119 - Resistance to antiplatelet drugs: molecular mechanisms and laboratory detection

Autor(s): M. Pugliano, M. Cattaneo

Issue: RIMeL - IJLaM, Vol. 5, N. 2, 2009 (MAF Servizi srl ed.)

Page(s): 119-124

Drugs that inhibit platelet function are widely used to decrease the risk of occlusive arterial events in patients with aterosclerosis. Aspirin irreversibly inhibits cyclo-oxygenase-1 (COX-1), thus affecting the arachidonate-thromboxane A 2 pathway, while clopidogrel affects the adenosine diphosphate (ADP) pathway, by irreversibly blocking the ADP receptor P2Y 12. Both these pathways contribute to the amplification of platelet activation and aggregation response to platelets agonists. The term “resistance” to a drug means the inability of a drug to hit its pharmacological target, demonstrable by a specific laboratory test. The prevalence of aspirin resistance, assessed by a specific laboratory test as serum thromboxane B 2 (TxB2), is about 1%; thus we can conclude that aspirin resistance does not exist or it is a very rare phenomenon. The most important cause of clopidogrel resistance is attributable to the inability of the hepatic cytochromes to metabolize the pro-drug to its active metabolite.
Key-words: blood platelets, drug resistance, platelet aggregation inhibitors.

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