Journal
LUPUS
Volume 25, Issue 2, Pages 129-136Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/0961203315603138
Keywords
Systemic lupus erythematosus; metabolic syndrome; endothelial progenitor cells; arterial stiffness; subclinical atherosclerosis
Categories
Funding
- Instituto de Salud Carlos III, Spain [PI10/01029]
- FundacioAL n para la InvestigacioAL n BiomeALdica Hospital Universitario Puerta de Hierro Majadahonda
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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 (6.882.20 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.
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