HPA1～6、15基因多态性与急性心肌梗死相关性研究

Correlation of human platelet alloantigens-1 to-6 and-15 polymorphisms with acute myocardial infarction

目的研究贵州地区人类血小板抗原(HPA1～6、15)基因多态性与急性心肌梗死(acute myocardial infarc-tion,AMI)的相关性。方法选择AMI患者86例(61.05±10.27岁),符合1979年WHO诊断标准,并行冠脉造影证实;对照组85例(60.74±6.88岁),排除心脑血管疾病及血栓性疾病。采用序列特异性引物-聚合酶链反应(SSP-PCR)技术扩增目的基因,进行HPA基因分型,回归分析其在AMI中的危险因素。结果①与对照组比较,AMI组HPA2基因多态性差异有统计学意义(P<0.01,OR=34.169,95%CI 14.553～80.221),而HPA1、3～6、15基因多态性差异无统计学意义(P>0.05);②影响AMI发病的多因素回归分析显示:与对照组比较,AMI组中HPA1ab基因型差异无统计学意义(P>0.05),但其在AMI发病的危险度比HPA1aa纯合子增加了4.256倍;HPA2aa基因型和HPA2b等位基因差异有统计学意义(P<0.01,OR=0.148,95%CI 0.071～0.307;P<0.01,OR=6.221,95%CI 3.201～12.091)。结论①HPA1ab杂合子患AMI的危险度较HPA1aa纯合子增加;②HPA2aa纯合子可能是AMI发病的保护因子,而HPA2b等位基因可能是AMI发病的独立遗传性危险因素。

Objective To investigate the correlation between gene polymorphism of human platelet antigens （HPA1-6, 15） in Guizhou Province and acute myocardial infarction （AMI）. Methods A total of 86 newly diagnosed AMI patients with a mean age of 61.05± 10.27 years, who were in line with 1979 WHO diag- nostic criteria, identified with coronary angiography and hospitalized in our affiliated hospital form April 2010 to October 2010 were enrolled in this study. Another 85 health individuals with a mean age of 60.74± 6.88 and without any cardiovascular disease and thrombosis served as control. Sequence-specific primer-polymerase chain reaction （SSP-PCR） was employed to amplify the target gene, and genotype HPA gene. Regression analysis was used to analyze whether its polymorphism was the risk factors of AMI. Results Compared with the control group, HPA2 polymorphism in AMI group had significantly difference （P 〈 0.01, OR = 26.36, 95% CI = 8. 317 to 83. 549）, while HPA1,3-6, 15 gene polymorphism had no difference （P 〉0.05）. Multiple regres- sion analysis showed there was no significant difference in HPAlab genotype between AMI group and control （ P 〉 0.05 ）, but HPAlab genotype had 4.3-fold higher risk in the incidence of AMI than HPA1 aa homozygote. There was statistically significant difference in HPA2aa genotype and HPA2b allele （ P 〈 0.01, OR = 0. 148, 95%CI=0.071 to0.307; P〈0. 01,OR=6.221,95%CI=3.201 to 12.091）. Conclusion HPAlab heter- ozygous carriers have a higher risk of AMI compared with those with HPAlaa homozygote. HPA2aa homozygote may be a protective factor for AMI onset, while HPA2b allele might be an independent genetic risk factor for incidence of AMI.