期刊
PHARMACOTHERAPY
卷 26, 期 11, 页码 1601-1607出版社
WILEY
DOI: 10.1592/phco.26.11.1601
关键词
statin; 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor; HMG-CoA reductase inhibitor; P-glycoprotein; P-gp; multidrug-resistant transporter protein 1; atorvastatin; fluvastatin; lovastatin; pravastatin; rosuvastatin; simvastatin
Understanding the mechanisms of drug interactions with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) has become increasingly important because of the potential for serious adverse effects, most notably myopathy. Most of the evidence supports the role of cytochrome P450 (CYP) isoenzymes in many of these drug interactions. However, P-glycoprotein (P-gp), an efflux protein located in the gastrointestinal tract, placenta, kidneys, brain, and liver, may also play a role. Results of several studies with in vitro models have shown that lovastatin, simvastatin, and atorvastatin are inhibitors for P-gp and may be substrates for this transporter as well. Pravastatin and fluvastatin consistently demonstrate no significant inhibition of P-gp. Drug interaction studies involving statins and digoxin support a role for P-gp. Many additional drugs such as diltiazem, verapamil, itraconazole, ketoconazole, and cyclosporine, as well as dietary supplements such as St. John's wort and grapefruit juice, interact with statins and are modulators of both CYP3A4 and P-gp. However, the role of P-gp in these specific drug interactions remains unclear.
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