Influence of autoimmunity and inflammation on endothelial function and thrombosis in systemic lupus erythematosus patients

Clin Rheumatol. 2018 Aug;37(8):2087-2093. doi: 10.1007/s10067-018-4104-4. Epub 2018 Apr 20.

Abstract

The aim of this study is to assess the relationship between autoimmunity and endothelial activation/damage (ICAM-1 and vWF serum levels) and the degree of prothrombotic activity (thrombin-antithrombin complexes-TAT serum levels) in SLE. In 60 clinically stable SLE patients, levels of the following parameters were estimated in their serum: lupus anticoagulant (LA), anticardiolipin antibodies in both IgG and IgM classes (aCL-IgG and aCL-IgM, respectively), antiβ2GPI antibodies in both IgG and IgM classes (antiβ2GPI-IgG and antiβ2GPI-IgM, respectively), ICAM, von Willebrand factor (vWF), TAT, CRP, C3c, C4, and IL-6. ICAM-1 values exceeded the upper reference limit in 9 (15%) patients. vWF levels were increased in 21 (35%) patients. In all patients with elevated ICAM-1 values, vWF were also increased. TAT concentrations were elevated in 12 (20%) people. ICAM-1 were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). Similarly, ICAM-1 were significantly higher in patients with elevated antiβ2-GPI-IgM (> 20 SMU vs ≤ 20 SMU; p < 0.05). There was no significant difference in ICAM-1 levels in relation to LA-positivity. vWF were not significantly different in relation to antiphospholipid antibodies nor the inflammation marker levels. TAT were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). In one third of young patients with stable SLE, signs of endothelial activation/damage were found, as shown by elevated plasma ICAM-1 or vWF. Increased prothrombotic tendency manifested by elevated TAT was found in one fifth of the patients. Elevated anticardiolipin (IgM) and anti-β2-glycoprotein I (IgM) antibodies influence endothelial dysfunction and enhance prothrombotic state.

Keywords: Atherosclerosis; Autoimmune diseases; Endothelial dysfunction; Systemic lupus erythematosus.

MeSH terms

  • Adult
  • Aged
  • Antibodies, Anticardiolipin
  • Antithrombin III
  • Autoimmunity*
  • Endothelium, Vascular / physiopathology*
  • Female
  • Humans
  • Inflammation / physiopathology
  • Intercellular Adhesion Molecule-1 / blood*
  • Lupus Erythematosus, Systemic / blood*
  • Male
  • Middle Aged
  • Peptide Hydrolases / blood*
  • Thrombosis / blood*
  • Young Adult
  • von Willebrand Factor / analysis*

Substances

  • Antibodies, Anticardiolipin
  • ICAM1 protein, human
  • antithrombin III-protease complex
  • von Willebrand Factor
  • Intercellular Adhesion Molecule-1
  • Antithrombin III
  • Peptide Hydrolases