Screening test for: Genetic Thrombophilia The GP IIb/IIIa complex is the most abundant receptor on platelet surface (about 80.000 copies/cell) and it’s formed by two protein chains non covalently associated, which role is to bind fibrinogen and von Willebrand factor. The protein chain gene GPIIIa (ITGB3 o GP3A) is localized on chromosome 17 locus q21.32 and has a SNP in exon 2, position 1565, with aminoacidic change in position 59, with leucine -> proline substitution. This genetic polymorphism is called HPA-1 or PlA1/PIA2. In this gene, it can be present the “a” allele (PlA1) or the “b” allele (PlA2). Homozygous aa subjects (PlA1/PlA1) are 74%, while heterozygous ab (PlA1/PlA2) are 24% of the population.

Homozygous bb subjects (PlA2/PlA2) are very rare, and represent about 2%. Platelets of subjects who bear the b allele (PlA2) in heterozygosis, and more over those of subjects bearing the b allele in homozygosis, have a higher capacity to bind fibrinogen and a bigger aggregability. Therefore, b allele (PlA2) has been associated to a higher risk for myocardial infarction, especially in young people and in smokers. It also could lead to increased risk for coronary restenosis after revascularization procedure with stent implantation. Finally, in this subject preventive therapy of restenosis e and complications should be modulated depending on the genotype, being b allele (PlA2) the most responsive to a combined treatment (aspirin + tyclopidin), compared to aspirin only treatment (aspirin resistance). Platelet polymorphism HPA-1 is also involved in pathogenetic mechanism of neonatal autoimmune thrombocytopenic purpura. In case of maternal-fetal incompatibility due to the allotypic system HPA-1, already during the first pregnancy there’s a transit of allo-immune antibodies from the mother to the fetus, with consequent neonatal thrombocytopenia. The kit is available in sizes from 24, 48 or 72 reactions.

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