摘要：
目的 探讨合并糖尿病的缺血性卒中患者阿司匹林治疗后血小板反应性变化及其影响因素.方法 纳入2016年9月至2017年12月期间在发病24 h内在威海市立医院神经内科住院治疗的急性缺血性卒中患者.所有患者均在入院后24 h内服用阿司匹林(100 mg/d),并于服药后(7±2)d应用PL-11血小板功能分析仪测定花生四烯酸(arachidonic acid,AA)诱导的血小板最大聚集率(maximum platelet aggregation ratio,MAR).记录患者基线资料,分析影响血小板高反应性(high platelet reactivity,HPR)的因素.结果 共纳入398例缺血性卒中患者,糖尿病组137例,非糖尿病组261例.糖尿病组MARAA(43.45％ ±14.11％ 对31.55％ ±19.39％;t=6.996,P<0.001)和HPR发生率(34.3％ 对19.9％;χ2=9.946,P=0.002)均显著高于非糖尿病组.在137例合并糖尿病的缺血性卒中患者中,47例存在HPR.HPR组高脂血症、既往卒中或短暂性脑缺血发作史的患者构成比以及基线NIHSS评分、稳态模型胰岛素抵抗指数(homeostatis model assessment-insulin resistance,HOMA-IR)、高敏C反应蛋白、空腹血糖和糖化血红蛋白均显著高于非HPR组(P均<0.05).多变量logistic回归分析显示,HOMA-IR[优势比(odds ratio,OR)1.153,95％ 可信区间(confidence interval,CI)1.027～1.295;P=0.016]、高敏C反应蛋白(OR 9.416,95％CI 2.271～39.049;P=0.002)、空腹血糖(OR 1.125,95％CI 1.025～1.235;P=0.013)、糖化血红蛋白(OR 1.458,95％CI 1.170～1.816;P=0.001)为发生HPR的独立危险因素.结论 合并糖尿病的缺血性卒中患者阿司匹林治疗期间血小板反应性仍较高,且血小板活性与炎症、胰岛素抵抗、血糖升高等多种机制有关.%Objective To investigate the changes of platelet reactivity and its influencing factors after aspirin treatment in patients with ischemic stroke complicated with diabetes. Methods From September 2016to December 2017, patients with acute ischemic stroke admitted to the Department of Neurology, Weihai Municipal Hospital within 24 h of onset were enrolled. All patients took aspirin (100 mg/d) within 24 h ofadmission, and after taking the drug (7 ±2 d), the PL-11 platelet function analyzer was used to determine the maximum platelet aggregation ratio (MAR) induced by arachidonic acid (AA). The baseline data of the patients were documented. The factors affecting high platelet reactivity (HPR) were analyzed. Results A total of 398 patients with ischemic stroke were enrolled, including 137 in the diabetes group and 261 in the non-diabetes group. MARAA (43. 45％ ± 14. 11％ vs. 31. 55％ ± 19. 39％; t = 6. 996, P < 0. 001) and the incidence of HPR (34. 3％ vs. 19. 9％; χ2 = 9. 946, P = 0. 002) in the diabetes group were significantly higher than in those in the non-diabetes group. Of the 137 patients with ischemic stroke complicated with diabetes, 47 had HPR. The proportions of patients with hyperlipidemia, previous history of stroke or transient ischemic attack and baseline NIHSS score, HOMA-IR (homeostatis model assessment-insulin resistance),high-sensitivity C-reactive protein, fasting blood glucose, and glycosylated hemoglobin in the HPR group were significantly higher than those in the non-HPR group (all P < 0. 05). Multivariate logistic regression analysis showed that HOMA-IR (odds ratio [OR] 1. 153, 95％ confidence interval [CI] 1. 027-1. 295; P =0. 016), high-sensitivity C-reactive protein (OR 9. 416, 95％ CI 2. 271-39. 049; P = 0. 002), fasting blood glucose (OR 1. 125, 95％ CI 1. 025-1. 235; P = 0. 013), and glycosylated hemoglobin (OR 1. 458, 95％ CI 1. 170-1. 816; P = 0. 001) were the independent risk factors for HPR. Conclusion The platelet reactivity during aspirin therapy in patients with ischemic stroke complicated with diabetes mellitus was high, and platelet activity was associated with multiple mechanisms, such as inflammation, insulin resistance, and hyperglycemia.
