title: Coagulation activation in patients with Binswanger disease.
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.
  
  
  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.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan. tomimoto@isola.kuhp.kyoto-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Tomimoto
authors.forename: I
authors.initials: I
authors.lastname: Akiguchi
authors.forename: H
authors.initials: H
authors.lastname: Wakita
authors.forename: A
authors.initials: A
authors.lastname: Osaki
authors.forename: M
authors.initials: M
authors.lastname: Hayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000990:Antithrombin III; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000097:blood* / Q000150:complications*; D001927:Brain Diseases / Q000097:blood; D016022:Case-Control Studies; D015140:Dementia, Vascular / Q000097:blood* / Q000209:etiology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases; D011516:Prothrombin / Q000378:metabolism
chemical_list: C046193:antithrombin III-protease complex; D000990:Antithrombin III; D011516:Prothrombin; D005340:Fibrinogen; D010447:Peptide Hydrolases