SummaryPrognosis of patients with early inflammatory arthritis (EIA) is highly variable. The aim of this study was to compare, longitudinally and crosssectionally, the levels of cytokine-expressing cells in peripheral blood (
In cardiovascular risks, OPG serum level might increase as a preventive compensatory mechanism to neutralize the RANKL level increment. The determination of the OPG-RANKL system is a diagnostic indicator for the intensity of vascular calcification and atherosclerosis in SSc patients.
AimThe aim of the study was to assess serum levels of interleukin (IL)-18 and IL-10 in systemic lupus erythematosus (SLE) patients and their relationship with disease activity.
Patients and methodsThirty patients with SLE and 20 healthy controls were investigated in this study. The serum IL-18 and IL-10 levels were determined using enzyme-linked immunosorbent assay and their correlations with the disease activity were measured using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), and laboratory parameters, including erythrocyte sedimentation rate, anti-ds DNA antibody, complement 3, and complement 4 levels were analyzed.
ResultsThe serum IL-18 and serum IL-10 levels were significantly higher (mean values 1770.2 ± 360.4 and 842.65 ± 315.37 pg/ml for IL-18 and IL-10, respectively) in SLE patients compared with the controls (110.65 ± 30.37 vs. 76 ± 14.2 pg/ml, respectively, P < 0.001). The increase in serum levels of IL-18 and IL-10 directly and significantly correlated with each other (r = 0.404, P = 0.037). Furthermore, such an increase in the levels of these two cytokines showed a highly significant positive correlation with the SLEDAI scores and anti-ds DNA in the studied patients (P < 0.001).
ConclusionThe circulating IL-18 and IL-10 concentrations were significantly elevated in SLE patients and correlated with the SLEDAI score. The study emphasized that there exists an upregulated proinflammatory as well as anti-inflammatory responses in patients with active SLE; however, the anti-inflammatory response is not enough to suppress the active disease. Identifying the exact contribution of the currently studied cytokines might provide future insights for targeted therapeutic strategies in SLE.[Downloaded free from http://www.err.eg.net on Sunday, June 07, 2015, IP: 49.204.26.195] Serum IL-18 and IL-10 in
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