title: Increased plasma fibrinolytic activity in bleeding gastrointestinal angiodysplasia.
abstract: OBJECTIVE
  Gastrointestinal angiodysplasia is a major cause of recurrent bleeding. Haemostatic abnormalities have been implicated in the haemorrhage from these common vascular lesions but their precise contribution remains to be established. Our aim was to investigate whether bleeding angiodysplasia is associated with any specific coagulation disorder.
  
  
  METHODS
  Clinical features and blood samples were prospectively obtained from 21 patients with bleeding gastrointestinal angiodysplasia 3 months after the last episode of haemorrhage. Plasma levels of von Willebrand factor, D-dimer, plasminogen activator inhibitor type 1 (PAI-1), tissue-plasminogen activator activity, tissue factor pathway inhibitor and activated factor VII (FVIIa-rTF) were measured. A group of 14 patients with bleeding duodenal ulcer were similarly studied as controls.
  
  
  RESULTS
  Mean plasma von Willebrand factor levels were higher in angiodysplasia patients (208+/-12%) than in controls (143+/-11%) (P<0.05). D-dimer levels (661+/-80 ng/ml) and tissue-plasminogen activator activity levels (2.04+/-0.14 IU/ml) were also higher than in controls: 395+/-99 ng/ml and 1.6+/-0.1 IU/ml, respectively (P<0.05), whereas levels of PAI-1, FVIIa-rTF and tissue factor pathway inhibitor were similar in both groups. However, PAI-1 levels (31.5+/-11 ng/ml) were lower in high-bleeding-rate angiodysplasia (more than two bleeding episodes/year) than in low-bleeding-rate angiodysplasia (< or = 2 bleeding episodes/year) (PAI-1 47+/-14 ng/ml) (P<0.05). In a multivariate regression analysis, the plasma level of PAI-1 was a predictor of haemorrhage from angiodysplasia (P<0.05).
  
  
  CONCLUSIONS
  Increased plasma fibrinolytic activity may contribute to bleeding from angiodysplasia. Low plasma PAI-1 levels constitute a risk factor for bleeding tendency in patients with angiodysplasia.
authors.affiliation: Digestive System Research Unit, Hospital General Vall d'Hebron, Autonomous University of Barcelona, P Vall d'Hebron, Barcelona, Spain.
authors.forename: Félix
authors.initials: F
authors.lastname: Junquera
authors.forename: Esteban
authors.initials: E
authors.lastname: Saperas
authors.forename: Ana
authors.initials: A
authors.lastname: Anglés
authors.forename: Carmen
authors.initials: C
authors.lastname: Abadía
authors.forename: Jasone
authors.initials: J
authors.lastname: Monasterio
authors.forename: Juan-Ramón
authors.initials: JR
authors.lastname: Malagelada
mesh_terms: D000368:Aged; D016888:Angiodysplasia / Q000097:blood / Q000150:complications*; D001778:Blood Coagulation Disorders / Q000097:blood / Q000150:complications*; D001800:Blood Specimen Collection / Q000379:methods; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis; D006471:Gastrointestinal Hemorrhage / Q000097:blood / Q000209:etiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D012044:Regression Analysis; D012307:Risk Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator