Sun Ying, Lu Qing, Tao Xuefei, Cheng Biao, Yang Guoxing
Department of Geriatric Cardiology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Department of Operations Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Front Genet. 2020 Dec 22;11:576046. doi: 10.3389/fgene.2020.576046. eCollection 2020.
In recent years, the relationship between *2 gene polymorphism and clopidogrel resistance reflected by platelet function assay has been studied extensively, but there is no clear conclusion yet. In order to evaluate the relationship between *2 gene polymorphism and clopidogrel resistance more accurately, meta-analysis was conducted in this study. The I value taking 50% as the limit, the heterogeneity is judged as high or low, and then a random effect model or a fixed effect model is selected for statistical analysis. PubMed, EMBASE, Web of Science, CNKI, and China Wanfang database were searched, and the related literatures from the establishment of the database to May 2020 were collected and analyzed by STATA 15.0 software. A total of 3,073 patients were involved in 12 studies, including 1,174 patients with clopidogrel resistance and 1,899 patients with non-clopidogrel resistance. The results of this study showed that allele model (A vs. G): OR = 2.42 (95%CI: 1.97-2.98); dominant model (AA+GA vs. GG): OR = 2.74 (95%CI: 2.09-3.59); recessive model (AA vs. GA+GG): OR = 4.07 (95%CI: 3.06-5.41); homozygous model (AA vs. GG): OR = 5.70 (95%CI: 4.22-7.71); heterozygote model (GA vs. GG): OR = 2.32 (95%CI: 1.76-3.07), the differences were statistically significant. Also, the analysis of the Ethnicity subgroup indicated that the Asian allele model and the other four gene models were statistically significant. In conclusion, *2 gene polymorphism is strongly associated with clopidogrel resistance. Allele A, genotype GA, AA, and GG + GA can increase clopidogrel resistance, especially in the Asian population.
近年来，关于通过血小板功能检测反映的2基因多态性与氯吡格雷抵抗之间的关系已得到广泛研究，但尚未得出明确结论。为了更准确地评估2基因多态性与氯吡格雷抵抗之间的关系，本研究进行了荟萃分析。以50%为界限取I值，判断异质性高低，然后选择随机效应模型或固定效应模型进行统计分析。检索了PubMed、EMBASE、Web of Science、CNKI和中国万方数据库，并收集了从数据库建立至2020年5月的相关文献，采用STATA 15.0软件进行分析。12项研究共纳入3073例患者，其中氯吡格雷抵抗患者1174例，非氯吡格雷抵抗患者1899例。本研究结果显示，等位基因模型（A对G）：OR = 2.42（95%CI：1.97 - 2.98）；显性模型（AA + GA对GG）：OR = 2.74（95%CI：2.09 - 3.59）；隐性模型（AA对GA + GG）：OR = 4.07（95%CI：3.06 - 5.41）；纯合子模型（AA对GG）：OR = 5.70（95%CI：4.22 - 7.71）；杂合子模型（GA对GG）：OR = 2.32（95%CI：1.76 - 3.07），差异具有统计学意义。此外，种族亚组分析表明，亚洲人的等位基因模型和其他四种基因模型具有统计学意义。总之，*2基因多态性与氯吡格雷抵抗密切相关。等位基因A、基因型GA、AA以及GG + GA可增加氯吡格雷抵抗，在亚洲人群中尤为明显。
