间接作用抗凝剂治疗效果评价方法的优化

D. S. Korolova
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引用次数: 0

摘要

目标间接抗凝剂(维生素K拮抗剂)的治疗需要一种个性化的方法来控制凝血酶原的总体水平及其脱羧形式的积累。这项工作的目的是优化间接抗凝剂治疗的监测方法。方法。对来自心血管疾病患者的41份血浆样本进行了分析。已使用活化部分凝血活酶时间(APTT)、凝血酶原时间、ecamulin时间、统计数据分析(“Statistica 7”)。后果APTT测试可以识别患者对间接抗凝剂的个体敏感性。特别是,20%的患者凝血酶原总水平下降,再加上脱羧形式的积累,导致出血风险。11%的患者对维生素K拮抗剂的作用不敏感。结论为了控制间接抗凝血剂治疗的疗效,我们开发了一种测试方法,其中使用ecamulin(来自棘皮蛇毒液的蛋白酶)作为凝血酶原激活剂,它不仅可以激活功能活性的凝血酶原,还可以激活其脱羧形式。ecamulin与凝血酶原同时使用不仅可以测定血浆中功能活性凝血酶原的含量,还可以测定凝血酶原的总水平,这使得控制脱羧凝血酶原的积累成为可能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
OPTIMIZATION OF THE EVALUATION METHOD OF THE PERFORMANCE OF THERAPY USING INDIRECT ACTION ANTICOAGULANTS
Aim. Treatment by indirect anticoagulants (vitamin K antagonists) requires a personalized approach for controlling the overall level of prothrombin and the accumulation of its decarboxylated forms. The purpose of this work was to optimize the method for monitoring of the therapy with indirect anticoagulants. Methods. An analysis was performed of 41 blood plasma samples from patients with cardiovascula pathologies. Activated partial thromboplastin time (APTT), prothrombin time, ecamulin time, statistical data analysis (“Statistica 7”) have been used. Results. APTT test allowed identifying the individual sensitivity of patients to indirect anticoagulants. In particular, 20% of patients showed a decrease in the total level of prothrombin, which, together with the accumulation of decarboxylated forms, leads to a risk of bleeding. Individual insensitivity to the action of vitamin K antagonists was determined in 11% of patients. Conclusion. To control the efficacy of indirect anticoagulants therapy, we developed test in which ecamulin (protease from the venom of Echis multisquamatis) was used as a prothrombin activator, which can activate not only functionally active prothrombin, but also its decarboxylated forms. Use of ecamulin simultaneously with thromboplastin allows determining in the blood plasma the content of not only functionally active prothrombin, but also the total level of prothrombin, which makes it possible to control the accumulation of decarboxylated prothrombin.
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