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| Clinical Background: | The formation of platelet aggregates requires the binding of fibrinogen and von Willebrand factor to a platelet surface receptor glycoprotein IIb/IIIa. Absence or defects in this receptor result in the platelet bleeding disorder Glanzmann’s thrombasthenia. Platelet membrane glycoproteins are highly polymorphous (eight human platelet antigen systems have been described) and alloimmune thrombocytopenias can result secondary to incompatibility of epitopes. Recently the PLA2 mutation of the glycoprotein IIIa gene was found to be associated with acute coronary events, especially in persons under 60 years of age. The prevalence of PLA2 was 2.1 times higher in persons wih myocardial infarction or unstable angina compared to matched controls without these conditions and a subgroup less than 60 years old had a PLA2 prevalence 3.6 times higher than controls. | |||||||||||||||||||
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