Patients with antiphospholipid syndrome display endothelial perturbation

Massimo Cugno, Maria Orietta Borghi, Laura Maria Lonati, Lorenzo Ghiadoni, Maria Gerosa, Claudia Grossi, Valentina De Angelis, Gaia Magnaghi, Angela Tincani, Daniela Mari, Piersandro Riboldi, Pier Luigi Meroni

Research output: Contribution to journalArticle

62 Citations (Scopus)

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. 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.

Original languageEnglish
Pages (from-to)105-110
Number of pages6
JournalJournal of Autoimmunity
Volume34
Issue number2
DOIs
Publication statusPublished - Mar 2010

Fingerprint

Antiphospholipid Syndrome
Thrombomodulin
E-Selectin
Brachial Artery
Vascular Cell Adhesion Molecule-1
von Willebrand Factor
Tissue Plasminogen Activator
Intercellular Adhesion Molecule-1
Vasodilation
Atherosclerosis
Healthy Volunteers
Endothelial Cells
Coagulants
Antiphospholipid Antibodies
Vitamin K
Endothelium
Case-Control Studies
Flow Cytometry
Animal Models
Phenotype

Keywords

  • Adhesion molecules
  • Anti-phospholipid syndrome
  • Endothelium
  • Risk factors

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Patients with antiphospholipid syndrome display endothelial perturbation. / Cugno, Massimo; Borghi, Maria Orietta; Lonati, Laura Maria; Ghiadoni, Lorenzo; Gerosa, Maria; Grossi, Claudia; De Angelis, Valentina; Magnaghi, Gaia; Tincani, Angela; Mari, Daniela; Riboldi, Piersandro; Meroni, Pier Luigi.

In: Journal of Autoimmunity, Vol. 34, No. 2, 03.2010, p. 105-110.

Research output: Contribution to journalArticle

Cugno, M, Borghi, MO, Lonati, LM, Ghiadoni, L, Gerosa, M, Grossi, C, De Angelis, V, Magnaghi, G, Tincani, A, Mari, D, Riboldi, P & Meroni, PL 2010, 'Patients with antiphospholipid syndrome display endothelial perturbation', Journal of Autoimmunity, vol. 34, no. 2, pp. 105-110. https://doi.org/10.1016/j.jaut.2009.07.004
Cugno, Massimo ; Borghi, Maria Orietta ; Lonati, Laura Maria ; Ghiadoni, Lorenzo ; Gerosa, Maria ; Grossi, Claudia ; De Angelis, Valentina ; Magnaghi, Gaia ; Tincani, Angela ; Mari, Daniela ; Riboldi, Piersandro ; Meroni, Pier Luigi. / Patients with antiphospholipid syndrome display endothelial perturbation. In: Journal of Autoimmunity. 2010 ; Vol. 34, No. 2. pp. 105-110.
@article{18a0a95ea4d34c3582240943d765ec56,
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. 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.",
keywords = "Adhesion molecules, Anti-phospholipid syndrome, Endothelium, Risk factors",
author = "Massimo Cugno and Borghi, {Maria Orietta} and Lonati, {Laura Maria} and Lorenzo Ghiadoni and Maria Gerosa and Claudia Grossi and {De Angelis}, Valentina and Gaia Magnaghi and Angela Tincani and Daniela Mari and Piersandro Riboldi and Meroni, {Pier Luigi}",
year = "2010",
month = "3",
doi = "10.1016/j.jaut.2009.07.004",
language = "English",
volume = "34",
pages = "105--110",
journal = "Journal of Autoimmunity",
issn = "0896-8411",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Patients with antiphospholipid syndrome display endothelial perturbation

AU - Cugno, Massimo

AU - Borghi, Maria Orietta

AU - Lonati, Laura Maria

AU - Ghiadoni, Lorenzo

AU - Gerosa, Maria

AU - Grossi, Claudia

AU - De Angelis, Valentina

AU - Magnaghi, Gaia

AU - Tincani, Angela

AU - Mari, Daniela

AU - Riboldi, Piersandro

AU - Meroni, Pier Luigi

PY - 2010/3

Y1 - 2010/3

N2 - 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.

AB - 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.

KW - Adhesion molecules

KW - Anti-phospholipid syndrome

KW - Endothelium

KW - Risk factors

UR - http://www.scopus.com/inward/record.url?scp=75349108595&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=75349108595&partnerID=8YFLogxK

U2 - 10.1016/j.jaut.2009.07.004

DO - 10.1016/j.jaut.2009.07.004

M3 - Article

C2 - 19656656

AN - SCOPUS:75349108595

VL - 34

SP - 105

EP - 110

JO - Journal of Autoimmunity

JF - Journal of Autoimmunity

SN - 0896-8411

IS - 2

ER -