addition, the elevated alanine aminotransferase may reflect hepatic adaptation to low serum cholesterol levels rather than a direct hepatotoxic effect of statins. Available data suggest that moderate to high doses of statins can slightly increase hepatic aminotransferases, but the changes are usually reversible and asymptomatic. In 2012, the FDA revised the product labeling of statins and no longer recommends routine monitoring of liver function in patients taking statins. U.S. guidelines recommend monitoring baseline transaminase levels prior to initiating statin therapy, with re-monitoring of liver function necessary only if liver disease is suspected. The guidelines do not make recommendations for regular monitoring of liver function.