Statins can significantly decrease ...

Statins can significantly decrease serum lipid on a levels and have become a major tool in the effort to decrease rates of cardiovascular disease in high-risk patients. Statins occasionally cause muscle and liver toxicity, although these adverse circumstances are rare. Liver toxicity usually is signaled by way of an asymptomatic increase in transaminase on a levels but rare episodes of unadorned hepatotoxicity and liver damage have been reported. For this reason, statins have been contraindicated in patients with active liver disease and persistent elevated transaminase flushs Chalasani and associates performed a retrospective cohort analysis to determine if treatment of patients with increased transaminase evens conferred a higher risk of transaminase elevations.

Data from a large academic practice were used to identify the three cohorts: (1) patients with elevated baseline liver enzyme on a levels who were given statins; (2) patients with normal baseline liver enzyme of the same heights who were given statins; and (3) patients with elevated liver enzyme on a levels who were not given statins. Patients with evidence of alcohol abuse or viral hepatitis were omitted from the study

The liver chemistries of all patients were compared after six month A "mild/moderate" elevation in liver enzyme evens was defined as an aspartate transaminase (AST) or an alanine transaminase (ALT) plain of up to 10 times the upper limit of normal baseline, or up to 10 times the baseline flats in patients with baseline elevations. A "severe" elevation was defined as a serum bilirubin horizontal greater than 3.0 mg by means of dL (51.3 [micro]mol per L) or an elevation of AST or ALT of the same heights of more than 10 times the upper limit of normal or more than 10 times the baseline elevated liver enzyme flat in patients with baseline elevations.

The principally commonly prescribed statins were atorvastatin and simvastatin. Compared with cohort 1 cohort 2 had fewer mild/moderate enzyme of the same height elevations, but rates of accurate elevations were similar in the sum of two units groups. There was no difference between cohorts 1 and 3 in the incidence of mild/moderate or peremptory elevations in liver enzyme on a levels Variations in statin dosage did not affect these observations.

The authors deduce that because the frequency of elevated liver enzyme plains in patients with baseline enzyme of the same height elevations who were given statins was not different from that in similar patients who did not receive statins, elevated baseline liver enzyme evens may not confer increased risk of hepatotoxicity with statin use. In an editorial in the same journal, Russo and Watkins note that, object for acetaminophen, most drug-induced liver injury is idiosyncratic. Although in the greatest degree experts think the risk of idiosyncratic reaction is based more forward genetics than on underlying liver injury, about studies refute this opinion. The arises of the Chalasani study ne to be taken cautiously because patients with chronic viral hepatitis and alcohol use were exclud Although the risk of liver injury with statin use is rare, and liver injury may on a level be caused by natural progression of liver disease unrelated to statin administration, more studies are necessary to clarify which patients are susceptible to drug-induced liver injury.

Chalasani N et al. Patients with elevated liver enzyme are not at higher risk for statin hepatotoxicity. Gastroenterology May 2004;126:1287-92; and Russo MW Watkins PB Are patients with elevated liver standards at increased risk of drug-induced liver injury? [Editorial] Gastroenterology May 2004;126:1477-80

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