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Coagulation Activation in Patients With Binswanger Disease
Hidekazu Tomimoto, MD;
Ichiro Akiguchi, MD;
Hideaki Wakita, MD;
Akihiko Osaki, MD;
Masamichi Hayashi, MD;
Yasumasa Yamamoto, MD
Arch Neurol. 1999;56:1104-1108.
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 fragment1+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 fragment1+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 fragment1+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 fragment1+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.
From the Departments of Neurology, Faculty of Medicine, Kyoto University (Drs Tomimoto, Akiguchi, Wakita, and Osaki) and Kyoto Second Red Cross Hospital (Drs Hayashi and Yamamoto), Kyoto, Japan.
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