TY - JOUR
T1 - Association of plasma soluble E-selectin and adiponectin with carotid plaque in patients with systemic lupus erythematosus
AU - Reynolds, Harmony R.
AU - Buyon, Jill
AU - Kim, Mimi
AU - Rivera, Tania L.
AU - Izmirly, Peter
AU - Tunick, Paul
AU - Clancy, Robert M.
N1 - Funding Information:
This work was supported by a research grant to R.M.C. from the Lupus Research Institute, New York, NY. and by NIH/NCRR M01 RR0096. P.M.I. was supported by SLE Foundation, Inc. H.C. was supported by the Arthritis Foundation, New York Chapter.
PY - 2010/6
Y1 - 2010/6
N2 - 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.
AB - 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.
KW - Adiponectin
KW - Atherosclerosis
KW - Carotid stenosis
KW - E-selectin
KW - Systemic lupus erythematosus
UR - http://www.scopus.com/inward/record.url?scp=77953231701&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77953231701&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2009.12.007
DO - 10.1016/j.atherosclerosis.2009.12.007
M3 - Article
C2 - 20044088
AN - SCOPUS:77953231701
SN - 0021-9150
VL - 210
SP - 569
EP - 574
JO - Atherosclerosis
JF - Atherosclerosis
IS - 2
ER -