目的:更多证据支持巴曲酶联合抗凝治疗对纠正急性脑静脉血栓形成(CVT)的益处。外周血血小板的动态波动,纤维蛋白溶解,并分析了该治疗期间的凝血生物标志物。
方法:我们研究了两种方案下巴曲酶对抗血栓系统的影响。治疗组包括在开始服用巴曲酶之前至少1周服用抗凝剂的患者。同时治疗组在入院时开始两种治疗。对照组仅接受抗凝治疗。巴曲酶隔天以10BU的剂量给予,5BU,和5BU,总共三个剂量。抗凝是连续的。基线数据为T0;每次巴曲酶给药后的第二天为T1、T2和T3。分析来自这四个时间点的数据。
结果:预处理组的时间点配对样本T检验结果[n=60;平均年龄(SD),43.3(16.5);38(63.35%)女性]显示巴曲酶显着抑制ADP诱导的血小板聚集率(T1-T0:p=0.015;T2-T0:p=0.025;T3-T0:p=0.013),纤维蛋白原水平降低(T1-T0:p<0.001;T2-T0:p<0.001;T3-T0:p<0.001),D-二聚体增加(T1-T0:p<0.001;T2-T0:p<0.001;T3-T0:p<0.001),TT(T1-T0:p=0.046;T2-T0:p=0.003;T3-T0:p<0.001),和APTT(T1-T0:p=0.021;T2-T0:p=0.012;T3-T0:p=0.026)。与对照组相比,同时治疗组显示显著高于TT(T2:p=0.002;T3:p=0.004)和D-二聚体(T1:p<0.001;T2:p<0.001;T3:p<0.001)值,而纤维蛋白原(T2:p<0.001;T3:p<0.001)水平显著降低。使用巴曲酶可以减轻抗凝剂引起的除TT以外的凝血指标变化幅度。以上结论与重复测量数据分析结果一致。
结论:巴曲酶能显著抑制ADP诱导的血小板聚集率,增加D-二聚体,降低纤维蛋白原,在抗凝剂存在下延长TT和APTT。使用巴曲酶可以减少抗凝剂引起的凝血指标变化的幅度。这些结果揭示了巴曲酶联合抗凝治疗CVT安全有效的潜在机制。
OBJECTIVE: More evidence supports the benefits of batroxobin combined with anticoagulation in correcting acute cerebral venous thrombosis (CVT). The dynamic fluctuations of peripheral blood platelets, fibrinolysis, and coagulation biomarkers during this therapy were analyzed.
METHODS: We investigated batroxobin\'s effects on the antithrombotic system under two regimens. The pretreatment group included patients on anticoagulants for at least 1 week before starting batroxobin. The simultaneous treatment group began both treatments upon admission. The control group received only anticoagulation. Batroxobin was given on alternate days at doses of 10BU, 5BU, and 5BU, totaling three doses. Anticoagulation was continuous. Baseline data were T0; the next day after each batroxobin dose was T1, T2, and T3. Data from these four time points was analyzed.
RESULTS: The time-point paired sample T-test results of the pretreatment group [n = 60; mean age (SD), 43.3(16.5); 38 (63.35%) women] showed that batroxobin significantly inhibited ADP-induced platelet aggregation rate (T1-T0: p = 0.015; T2-T0: p = 0.025; T3-T0: p = 0.013), decreased fibrinogen level (T1-T0: p < 0.001; T2-T0: p < 0.001; T3-T0: p < 0.001), and increased D-dimer (T1-T0:p < 0.001; T2-T0: p < 0.001; T3-T0: p < 0.001), TT (T1-T0:p = 0.046; T2-T0: p = 0.003; T3-T0: p < 0.001), and APTT (T1-T0:p = 0.021; T2-T0: p = 0.012; T3-T0: p = 0.026). Compared to the control group, the simultaneous treatment group showed significantly higher TT (T2: p = 0.002; T3: p = 0.004) and D-dimer (T1: p < 0.001; T2: p < 0.001; T3: p < 0.001) values, while fibrinogen (T2: p < 0.001; T3: p < 0.001) levels were significantly lower. Using batroxobin can alleviate the amplitude of changes in coagulation indicators other than TT caused by anticoagulants. The above conclusions are consistent with the results of repeated measurement data analysis.
CONCLUSIONS: Batroxobin can significantly inhibit ADP-induced platelet aggregation rate, increase D-dimer, decrease fibrinogen, and prolong TT and APTT in the presence of anticoagulant agents. Using batroxobin can reduce the amplitude of changes in coagulation indicators caused by anticoagulants. These results reveal the potential mechanism of batroxobin combined with anticoagulation in the safe and effective treatment of CVT.