Patients with antiphospholipid syndrome display endothelial perturbation

J Autoimmun. 2010 Mar;34(2):105-10. doi: 10.1016/j.jaut.2009.07.004. Epub 2009 Aug 4.


Background: There is strong evidence that antiphospholipid antibodies (aPL) perturb endothelium both in vitro and in experimental animal models. by inducing a vasculopathy and an endothelial pro-inflammatory/coagulant phenotype. However, few contrasting studies raised the issue about the possibility to detect a comparable endothelial perturbation in anti-phospholipid syndrome (APS) patients. The aim of this observational case-control study was to evaluate several parameters of endothelial perturbation in patients with APS and without any other atherosclerosis risk factor.

Patients and methods: We investigated plasma levels of soluble adhesion molecules (s-ICAM-1, s-VCAM-1, s-E-selectin), soluble thrombomodulin (sTM), von Willebrand factor (vWF) and tissue plasminogen activator (t-PA) by solid-phase assays in 40 selected APS patients and 40 age- and sex-matched healthy subjects. In addition, we evaluated circulating endothelial cells by flow cytometry and brachial artery flow-mediated vasodilation. Patients and controls were free of conditions known to affect both the biological and the functional endothelial parameters.

Results: Plasma levels of sTM, s-E-selectin and s-VCAM-1 did not differ from controls, while a significant increase in s-ICAM-1 (P = 0.029), t-PA (P = 0.003) and vWF titres (P = 0.002) was found. Circulating mature endothelial cells were also significantly higher in patients than in controls (P = 0.05) and decreased during both vitamin K antagonists (P = 0.001) and antiplatelet (P = 0.032) treatments. Mean brachial artery flow-mediated vasodilation responses were significantly impaired compared to healthy subjects (P = 0.0001).

Conclusions: As a whole these findings indicate that APS patients display an endothelial perturbation in the absence of other detectable traditional risk factors for atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antibodies, Antiphospholipid / immunology
  • Antibodies, Antiphospholipid / metabolism*
  • Antiphospholipid Syndrome / blood
  • Antiphospholipid Syndrome / immunology*
  • Antiphospholipid Syndrome / pathology
  • Antiphospholipid Syndrome / physiopathology
  • Atherosclerosis
  • Brachial Artery / physiology*
  • Carotid Arteries / pathology*
  • Case-Control Studies
  • Cell Adhesion Molecules / blood
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Dilatation, Pathologic
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / immunology
  • Endothelium, Vascular / metabolism*
  • Endothelium, Vascular / pathology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Platelet Aggregation Inhibitors / pharmacology
  • Tissue Plasminogen Activator / blood
  • Tissue Plasminogen Activator / genetics
  • Tissue Plasminogen Activator / metabolism
  • von Willebrand Factor / genetics
  • von Willebrand Factor / metabolism


  • Antibodies, Antiphospholipid
  • Cell Adhesion Molecules
  • Platelet Aggregation Inhibitors
  • von Willebrand Factor
  • Tissue Plasminogen Activator