妊娠合并子痫前期内皮功能障碍与凝血电位障碍的发病关系[j]。

Sergeeva On, N. Chesnokova, E. Ponukalina, Rogozhina Ie, T. Glukhova
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引用次数: 9

摘要

到目前为止,内皮功能障碍在子痫前期不同器官和组织的凝血电位和微循环障碍机制中的作用还没有系统的信息。目的:我们的目的是通过建立内皮功能障碍在凝血潜在违规机制中的作用来扩展现有的先兆子痫诊断原则。方法采用前瞻性比较研究。常规技术研究的凝血过程条件,功能内皮参数(血浆中一氧化氮代谢物、内皮素1、血栓反应蛋白、血栓调节蛋白和细胞间粘附分子)- ELISA。结果研究组包括55例中度先兆子痫患者和49例重度先兆子痫孕妇,对照组为40例生理性妊娠。与对照组相比,中度子痫前期患者血浆内皮素-1 (p < 0.001)、血小板反应蛋白(p < 0.001)、细胞间黏附分子(p < 0.001)升高,一氧化氮水平降低(p < 0.001),纤溶时间增加(p < 0.050),国际标准化比值降低(p < 0.050)。随着子痫前期严重程度的增加,研究人员在患者血浆中检测到内皮素1 (p1 < 0.020)、血小板反应蛋白(p1 < 0.001)、细胞间粘附分子(p1 < 0.001)的逐渐增加,一氧化氮代谢物(p1 < 0.001)和血栓调节蛋白(p1 < 0.001)的减少;最后一种联合激活促凝剂止血。结论内皮功能障碍的发生、凝血潜能的损害与子痫前期临床症状的严重程度有一定的病理关系。为了扩大现有诊断子痫前期严重程度的技术数量,我们建议测量血浆中的内皮素1、血栓调节素、血栓反应蛋白、细胞间粘附分子和一氧化氮代谢物,并使用传统的指标来评估止血系统。
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[Pathogenetic Relationship between Endothelial Dysfunction and Disorders of Blood Coagulation Potential in Pregnancy Complicated by Pre-Eclampsia].
UNLABELLED Until now, there is no systematic information on the role of endothelial dysfunction in the mechanisms of disorders of blood coagulation potential and microcirculation in different organs and tissues in preeclampsia. OBJECTIVE Our aim was to extend the existing principles of diagnosis of pre-eclampsia by establishing the role of endothelial dysfunction in the mechanisms of blood coagulation potential violations. METHODS A prospective comparative study was performed. Condition of coagulation processes studied by conventional techniques, parameters of a functional endothelium (nitric oxide metabolites, endothelin 1, thrombospondin, thrombomodulin and intercellular adhesion molecules in blood plasma)--by ELISA. RESULTS The study group included 55 patients with moderate preeclampsia and 49 pregnant women with severe pre-eclampsia, in the control group--40 women with physiological pregnancy. In patients with pre-eclampsia moderate observed increase in plasma endothelin-1 (p < 0.001), thrombospondin (p < 0.001), intercellular adhesion molecules (p < 0.001) while reducing the level of nitrogen oxide (p < 0.001), increase in time of fibrinolysis (p < 0.050) and decreased international normalized ratio (p < 0.050) compared with the control group. With increasing severity of preeclampsia the researchers detected in blood plasma of patients a progressive increase in endothelin 1 (p1 < 0.020), thrombospondin (p1 < 0.001), intercellular adhesion molecules (p1 < 0.001) and decrease of nitric oxide metabolites (p1 < 0.001) and thrombomodulin (p1 < 0.001); the last combined with the activation of procoagulant hemostasis. CONCLUSION There is a pathogenetic relationship between the development of endothelial dysfunction, impaired blood coagulation potential and the severity of clinical signs ofpreeclampsia. To widen the number of existing techniques to diagnose the severity of pre-eclampsia we recommende to mesure endothelin 1, thrombomodulin, thrombospondin, intercellular adhesion molecules and nitric oxide metabolites in the blood plasma, and use traditional indicators to assess the hemostatic system.
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