Platelet aggregation abnormalities in patients with fetal losses: the GP6 gene polymorphism

ObjectiveTo evaluate the GP6 gene polymorphism in patients with sticky platelet syndrome (SPS) and fetal loss.DesignGenetic association study.SettingPerinatal center.Patient(s)Twenty-seven patients with SPS, manifested as fetal loss, and 42 control subjects without SPS and no history of fetal loss and thrombosis.Intervention(s)SPS was diagnosed by platelet aggregometry (PACKS-4 aggregometer; Helena Laboratories). 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.Result(s)We found a higher occurrence of three SNPs of the GP6 gene in SPS patients versus control subjects (rs1671153: 0.204 vs. 0.048, odds ratio [OR] 5.116, 95% confidence interval [CI] 1.536–17.03; rs1654419: 0.204 vs. 0.071, OR 3.326, 95% CI 1.149–9.619; rs1613662: 0.204 vs. 0.071, OR 3.326, 95% 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, 95% CI 1.142–11.14; and CGATAG in haplotype 6: 0.204 vs. 0.048, OR 4.961, 95% CI 1.488–16.53).Conclusion(s)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.