Coagulation activation in patients with Binswanger disease.
Coagulation activation in patients with Binswanger disease.
复制标题
Binswanger 病患者的凝血激活。
作者：
H. Tomimoto;I. Akiguchi;H. Wakita;A. Osaki;M. Hayashi;Yasumasa Yamamoto
背景
高凝状态通常与脑血管病（CVD）中的急性卒中相关。然而，在宾斯旺格病（BD），没有信息是可用的凝血-纤溶途径，除了存在高血浆纤维蛋白原水平。
目的
探讨BD与凝血-纤溶通路激活的关系。
患者和方法
我们检测了17例BD患者、24例无CVD的神经系统患者和26例急性或慢性腔隙性脑梗死患者的纤维蛋白原、凝血酶-抗凝血酶复合物、凝血酶原片段（1+2）和交联D-二聚体水平。
结果
与非CVD组和腔隙性脑梗死组相比，BD患者的凝血酶-抗凝血酶复合物（P<0.001）、凝血酶原片段（1+2）（P<0.05）和交联D-二聚体（P<0.01）水平显著升高。与非CVD组相比，纤维蛋白原水平也显著升高（P<0.05）。在BD组中，8例病情稳定的患者（即过去3个月内无明显神经功能缺损的患者）的纤维蛋白原、凝血酶-抗凝血酶复合物、凝血酶原片段（1+2）或交联D-二聚体水平正常或轻度升高。相反，9例局灶性或皮质下脑功能亚急性恶化的BD患者（恶化组）与稳定患者相比，凝血酶-抗凝血酶复合物水平显著升高（P<0.01）。同样，纤维蛋白原、凝血酶原片段（1+2）和交联D-二聚体水平在恶化患者中升高，但这种趋势未达到统计学显著性。
结论
这些结果表明，凝血-纤溶途径被激活的BD患者的亚急性加重。凝血激活可能导致这些患者脑内形成微血栓和微循环障碍，从而促进进一步的生物学和神经损伤。
BACKGROUND
A hypercoagulable state is often associated with an acute stroke in cerebrovascular disease (CVD). However, in Binswanger disease (BD), no information is available on the coagulation-fibrinolysis pathway except for the presence of high plasma fibrinogen levels.
OBJECTIVE
To determine the association of BD and coagulation-fibrinolysis pathway activation.
PATIENTS AND METHODS
We examined the levels of fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), and cross-linked D-dimer in 17 patients with BD, 24 neurologic patients without CVD, and 26 patients with lacunar infarction in either the acute or chronic stage.
RESULTS
As compared with the non-CVD and lacunar infarction groups, the patients with BD had significantly elevated levels of thrombin-antithrombin complex (P<.001), prothrombin fragment(1+2) (P<.05), and cross-linked D-dimer (P<.01). There was also a significant increase in fibrinogen levels compared with the non-CVD group (P<.05). In the BD group, 8 patients in stable condition (ie, those without obvious neurologic deficits in the past 3 months) showed normal levels or a mild increase in their fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), or cross-linked D-dimer levels. In contrast, 9 patients with BD with a subacute aggravation of their focal or subcortical cerebral functions (deteriorating group) showed a significant increase in their thrombin-antithrombin complex levels compared with the stable patients (P<.01). Similarly, the fibrinogen, prothrombin fragment(1+2), and cross-linked D-dimer levels were elevated in the deteriorating patients, but this trend did not reach statistical significance.
CONCLUSIONS
These results indicate that the coagulation-fibrinolysis pathway is activated in patients with BD with a subacute aggravation. Coagulation activation may result in the formation of microthrombi and microcirculatory disturbances in the brains of these patients, and thus promote further biological and neurologic insults.