机构地区:[1]天津市天津医院感染免疫风湿科,300211 [2]天津市天津医院放射科,300211
出 处:《中华危重病急救医学》2016年第9期834-838,共5页Chinese Critical Care Medicine
基 金:天津市医药卫生科技基金(2011KY26)
摘 要:目的探讨外周血接触系统的激活在系统性红斑狼疮(SLE)患者血栓事件发生机制中的作用。方法采用随机抽样方法,入选2014年6月至2016年2月天津医院风湿科收治的69例SLE患者,根据是否合并心血管疾病(VD)将患者分为单纯SLE组(38例)和SLE+VD组(31例),后者再根据合并VD的种类分为SLE合并心肌梗死(sLE+MI,10例)、SLE合并深静脉血栓(SLE+DVT,13例)、SLE合并动脉血栓(SLE+AT,8例)3个亚组;同期选取68例年龄、性别相匹配的健康体检志愿者作为健康对照组。采用酶联免疫吸附试验(ELISA)检测各组血浆Ⅻ因子-C抑制剂复合物(FⅫa-CIINH)和Ⅻ因子抗凝血酶复合物(FⅫa-AT)水平,流式细胞仪分析SLE患者血小板相关因子的含量;Spearman相关分析FⅫIa-CIINH和FⅫa-AT与血小板相关因子的相关性。绘制受试者工作特征曲线(ROC),分析FⅫa-cIINH和FⅫIa-AT对SLE血栓事件发生的预测价值。结果与健康对照组比较,SLE组血浆FⅫa-CIINH水平显著下降[nmol/L:0.00(0.00,0.07)比0.08(0.03,0.13),P〈0.01],FⅫa-AT水平显著升高[mnol/L:0.18(O.07,0.38)比0.16(0.12,0.26),P〈0.05]。与单纯SLE组相比,SLE+DVT组和SLE+AT组FⅫa-cIINH水平显著下降[nrnol/L:0.03(0.02,0.07)、0.02(0.01,0.04)比0.07(0.02,0.11),均P〈0.05],SLE+AT组血浆FⅫa-AT水平显著升高[nmol/L:0.34(0.21,0.52)比0.17(0.06,0.30),P〈0.01]。相关分析显示,SLE患者FⅫa-C11NH与FⅫa-AT呈显著负相关(r=-0.24,P=0.0416);干扰素介导跨膜蛋白1(IFITMl)、干扰素诱导双链RNA依赖性激活剂(PRKRA)的产生与FⅫa-AT上调和FⅫa-cIINH下降均有相关性(IFITM1与FⅫa-AT:r=0.39、P=O.0012,IFITMl与FⅫa-c1INH:r=-0.30、P=0.0146,PRKRA与FⅫa-AT:r=0.29、P=O.0176,PRKRA与FⅫa-Objective To explore the role of contact system activation in the mechanism of systemic lupus erythematosus (SLE) patients with thrombotic events. Methods A simple sample drawing study was conducted. Sixty-nine patients with SLE admitted to Department of Rheumatism in Tianjin Hospital from June 2014 to Februay 2016 were enrolled. The patients were divided into simple SLE group (n = 38) and SLE + vascular diseases (VD) group (n = 31) according to whether the patients complicated with VD or not. The VD patients were subdivided into three subgroups including SLE complicated with myocardial infarction (SLE + MI, n = 10), SLE complicated with deep vein thrombosis (SLE + DVT, n = 13), and SLE complicated with arterial thrombosis (SLE + AT, n = 8). Sixty-eight healthy age and gender-matched volunteers without history of VD were served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to detect the content of FⅫa-C1 inhibitor (FⅫa-CIINH) and FⅫa-antithrombin (FⅫa-AT) in plasma. Flow cytometry was used to analyze the contents of platelets associated factors. The correlation between platelet associated factor and FⅫA-CIINH and FX]/a-AT was analyzed by Spearman correlation analysis. Receiver operating characteristic curve (ROC) was plotted to analyze the predictive value of FXUA-CIINH and FⅫa-AT for SLE thrombotic events. Results Compared with health control group, the expression of FⅫa-CIINH in plasma in SLE group was significantly decreased [nmol/L: 0.00 (0.00, 0.07) vs. 0.08 (0.03, 0.13), P 〈 0.01], the expression of FⅫa-AT was significantly up-regulated [nmol/L: 0.18 (0.07, 0.38) vs. 0.16 (0.12, 0.26), P 〈 0.05]. Compared with the simple SLE group, the expression of FⅫa-CIINH in SLE + DVT and SLE + AT groups was significantly decreased [nmol/L: 0.03 (0.02, 0.07), 0.02 (0.01, 0.04) vs. 0.07 (0.02, 0.11), both P 〈 0.05], and the expression of FⅫa-AT in plasma in SLE + AT group was significant
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