1Centro de Hematología y Medicina Interna de Puebla, Mexico.
Clin Appl Thromb Hemost. 2013 Nov-Dec;19(6):689-92. doi: 10.1177/1076029612448418. Epub 2012 Jun 29.
The sticky platelet syndrome (SPS) seems to be a common cause of thrombosis, although no molecular substrate to explain platelet hyperaggregability has been found.
To analyze an association between the SPS phenotype and the platelet glycoprotein (GP) IIIa PL(A1/A2) (human platelet antigen [HPA]-1a/b) gene polymorphism.
Along an 18-month period, Mexican mestizo thrombophilic patients were prospectively accrued. The SPS phenotype was assessed by aggregometry, whereas a tetra-primer amplification refractory mutation system (ARMS) polymerase chain reaction analysis was used to detect the PLA1 and PLA2 alleles.
A total of 95 individuals with SPS and 127 healthy donors were studied; in 11 of the donors and 16 of the patients with SPS the A2 allele of the GP IIb/IIIA was found, yielding a weak and nonsignificant association (odds ratio 2.14, 95% CI 0.94-4.85).
In Mexican mestizo patients, the platelet GP IIIa PL(A1/A2) gene polymorphism does not lead to the SPS phenotype.
粘性血小板综合征(SPS)似乎是血栓形成的常见原因,尽管尚未发现可解释血小板高聚集性的分子基础。
分析 SPS 表型与血小板糖蛋白(GP)IIIa PL(A1/A2)(人类血小板抗原[HPA]-1a/b)基因多态性之间的关联。
在 18 个月的时间内,前瞻性地招募了墨西哥混血血栓形成倾向患者。通过聚合酶链反应分析聚合酶链反应分析来评估 SPS 表型,而四引物扩增耐突变系统(ARMS)聚合酶链反应分析用于检测 PLA1 和 PLA2 等位基因。
共研究了 95 名 SPS 患者和 127 名健康献血者;在 11 名献血者和 16 名 SPS 患者中发现了 GP IIb/IIIa 的 A2 等位基因,这与较弱且无统计学意义的相关性(比值比 2.14,95%置信区间 0.94-4.85)。
在墨西哥混血患者中,血小板 GP IIIa PL(A1/A2)基因多态性不会导致 SPS 表型。