Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement

The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.

Association of Soluble E-Selectin and Adiponectin with Carotid Plaque, Independent of Clinical Activity, in Patients with Systemic Lupus Erythematosus

Izmirly1,  Peter M., Reynolds1,  Harmony R., Rivera1,  Tania L., Kim2,  Mimi Y., Tunick1,  PA, Buyon1,  Jill P., Clancy1,  Robert M.

NYU School of Medicine, New York, NY,
AECOM, Bronx, NY


The mechanisms underlying premature atherosclerosis in SLE are not understood. The endothelium merits focus since it provides the physiologic boundary which limits extravasation and diapedesis of inflammatory cells.


One hundred and nineteen patients with SLE, predominantly non-Caucasian, and 71 healthy controls matched for age, sex and race, underwent carotid ultrasonography and donated blood for evaluation of circulating endothelial cells (CEC), soluble endothelial protein C receptor (sEPCR) and gene polymorphism at A6936G, soluble E-selectin, and adiponectin.


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 (0.59mm±0.19 vs 0.54mm±0.11, p=0.03). Levels of CEC (19 vs 3 CECs/mL, p<0.0001) and sE-selectin (64 vs 36 ng/ml, p<0.0001) were significantly elevated in patients compared to controls. Unexpectedly, adiponectin was also significantly higher in patients compared to controls (16 ug/mL versus 11 ug/mL, p=0.0001) but no differences were seen in the levels of sEPCR or the distribution of genotype. Independent predictors of plaque status using logistic regression models included: age (p<0.0001; OR=2.1 per 10 year increase; 95% CI: 1.5–3.0), SLE status (p=0.015; OR=3.4 for SLE vs control; 95% CI: 1.3–9.1), sE-selectin (p=0.016; OR=1.2 per 10 unit increase; 95% CI: 1.0–1.4) and adiponectin (p=0.050; OR=1.5 per 10 unit increase; 95% CI: 1.0–2.4). Comparing SLE patients with and without plaque, there were no differences in cardiac CRP, complement, anti-dsDNA ab, CEC, sEPCR levels and EPCR SNP. However, sE-selectin and adiponectin levels were significantly higher in SLE with plaque compared to those without (sE-selectin 78 vs 52 ng/ml; p=0.006; adiponectin 18 vs 14 ug/ml; p=0.033). The estimated odds ratios for plaque in the final logistic regression model were: ORselectin= 1.3 per 10 ng/ml increase (95% CI: 1.1–1.5) and ORadiponectin=1.8 per 10 ug/ml increase (95% CI: 1.1–3.0). SELENA-SLEDAI scores were similar between groups, and the proportion of patients with SLEDAI<= 4 did not segregate with the absence of plaque. Neither past nor current medications significantly associated with plaque. In the stable subjects (SLEDAI <=4), age (p=0.007), sE-selectin (p=0.02) and adiponectin (p=0.02) remained associated with plaque. The prevalence of plaque was greatest in the stable patients with high sE-selectin plus high adiponectin (55%; p =0.0009) confirming the multivariable analyses. Sixty-two patients donated blood at a second visit. High sE-selectin and adiponectin were sustained in plaque patients compared to non-plaque patients (p=0.0009 and p=0.0011 respectively).


These results confirm that SLE patients, irrespective of race, are at increased risk for premature atherosclerosis and support the hypothesis that endothelial perturbation is contributory even in the absence of clinically measurable disease activity.

To cite this abstract, please use the following information:
Izmirly, Peter M., Reynolds, Harmony R., Rivera, Tania L., Kim, Mimi Y., Tunick, PA, Buyon, Jill P., et al; Association of Soluble E-Selectin and Adiponectin with Carotid Plaque, Independent of Clinical Activity, in Patients with Systemic Lupus Erythematosus [abstract]. Arthritis Rheum 2009;60 Suppl 10 :1562
DOI: 10.1002/art.26636

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