Platelet aggregation abnormalities in patients with fetal losses The GP6 gene polymorphism

This work evaluates the GP6 gene polymorphism in 27 patients with sticky platelet syndrome and fetal loss and in 42 healthy control subjects. Higher occurrence of two haplotypes in the patients shows that GP6 gene polymorphism may be associated with platelet hyperaggregability.

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Juraj Sokol, M.D., Kamil Biringer, M.D., Ph.D., Maria Skerenova, M.Sc., Miroslav Hasko, M.D., Lenka Bartosova, M.D., Ph.D., Jan Stasko, M.D., Ph.D., Jan Danko, M.D., Ph.D., Peter Kubisz, M.D., Ph.D.

Vol 98, Issue 5, Pages 1170-1174



To evaluate the GP6 gene polymorphism in patients with Sticky platelet syndrome (SPS) and fetal loss.


Genetic association study.


Perinatal center.


Twenty-seven patients with SPS, manifested as fetal loss, and 42 control subjects without SPS and no history of fetal loss and thrombosis.


SPS was diagnosed by platelet aggregometry (PACKS-4 aggregometer, Helena Laboratories, USA). Seven single nucleotide polymorphisms (SNPs) of the GP6 gene were evaluated.

Main Outcome Measure(s):

Occurrence of SNPs of the GP6 gene in SPS patients versus control subjects.


We found a higher occurrence of three SNPs of the GP6 gene in SPS patients vs. controls (rs1671153: 0.204 vs. 0.048, OR 5.116, CI 1.536-17.03; rs1654419: 0.204 vs. 0.071, OR 3.326, CI 1.149-9.619, rs1613662: 0.204 vs. 0.071, OR 3.326, CI 1.149-9.619). The haplotype analysis showed a significantly higher occurrence of two haplotypes (CTGAG in haplotype 5: 0.185 vs. 0.059, OR 3.568. CI 1.142-11.14, and CGATAG in haplotype 6: 0.204 vs. 0.048, OR 4.961, CI 1.488-16.53).


Our results, especially the higher occurrence of haplotypes CTGAG and CGATAG in SPS patients, support the idea that GP6 gene polymorphism may be associated with platelet hyperaggregability, a possible cause of fetal loss.

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