急性脑梗塞患者AECA、TM检测的临床意义被引量：6

The Detections and Clinical Significances of AECA and TM in Patients with Acute Cerebral Infarction

下载PDF

导出

摘要目的:通过对急性脑梗塞患者血清抗血管内皮细胞抗体(Antiendothelialcellantibodies,AECA)和血浆可溶性血栓调节蛋白(solublethrombomdulin,sTM)的联合检测,旨在探讨急性脑梗塞临床发病与血管内皮细胞损伤的内在关系。方法:采用间接荧光免疫法和双抗体夹心ELISA法检测66例急性脑梗塞患者(急性脑梗塞组)和35例献血员标本(对照组)的AECA、sTM水平。结果:急性脑梗塞组的AECA阳性率显著高于对照组(P<0.01);急性脑梗塞组治疗前sTM水平显著高于对照组(P<0.01);急性脑梗塞组治疗3～4周后sTM水平与对照组相比无显著性差异(P>0.05)。结论:AECA、TM的检测可作为急性脑梗塞血管内皮损伤的观察指标,有助于脑血管病变的诊断和治疗。 Objective:To examine serum antiendothelial cell antibodies (AECA) and plasma soluble thrombomdulin (sTM) in patients with acute cerebral infarction and interrelationship in the onset of acute cerebral infarction and endothelial cellular damage. Methods: AECA and TM were detected in 66 patients with acute cerebral infarction and in the controls with IIF and ELISA. Results: In 66 cases of acute cerebral infarction, the positive rate of AECA was 37.9% (25/66), and was much higher than that in the controls (P<0.01). In first 2 weeks of the disease, the sTM level was much higher than that of the normal group (P<0.01). After 4 weeks, the sTM level in treated patients was no difference from that in the normal group (P>0.05). Conclusion: The results suggest that the determinations of AECA and TM in patients with acute cerebral infarction have a certain value for the diagnosis and Treatments.

作者樊有龙徐建民王外梅李华

机构地区江西医学院第二附属医院检验科

出处《实用临床医学（江西）》 CAS 2005年第3期12-14,共3页 Practical Clinical Medicine

关键词脑梗塞急性抗血管内皮细胞抗体血栓调节蛋白 cerebral infarction,acute antiendothelial cell antibodies soluble thrombomdulin

分类号 R743.33 [医药卫生—神经病学与精神病学] R446.62 [医药卫生—诊断学]

引文网络
相关文献

参考文献7

1邓学新,曾学军.抗内皮细胞抗体临床意义及致病机制[J].中华风湿病学杂志,2003,7(3):175-177. 被引量：11
2周志中,吴竞生,叶山东,徐修才,莫蔚林.血管内皮损伤标记物在糖尿病肾病患者中的变化[J].血栓与止血学,2001,7(3):115-117. 被引量：5
3Cines DB,Lyss AP.Reeber LM,et al.Prseence of complement-fixing anti-endothelial cell antibidies in systemic lupus erythenatosus[J].Clin lnvest,1984,73:611～625.
4Aso Y,Inukai T,Takemura Y,et al.Mechanisms of elevation of serum and urinary concentrations of soluble thrombomdulin in diabetis patients:possible application as a marker for vascular endothelial injury[J].Metabolism,1998,47:362～365.
5Boffa MC,Karmochkine M,Thrombomodulin:an overview and potential implications in vascular disorders,lupus[J].1998,7(Suppl 2):120～125.
6Fukudome K,Ye X.Activation mechanism of anticoagulant protein C in large blood vessels involving the endothelial cell protein C receptor[J].Exp Med,1998,187:1 029～1 035.
7王建茹,冯忠军,李娜,曹志坤.急性脑梗塞患者血IL-1、IL-6、TNF、TM水平的变化及临床意义[J].中国免疫学杂志,2004,20(6):431-432. 被引量：13

二级参考文献16

1[1]Fukudome K, Ye X, Tsuneyoshi N, et al. Activation mechanism of anticoagulant protein C in large blood vessels involving the endothelial cell protein C receptorv. J Exp Med, 1998, 187:1029-1035.
2[2]Laszik Z, Mitro A, Taylor FB, et al. Human protein C receptor is present primarily on endothelium of large blood vessels: implications for the control of the protein C pathway. Circulation, 1997, 96: 3633-3640.
3[3]Fukudome K, Esmon CT. Identification, cloning and regulation of a novel endothelial cell protein C/activated protein C receptorv. J Biol Chem, 1994, 269: 26486-26491.
4[4]Stearns-Kurosawa DJ, Kurosawa S, Mollica JS, et al. The endothelial cell protein C receptor augments protein C activation by the thrombin-thrombomodulin complx. Proc Natl Acad Sci USA, 1996, 93:10212-10216.
5[6]Boffa MC, Karmocbkine M. Thrombomodulin: an overview and potential implications vascular disorders. Lupus, 1998,7:120-121.
6[7]Rinno H, Kuramoto T, Iijima T, et al. Measurement of soluble thrombonodulin in sera from various clinical stages of diabetic nephropathy. J Clin Lab Anal, 1996, 10: 119-124.
7[9]Aso Y, lnukai T, Takemura Y. Mechanism of elevation of serum and urinary concentrations of soluble thrombomodulin in diabetic patients: possible application as a marker for vascular endothelial injury. Metabolism, 1998, 47:362-365.
8[10]Sumida Y, Wada H, Fujii M, et al. Increased soluble febrin monomer and soluble thrombomodulin levels in non-insulin-dependent diabetes mellitus. Blood Coagul Fibrinolysis, 1997, 8:303-307.
9[1]Saliba E , Henrot A. Inflammatory mediators and neonatal brain damage[J]. Biology of the Neonate , 2001; 79(3-4):224-227.
10[2]Gregersen R , Lambertsem K , Finsen B . Microglia and macrophages are the major source of tumor necrosis factor in pernanent middle cerebral artery occlusion in mice[J]. J Cereb Blood Flow Metab, 2000;20(1):53-65.