Coagulation activation in patients with Binswanger disease

Hidekazu Tomimoto, Ichiro Akiguchi, Hideaki Wakita, Akihiko Osaki, Masamichi Hayashi, Yasumasa Yamamoto

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)1104-1108
Number of pages5
JournalArchives of Neurology
Volume56
Issue number9
DOIs
Publication statusPublished - 01-09-1999

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Vascular Dementia
Fibrinogen
Cerebrovascular Disorders
Fibrinolysis
Lacunar Stroke
Nervous System
Activation
Neurologic Manifestations
Stroke

All Science Journal Classification (ASJC) codes

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

Cite this

Tomimoto, H., Akiguchi, I., Wakita, H., Osaki, A., Hayashi, M., & Yamamoto, Y. (1999). Coagulation activation in patients with Binswanger disease. Archives of Neurology, 56(9), 1104-1108. https://doi.org/10.1001/archneur.56.9.1104
Tomimoto, Hidekazu ; Akiguchi, Ichiro ; Wakita, Hideaki ; Osaki, Akihiko ; Hayashi, Masamichi ; Yamamoto, Yasumasa. / Coagulation activation in patients with Binswanger disease. In: Archives of Neurology. 1999 ; Vol. 56, No. 9. pp. 1104-1108.
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abstract = "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.",
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Tomimoto, H, Akiguchi, I, Wakita, H, Osaki, A, Hayashi, M & Yamamoto, Y 1999, 'Coagulation activation in patients with Binswanger disease', Archives of Neurology, vol. 56, no. 9, pp. 1104-1108. https://doi.org/10.1001/archneur.56.9.1104

Coagulation activation in patients with Binswanger disease. / Tomimoto, Hidekazu; Akiguchi, Ichiro; Wakita, Hideaki; Osaki, Akihiko; Hayashi, Masamichi; Yamamoto, Yasumasa.

In: Archives of Neurology, Vol. 56, No. 9, 01.09.1999, p. 1104-1108.

Research output: Contribution to journalArticle

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T1 - Coagulation activation in patients with Binswanger disease

AU - Tomimoto, Hidekazu

AU - Akiguchi, Ichiro

AU - Wakita, Hideaki

AU - Osaki, Akihiko

AU - Hayashi, Masamichi

AU - Yamamoto, Yasumasa

PY - 1999/9/1

Y1 - 1999/9/1

N2 - 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.

AB - 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.

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Tomimoto H, Akiguchi I, Wakita H, Osaki A, Hayashi M, Yamamoto Y. Coagulation activation in patients with Binswanger disease. Archives of Neurology. 1999 Sep 1;56(9):1104-1108. https://doi.org/10.1001/archneur.56.9.1104