Platelet polymorphisms in thrombotic disorders - 01/01/01
S. Santoso * *Correspondence and reprints:
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Résumé |
Plaque rupture and/or endothelial damage lead to exposure of von Willebrand factor (VWF) and collagen which facilitate the adhesion of circulating platelets via glycoprotein (GP) GPIb-IX-V and integrin α2β1, respectively, to the damaged vessel wall. This process activates the platelets and leads to a conformational change of a second integrin αIIbβ3 that facilitates fibrinogen binding and platelet aggregation. Thrombin generated at the blood-plaque interface converts fibrinogen to fibrin, which stabilizes thrombus growth. Therefore, any genetic differences that might alter surface expression or activity of these receptors could influence the risk for adverse outcome as a result of the hemostatic process. In the last five years, there has been a rapid accumulation of literature concerning the relationship between genetic variations in platelet glycoproteins and risk for coronary heart disease. In this study, we have presented a comprehensive review of the impact of platelet receptor polymorphisms and thrombotic risk.
Mots clés : acute myocardial infarction ; platelet receptor polymorphism ; thrombotic disorder ; thrombotic risk.
Plan
Vol 8 - N° 3
P. 261-266 - juin 2001 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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