Patients with elevated liver enzymes are not at higher risk for statin hepatotoxicity
Autor: | Joe Kesterson, Hisham Aljadhey, Naga Chalasani, Michael D. Murray, Stephen D. Hall |
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Rok vydání: | 2004 |
Předmět: |
Adult
Male medicine.medical_specialty Statin medicine.drug_class Elevated liver enzymes Hyperlipidemias Risk Assessment Gastroenterology Cohort Studies Internal medicine medicine Humans Aspartate Aminotransferases Aged Hepatology business.industry Incidence (epidemiology) Case-control study Alanine Transaminase Middle Aged Discontinuation Endocrinology Liver Case-Control Studies Cohort Female Hydroxymethylglutaryl-CoA Reductase Inhibitors Risk assessment business Cohort study |
Zdroj: | Gastroenterology. 126:1287-1292 |
ISSN: | 0016-5085 |
DOI: | 10.1053/j.gastro.2004.02.015 |
Popis: | Background & Aims: Studies that evaluate the risk of hepatotoxicity from statins in hyperlipidemic subjects with elevated baseline serum transaminases are lacking. We conducted a study to test the hypothesis that patients with elevated baseline liver enzymes have higher risk of statin hepatotoxicity. Methods: Our study consisted of the following 3 cohorts of patients seen between January 1, 1998 and June 31, 2002: Cohort 1: 342 hyperlipidemic patients with elevated baseline enzymes (AST >40 IU/L or ALT >35 IU/L) who were prescribed a statin; cohort 2: 1437 hyperlipidemic patients with normal transaminases who were prescribed a statin; and cohort 3: 2245 patients with elevated liver enzymes but who were not prescribed a statin. The effect of statins on liver biochemistries was assessed over a 6-month period after statins were prescribed. Elevations in liver biochemistries during follow-up were categorized into mild-moderate or severe based on predefined criteria. Results: The incidence of mild-moderate elevations and severe elevations in liver biochemistries in cohort 1 were 4.7% and 0.6%, respectively. Compared with cohort 1, individuals in cohort 2 had lower incidence of mild-moderate elevations (1.9%, P = 0.002) but not severe elevations (0.2%, P = 0.2). However, between cohorts 1 and 3, there were no differences in the incidence of mild-moderate elevations (4.7% vs. 6.4%, respectively, P = 0.2) or severe elevations (0.6% vs. 0.4%, respectively, P = 0.6). Statin discontinuation during the follow-up was similar between cohorts 1 and 2 (11.1% vs. 10.7%, respectively, P = 0.8). Conclusions: These data suggest that individuals with elevated baseline liver enzymes do not have higher risk for hepatotoxicity from statins. |
Databáze: | OpenAIRE |
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