%0 Journal Article
%T Small artery elasticity is decreased in patients with systemic lupus erythematosus without increased intima media thickness
%A Hans LA Nienhuis
%A Karina de Leeuw
%A Johan Bijzet
%A Jasper J van Doormaal
%A Arie M van Roon
%A Andries J Smit
%A Reindert Graaff
%A Cees GM Kallenberg
%A Marc Bijl
%J Arthritis Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/ar3145
%X Thirty SLE patients with inactive disease and 30 age- and sex-matched healthy controls were included. Twenty patients with essential hypertension (EH) served as positive control. SAE was assessed by pulse-wave analysis using tonometric recordings of the radial artery. IMT of the carotid arteries was measured by ultrasound. AGE accumulation was assessed with an AGE-reader. Endothelial activation markers and C-reactive protein (CRP) were determined by enzyme-linked immunosorbent assay (ELISA).SAE was decreased in SLE (P = 0.01) and further decreased in EH (P < 0.01) compared to healthy controls. IMT was increased in EH (P < 0.05), but not in SLE. AGE accumulation was increased in SLE (P < 0.05) and further increased in EH (P < 0.01) compared to healthy controls. Endothelial activation markers and CRP were increased in SLE but not in EH. SAE related to AGE accumulation (r = -0.370, P < 0.05), CRP (r = -0.429, P < 0.05) and creatinine clearance (r = 0.440, P < 0.05), but not to IMT and endothelial activation markers. In multivariate analysis SLE was an independent predictor of SAE.SAE is decreased in SLE patients without increased IMT, independently of traditional cardiovascular risk factors. Longitudinal studies are needed to investigate whether SAE, endothelial activation and AGE accumulation are early markers for cardiovascular disease in SLE.Systemic lupus erythematosus (SLE) is associated with an increased prevalence of cardiovascular disease (CVD), due to accelerated atherosclerosis [1,2]. Traditional cardiovascular risk factors cannot fully explain the presence of accelerated atherosclerosis in these patients, suggesting that other factors are involved [3-5]. A potential non-traditional risk factor in these patients is formation and accumulation of advanced glycation end products (AGEs). We previously showed that accumulation of AGEs is increased in SLE patients and that AGE accumulation is related to intima media thickness (IMT), a surrogate marker for atheroscl
%U http://arthritis-research.com/content/12/5/R181