title: No evidence of activated blood coagulation in Crohn's disease.
abstract: BACKGROUND
  Thromboembolism seems to be a significant and serious complication in Crohn's disease (CD), and multifocal microvascular infarction of the intestinal mucosa may be an important effector mechanism in the pathogenesis of CD. Therefore, it has been hypothesized that an increased activation of the blood coagulation system may favour thromboembolic complications.
  
  
  OBJECTIVE
  To assess the activity of blood coagulation as a potential index of thromboembolic risk in CD using thrombin-antithrombin III complex (TAT).
  
  
  METHODS
  Prospective evaluation of TAT.
  
  
  METHODS
  Out-patients at the gastroenterological department of a university hospital.
  
  
  METHODS
  Eighty patients with CD, 47 with inactive (Crohn's disease activity index (CDAI) < 150) and 33 with active disease, and 80 healthy controls were investigated in this study.
  
  
  METHODS
  TAT and fibrinogen were used as parameters of blood coagulation. C-reactive protein and orosomucoid were used as serum inflammatory parameters.
  
  
  RESULTS
  Fibrinogen was significantly higher in patients with active CD (median 535 mg/dl; interquartile range 402-620 mg/dl) than in patients with inactive CD (357 mg/dl; 300-467 mg/dl) or controls (268 mg/dl; 231-299 mg/dl). Fibrinogen correlated with CDAI, C-reactive protein and orosomucoid. TAT did not show any difference between patients with active CD (3.2 ng/ml; 2.5-4.6 ng/ml), inactive CD (3.0 ng/ml; 2.4-3.9 ng/ml) and controls (3.1 ng/ml; 2.3-3.6 ng/ml). Correspondingly, TAT correlated neither with serum inflammatory parameters and CDAI nor with fibrinogen.
  
  
  CONCLUSIONS
  We could not find evidence of activation of the blood coagulation system as determined by TAT plasma levels in CD, not even in patients with active disease. TAT is not, therefore, a potential index of thromboembolic risk in CD and of microvascular infarction as an effector mechanism in the pathogenesis of CD.
authors.affiliation: Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Vienna, Austria.
authors.forename: G
authors.initials: G
authors.lastname: Novacek
authors.forename: S
authors.initials: S
authors.lastname: Kapiotis
authors.forename: G
authors.initials: G
authors.lastname: Moser
authors.forename: W
authors.initials: W
authors.lastname: Speiser
authors.forename: A
authors.initials: A
authors.lastname: Gangl
authors.forename: H
authors.initials: H
authors.lastname: Vogelsang
mesh_terms: D000328:Adult; D000990:Antithrombin III / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D003424:Crohn Disease / Q000097:blood* / Q000150:complications; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000378:metabolism*; D011446:Prospective Studies; D012307:Risk Factors; D018709:Statistics, Nonparametric; D013923:Thromboembolism / Q000209:etiology
chemical_list: D015415:Biomarkers; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D005340:Fibrinogen; D010447:Peptide Hydrolases