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Abstract

Clopidogrel (Plavix®) is an orally administered pro-drug, whose pharmacology and therapeutic role has been extensively reviewed in recent publications.1-5 In essence, it results in selective and irreversible antagonism of ADP-induced platelet aggregation. Such aggregation normally results in the surface expression of platelet glycoprotein (GP) IIb/IIIa receptors, which facilitate fibrinogen binding as well as consequential further platelet aggregation – the final common pathway of vascular occlusion. Specific cytochrome P450 enzymes are thought to generate the responsible active metabolite (believed to persist transiently). However, dosage adjustment is not recommended in hepatic impairment (unless severe) and drug-drug interactions and co-administration with meals are believed to be unimportant.

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