title: Association of plasma soluble E-selectin and adiponectin with carotid plaque in patients with systemic lupus erythematosus.
abstract: BACKGROUND
  Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis but the mechanisms underlying this association are not understood. The role of endothelial dysfunction is hypothesized.
  
  
  METHODS
  In predominantly non-Caucasian patients with SLE (N=119) and controls (N=71), carotid ultrasonography was performed and circulating endothelial cells (CECs), soluble endothelial protein C receptor and gene polymorphism at A6936G, soluble E-selectin (sE-selectin), and adiponectin were assessed.
  
  
  RESULTS
  Carotid plaque was more prevalent among patients than controls (43% vs 17%, p=0.0002). Mean CCA IMT was greater in patients compared to controls (0.59+/-0.19 mm vs 0.54+/-0.11 mm, p=0.03). Among SLE patients, plaque was not associated with smoking, body-mass index, LDL, triglycerides, homocysteine, C-reactive protein, anti-ds DNA antibody, C3, C4, SLE activity, or medications. Age and levels of soluble E-selectin and adiponectin were significantly higher in the SLE patients with plaque compared to those without plaque in univariate and multivariate analyses. sE-selectin and adiponectin were found to serve as independent predictors of carotid plaque and that elevations were persistent over more than one visit. Unexpectedly, these biomarkers were present despite clinical quiescence.
  
  
  CONCLUSIONS
  Premature atherosclerosis is a consistent feature of SLE and extends across ethnicities. Higher levels of adiponectin may represent a physiological attempt to limit further endothelial damage already reflected by the elevation in sE-selectin and the observed increase in plaque represents overwhelming of this reparative process by atherogenic stimuli.
authors.affiliation: Department of Medicine, Division of Cardiology, New York University Langone School of Medicine, New York, NY 10016, USA.
authors.forename: Harmony R
authors.initials: HR
authors.lastname: Reynolds
authors.forename: Jill
authors.initials: J
authors.lastname: Buyon
authors.forename: Mimi
authors.initials: M
authors.lastname: Kim
authors.forename: Tania L
authors.initials: TL
authors.lastname: Rivera
authors.forename: Peter
authors.initials: P
authors.lastname: Izmirly
authors.forename: Paul
authors.initials: P
authors.lastname: Tunick
authors.forename: Robert M
authors.initials: RM
authors.lastname: Clancy
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D002340:Carotid Artery Diseases / Q000150:complications / Q000473:pathology*; D019040:E-Selectin / Q000096:biosynthesis / Q000097:blood*; D042783:Endothelial Cells / Q000166:cytology; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D012306:Risk
chemical_list: D052242:Adiponectin; D019040:E-Selectin