title: Patients with antiphospholipid syndrome display endothelial perturbation.
abstract: 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.
  
  
  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.
authors: Department of Internal Medicine, University of Milan, IRCCS Foundation Maggiore Hospital Policlinico, Mangiagalli, Regina Elena, Italy.
authors: Massimo
authors: M
authors: Cugno
authors: Maria Orietta
authors: MO
authors: Borghi
authors: Laura Maria
authors: LM
authors: Lonati
authors: Lorenzo
authors: L
authors: Ghiadoni
authors: Maria
authors: M
authors: Gerosa
authors: Claudia
authors: C
authors: Grossi
authors: Valentina
authors: V
authors: De Angelis
authors: Gaia
authors: G
authors: Magnaghi
authors: Angela
authors: A
authors: Tincani
authors: Daniela
authors: D
authors: Mari
authors: Piersandro
authors: P
authors: Riboldi
authors: Pier Luigi
authors: PL
authors: Meroni
mesh_terms: D000328:Adult; D000368:Aged; D017152:Antibodies, Antiphospholipid / Q000276:immunology / Q000378:metabolism*; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D050197:Atherosclerosis; D001916:Brachial Artery / Q000502:physiology*; D002339:Carotid Arteries / Q000473:pathology*; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood / Q000235:genetics / Q000378:metabolism; D004108:Dilatation, Pathologic; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D010959:Tissue Plasminogen Activator / Q000097:blood / Q000235:genetics / Q000378:metabolism; D014841:von Willebrand Factor / Q000235:genetics / Q000378:metabolism
chemical_list: D017152:Antibodies, Antiphospholipid; D015815:Cell Adhesion Molecules; D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator