Effect of acute exacerbations on circulating endothelial, clotting and fibrinolytic markers in COPD patients

Intern Emerg Med. 2013 Oct;8(7):567-74. doi: 10.1007/s11739-011-0636-1. Epub 2011 Jun 10.


Patients with chronic obstructive pulmonary disease (COPD) are prone to clinical exacerbations that are associated with increased airway inflammation, a potent pro-thrombotic stimulus. Limited information is available on the mechanisms underlying the putative alterations of the endothelial-coagulative system during acute exacerbations. The aim was to investigate whether the activation of the endothelial-coagulative system occurs in association with the acute inflammatory response of COPD exacerbation. We monitored the blood levels of surrogate markers of inflammation: interleukin-6 (IL-6); endothelium damage: von Willebrand's factor (vWF); clotting activation: D-dimer (D-D), and prothrombin fragment 1+2 (F1+2); fibrinolytic response: plasminogen activator inhibitor 1 (PAI-1), in COPD subjects, during hospital admission and after clinical resolution. In 30 COPD subjects, IL-6, vWF, D-D and F1+2 levels were elevated during exacerbation and decreased significantly at clinical stability (IL-6, p = 0.005; vWF, p < 0.001; D-D, p < 0.001; F1+2, p < 0.001). PAI-1 levels did not change at exacerbation compared to clinically stable situations. Positive correlations were observed between several of the markers measured. Elevation of IL-6, vWF, D-D and F1+2 levels during COPD exacerbations implies a strict association between acute inflammation, endothelial activation and clotting initiation. This was not associated with a change in PAI-1, implying an increase in the fibrinolytic response to inflammation. The pro-thrombotic nature of COPD exacerbations sustained by enhanced clotting activation appears to be mitigated by excessive fibrinolysis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Biomarkers / blood*
  • Blood Coagulation / physiology*
  • Blood Gas Analysis
  • Endothelium, Vascular / physiopathology*
  • Female
  • Fibrin Fibrinogen Degradation Products / metabolism
  • Humans
  • Inflammation / blood
  • Interleukin-6 / blood
  • Male
  • Peptide Fragments / blood
  • Plasminogen Activator Inhibitor 1 / blood
  • Prothrombin
  • Pulmonary Disease, Chronic Obstructive / blood*
  • Pulmonary Disease, Chronic Obstructive / drug therapy
  • Pulmonary Disease, Chronic Obstructive / physiopathology*
  • Spirometry
  • von Willebrand Factor / metabolism


  • Biomarkers
  • Fibrin Fibrinogen Degradation Products
  • Interleukin-6
  • Peptide Fragments
  • Plasminogen Activator Inhibitor 1
  • fibrin fragment D
  • prothrombin fragment 1.2
  • von Willebrand Factor
  • Prothrombin