Circulating Endothelial Cells as a Marker of Vascular Dysfunction in Patients With Systemic Lupus Erythematosus by Real-Time Polymerase Chain Reaction

Context.-Systemic lupus erythematosus (SLE) is associated with an increased risk of atherosclerosis; endothelial dysfunction represents the first step in its pathogenesis. Objective.-To assess endothelial dysfunction in SLE by circulating endothelial cells (CECs) and to characterize SLE-specific factors that contribute to its appearance. Design.-Case-control study was conducted on 60 subjects, divided into 2 groups: group A (30 patients with SLE) and group B (30 healthy sex-and age-matched controls). Total cholesterol, triglycerides, antinuclear antibodies, anti-double-stranded DNA antibodies, and C3 were determined in all patients. Systemic lupus erythematosus activity was assessed using the SLE Disease Activity Index. Endothelial function was assessed by means of flow-mediated dilation of the brachial artery using B-mode ultrasonography and relative quantification of CD 146 mRNA by real-time polymerase chain reaction. Results.-The group of SLE patients was formed of 20 females and 10 males, with a mean age of 31.16 +/- 9.69 years. The values of SLE-specific tests and SLE Disease Activity Index were represented by anti-double-stranded DNA antibodies 160 +/- 40.5, C3 68.91 +/- 11.91 mg/dL, total cholesterol 188.66 +/- 49.63 mg/dL, triglycerides 143.41 +/- 46.26 mg/dL, and SLE Disease Activity Index 12.66 +/- 3.70. Values for flow-mediated dilation were 8.85% +/- 2.02% (group A) and 20.33% +/- 6.19% (group B), P < .001, and CECs were 300 +/- 40.5 mu L-1 blood (group A) and 10 +/- 2.5 mu L-1 blood (group B). The statistical analysis showed a strong inverse correlation between CECs and SLE Disease Activity Index, a strong correlation between CECs and C3, a strong correlation between CECs and anti-double-stranded DNA antibodies, and a moderate inverse correlation between CECs and total cholesterol. Conclusion.-Endothelial dysfunction is present in SLE patients even in the absence of traditional cardiovascular risk factors due to disease activity. (Arch Pathol Lab Med. 2011;135:1482-1485; doi:10.5858/arpa.2010-0731-OA)