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AB0184 A Link of Autoimmune Inflammation and Cardiovascular Risk Factors in Patients with Systemic Lupus Erythematosus

Background According to many studies systemic lupus erythematosus (SLE) is associated with an elevated risk of cardiovascular diseases due to early development of atherosclerosis. Several investigators have found that cytokines, C-reactive protein are increased both in patients with systemic inflammatory disease and with cardiovascular pathology. However the evidences of the autoimmune etiology of atherogenesis are discussed. Objectives The aim of our study was to determine an association of antiphospholipid antibodies (aPL), inflammatory markers and cardiovascular risk factors in patients with systemic lupus erythematosus and atherosclerotic alterations of the vessel wall. Methods The study included 40 female patients with SLE (met the ACR diagnostic criteria 1997), mean age 33,5 (27,5; 44,5) years old, disease duration 8,0 (5,0; 14,5) years, disease activity SLEDAI-2K 7,0 (4,0; 11,5) points. The control group was formed by 28 healthy women of the same age. The levels of LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glycoprotein-1 (aβ2-GP1), high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor - α (TNF-α), were determined with ELISA, according to the instruction of the manufactures. The presence of traditional (age, smoking, arterial hypertension, obesity, hypercholesterolemia) and non-traditional (disease duration, disease activity, the dose of prednisone) risk factors was assessed in patients with SLE. The atherosclerotic alterations of the common carotid artery were revealed ultrasonographically according to standard procedures. Results The asymptomatic atherosclerotic alterations of the vessel wall were found in 60,00% patients with SLE, 28,57% in the control group. The comparative analysis of aPL, inflammatory markers revealed an increase of aCL IgG, aβ2-GP1 IgG, LA, hs-CRP, IL-6, TNF-α levels in SLE patients with atherosclerosis as compared to the control subjects without it (p<0,0001, p=0,0007, p=0,002, p=0,011, p<0,0001, p=0,00007, respectively). The levels of aCL IgG/IgM, aβ2-GP1 IgG/IgM, LA, IL-6, TNF-α in patients with SLE without atherosclerosis were higher than in the control group, but the levels of inflammatory markers and antibodies under study were lower, than in SLE patients with atherosclerosis. An association between aCL IgG and TNF-α in patients with atherosclerosis was revealed during correlation analysis. We did not find any correlations between aPL and inflammatory markers in SLE patients without atherosclerosis. Selection by traditional and non-traditional risk factors in subjects with atherosclerotic alterations revealed positive correlation between aCL IgG and TNF-α in obesity (r=0,610, p=0,021), in arterial hypertension (r=0,509, p=0,044), in nonsmokers (r=0,587, p=0,013), in the disease duration less than 10 years (r=0,626, p=0,039). Conclusions Thus, we revealed an association between disease duration, disease activity, detected by the degree of increased proinflammatory cytokines (TNF-α) and by the presence of cardiovascular risk factors, which confirms polyetiology of atherosclerotic damage of the vessel wall in patients with SLE. Disclosure of Interest None declared