Metabolic syndrome is associated with decreased circulating endothelial progenitor cells and increased arterial stiffness in systemic lupus erythematosus

Abstract

Objectives

Metabolic syndrome (MetS) is highly prevalent in patients with systemic lupus erythematosus (SLE) and it has been associated with increased cardiovascular risk. We examined the contribution of MetS to inflammatory markers, arterial stiffness and circulating endothelial progenitor cells (EPCs) as surrogates of subclinical atherosclerosis.

Methods

Cardiovascular risk factors, SLE-specific factors and peripheral blood EPCs were assessed in 50 female SLE patients. MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III. Simultaneously, atherosclerosis was assessed by measuring the carotid–femoral pulse wave velocity (PWV) by doppler velocimetry.

Results

Beyond the factors included in the definition, SLE patients with MetS have a significantly higher serum level of uric acid (6.88 ± 2.20 vs 4.45 ± 1.17, p < 0.001) and some inflammatory biomarkers such as homocysteine, IL-8, sICAM-1 or complement molecules. The presence of MetS in our patients was closely linked with a significantly increased patient organ damage score (3.20 ± 1.97 vs 1.60 ± 1.67, p = 0.008), a decreased percentage of circulating EPCs (0.53 ± 0.24 vs 0.85 ± 0.57, p = 0.007) and an increased arterial stiffness (9.89 ± 2.40 vs 7.13 ± 1.51, p < 0.001).

Conclusions

MetS may contribute to the development of atherosclerosis by significantly increasing inflammation levels and arterial stiffness and decreasing circulating EPCs. This finding would justify close monitoring of these patients.