Abstract
To examine serum interleukin 18 (IL-18), fetuin-A, soluble intercellular adhesion molecule-1 (sICAM-1), and endothelin-1 (ET-1) levels in ankylosing spondylitis (AS), psoriatic arthritis (PsA), and Synovitis Acne Pustulosis Hyperostosis Osteitis syndrome (SAPHO). We studied 81 AS, 76 PsA, and 34 SAPHO patients. We measured serum IL-18, fetuin-A, sICAM-1, ET-1, IL-6, IL-23, vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF). IL-18 levels were higher in AS (p = 0.001), PsA (p = 0.0003), and SAPHO (p = 0.01) than in controls, and were positively correlated with CRP (p = 0.03), VEGF (p = 0.03), and total cholesterol (TC, p = 0.006) in AS and with IL-6 (p = 0.03) in PsA. Serum fetuin-A levels were lower in AS (p = 0.001) and PsA (p = 0.001) than in controls, and negatively correlated with C-reactive protein (CRP) in AS (p = 0.04) and SAPHO (p = 0.03). sICAM-1 positively correlated with CRP (p = 0.01), erythrocyte sedimentation rate (ESR, p = 0.01), and IL-6 (p = 0.008) in AS, and with IL-6 (p = 0.001) in SAPHO. Serum ET-1 levels were lower in AS (p = 0.0005) than in controls. ET-1 positively correlated with ESR (p = 0.04) and Disease Activity Score 28 (DAS28, p = 0.003) in PsA. In spondyloarthritis, markers of endothelial function correlated with disease activity and TC.
Highlights
There is evidence of an increased risk of atherosclerosis and cardiovascular disease (CVD) in inflammatory rheumatic diseases [1,2,3,4,5,6,7,8,9]
We found no differences in serum Interleukin 18 (IL-18) levels between the Ankylosing spondylitis (AS), psoriatic arthritis (PsA), and SAPHO groups
The results of our study suggest that active inflammation in the course of SpA is connected with an increased IL-18 level, which stimulates endothelial dysfunction and may increase the risk of atherosclerosis in this group
Summary
There is evidence of an increased risk of atherosclerosis and cardiovascular disease (CVD) in inflammatory rheumatic diseases [1,2,3,4,5,6,7,8,9]. Inflammation in the course of arthritis, as well as traditional risk factors of atherosclerosis together with cytokines and adhesion molecules, influence endothelial activation and dysfunction. Interleukin 18 (IL-18), fetuin-A, soluble intercellular adhesion molecule-1 (sICAM-1), and endothelin-1 (ET-1) are a group of cytokines and adhesion molecules which activate and deregulate endothelial function, and could increase the risk of atherosclerosis [13,14,15,16,17,18,19,20]. Angiogenesis, stimulated by vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF), plays a role in the pathogenesis of SpA [23,24,25,26]
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