title: Endothelial cell activation and blood coagulation in critically ill patients with lung injury.
abstract: BACKGROUND
  Adult respiratory distress syndrome is a life-threatening disease that requires respiratory assistance. It is associated with endothelial cell damage, coagulation activation, and intravascular fibrin deposition. This prospective study was conducted to determine whether the plasma levels of specific markers of endothelial cell function and coagulation activation are related to the degree of pulmonary disturbance.
  
  
  METHODS
  Fourteen patients (8 male, 6 female, median age 69 years), admitted to a medical intensive care unit with various stages of lung injury needing mechanical ventilation, were compared with 16 healthy age- and sex-matched control subjects.
  
  
  RESULTS
  Markers of endothelial cell damage and coagulation activation were significantly elevated in patients with lung injury compared with controls: von Willebrand factor (vWF) 4.12 vs. 1.25 U/ml, p < 0.0001; F VIII 4.40 vs. 1.88 U/ml, p = 0.0001; tissue-type plasminogen activator (tPA) 11.6 vs. 8.7 ng/ml, p = 0.02; plasminogen activator inhibitor-1 (PAI) 48.9 vs. 14.6 ng/ml, p < 0.0001; D-dimer 2.9 vs. 0.6 microgram/ml, p < 0.0001; thrombin-antithrombin III complex (TAT) 7.9 vs. 2.2 ng/ml, p < 0.0001 (median values; Mann-Whitney U-test). vWF, tPA, PAI and D-Dimer were significantly correlated with the PaO2/FiO2 ratio (p = 0.0003, 0.003, 0.04, 0.02, respectively; Spearman's rank correlation).
  
  
  CONCLUSIONS
  These findings suggest that the endothelial cell disturbance and the activation of the coagulation system in patients with lung injury are related to the degree of pulmonary dysfunction.
authors.affiliation: Department of Internal Medicine I, University of Vienna, Vienna, Austria.
authors.forename: Catharina
authors.initials: C
authors.lastname: Wenzel
authors.forename: Julia
authors.initials: J
authors.lastname: Kofler
authors.forename: Gottfried J
authors.initials: GJ
authors.lastname: Locker
authors.forename: Klaus
authors.initials: K
authors.lastname: Laczika
authors.forename: Peter
authors.initials: P
authors.lastname: Quehenberger
authors.forename: Michael
authors.initials: M
authors.lastname: Frass
authors.forename: Paul
authors.initials: P
authors.lastname: Knöbl
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers; D001777:Blood Coagulation / Q000502:physiology*; D001780:Blood Coagulation Tests; D016638:Critical Illness; D003627:Data Interpretation, Statistical; D004730:Endothelium, Vascular / Q000166:cytology*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D007362:Intensive Care Units; D008168:Lung / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010447:Peptide Hydrolases / Q000032:analysis; D011175:Positive-Pressure Respiration; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; D000990:Antithrombin III; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator