Association of plasma soluble E-selectin and adiponectin with carotid plaque in patients with systemic lupus erythematosus

• Published in: Atherosclerosis Vol. 210; no. 2; pp. 569 - 574
• Main Authors: Reynolds, Harmony R, Buyon, Jill, Kim, Mimi, Rivera, Tania L, Izmirly, Peter, Tunick, Paul, Clancy, Robert M
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01-06-2010; Elsevier
• Subjects: Adiponectin; Adiponectin - blood; Adult; Atherosclerosis; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cardiovascular; Carotid Artery Diseases - complications; Carotid Artery Diseases - pathology; Carotid stenosis; Coronary heart disease; E-selectin; E-Selectin - biosynthesis; E-Selectin - blood; Endothelial Cells - cytology; Endothelium, Vascular - pathology; Female; Gene Expression Regulation; Heart; Humans; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - complications; Lupus Erythematosus, Systemic - pathology; Male; Medical sciences; Middle Aged; Polymorphism, Genetic; Regression Analysis; Risk; Systemic lupus erythematosus; Carotid stenosis; E-selectin; Systemic lupus erythematosus; Atherosclerosis; Adiponectin; Human; Immunopathology; Connective tissue disease; Skin disease; Nervous system diseases; E Selectin; Autoimmune disease; Cardiovascular disease; Artery; Cerebral disorder; Arterial disease; Vascular disease; Blood vessel; Carotid; Systemic disease; Central nervous system disease; Circulatory system; Cerebrovascular disease
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/j.atherosclerosis.2009.12.007

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. Conclusion 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.