Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Weber, A.A. et al.

Weber, Meila, Jacobs, Weber, Kelm, Strauer, Zotz, Scharf, Schrör,

Low incidence of paradoxical platelet activation by glycoprotein IIb/IIIa inhibitors.

The human platelet antigen-1 (HPA-1, Pl(A)) polymorphism has been proposed to influence the inhibitory actions of abciximab. Thus, we hypothesized that this polymorphism might also be the cause for paradoxical activation of platelets by GPIIb/IIIa inhibitors. The effects of abciximab (1-10 microg/ml), tirofiban (3-30 nM), or eptifibatide (0.3-3 microg/ml) on basal and ADP (3 microM)-induced CD62P externalization were measured in n=62 healthy blood donors and n=177 patients with stable coronary artery disease. All subjects were genotyped for the human platelet antigen-1 (HPA-1, Pl(A)) polymorphism by GALIOS(R) and fluorescence correlation spectroscopy. Although a significant platelet hyperreactivity was observed in the patients, the HPA-1 genotype did not influence basal or ADP- induced CD62P expression. A moderate (twofold) stimulation of CD62P expression by abciximab but not by tirofiban or eptifibatide was observed in one patient. Interestingly, this patient carried the HPA-1 b/b genotype. In no other subject any activation of platelets by GP IIb/IIIa inhibitors was observed and there were no statistically significant differences between HPA-1 genotypes with respect to the effects of GP IIb/IIIa inhibitors on basal or ADP- stimulated CD62P expression. It is concluded that paradoxical platelet activation by abciximab is a rare (<2%) phenomenon. HPA-1 b/b genotype might be a contributing factor but clearly does not predict platelet activation by GP IIb/IIIa inhibitors.[1]

References

Low incidence of paradoxical platelet activation by glycoprotein IIb/IIIa inhibitors. Weber, A.A., Meila, D., Jacobs, C., Weber, S., Kelm, M., Strauer, B.E., Zotz, R.B., Scharf, R.E., Schrör, K. Thromb. Res. (2002) [Pubmed]

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