摘要
目的:探讨老年不稳定心绞痛患者P2Y12受体基因多态性对氯吡格雷抑制血小板聚集率的影响。方法:筛选255名老年不稳定型心绞痛患者,检测P2Y12外显子C34T和G52T多态性。测定服氯吡格雷前及服该药300mg后6 h血小板聚集率。结果:P2Y12外显子C34T、G52T的位点基因突变频率分别为16.01%和25.00%,其频率分布符合Hardy-Weinberg平衡。在5μmol/LADP诱导血小板聚集实验中,34T突变型组血小板聚集率降低的程度显著大于34C野生型组;52T突变型组血小板聚集率降低的程度显著小于52G野生型组。结论:老年不稳定心绞痛患者存在P2Y12受体基因多态性,P2Y12受体外显子C34T突变增强氯吡格雷抑制血小板聚集的作用,G52T突变减弱氯吡格雷抑制血小板聚集作用。
Objective To assess whether the clopidogrel response may be influenced by the C34T and G52T in P2Y12 gene polymorphism in patients. Methods 255 patients were included in our study and were divided into2 groups: CC homozygotes,CT heterozygotes with TT homozygotes. All patients received loading doses of 300 mg clopidogrel loading dose. Clopidogrel response was assessed by post-treatment 5 μmoL /-induced platelet aggregation. Results Significant variability in the distribution of platelet parameters was observed in the overall study population. The genotype frequencies of the C34T and G52T polymorphism were fit of a population to Hardy-Weinberg structure. Mutations in exons C34T and G52T influence individual response to ADP induced platelet aggregation. Conclusion Our study did show both C34T and G52T polymorphism of the P2Y12 receptor gene on clopidogrel response assessed in all patients. Clopidogrel response variability exists,52G > T which may result in increased risk for cerebrovascular events. Whether identification of the 34C > T polymorphism as a contributor to Improve curative effect,or rise adverse reaction. These findings imply that P2Y12 polymorphism have a impact on the future anti-aggregant strategies for patients on clopidogrel treatment.
出处
《湖南师范大学学报(医学版)》
2014年第2期49-51,共3页
Journal of Hunan Normal University(Medical Sciences)