AB1116 CORRELATION BETWEEN SERUM RESISTIN AND CAROTID INTIMA-MEDIA THICKNESS AS A MARKER OF SUBCLINICAL ATHEROSCLEROSIS IN SYSTEMIC LUPUS ERYTHEMATOSUS
Authors: Omnia Ahmed, Mona Abdel Mageed, Mohamed Barakat, Dalia Elneily, Ahmed Shaaban
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Although SLE management has improved markedly in the last few decades, cardiovascular disease (CVD) is still one of the most important leading cause of death. Subclinical atherosclerosis is increased in patients with SLE and it is not fully explained by traditional cardiovascular risk factors. Evidences suggest that resistin is involved in pathological processes leading to CVD including; inflammation, endothelial dysfunction, thrombosis, angiogenesis and smooth muscle cell dysfunction. Objectives: to determine the relation between serum resistin level and carotid intima-media thickness by doppler technique as a marker of premature or subclinical atherosclerosis in SLE patients. Methods: this is a cross-sectional study, carried on thirty Egyptian SLE patients who fulfilled the 2012 Systemic Lupus International Collaborating Clinics (SLICC) criteria. All patients had metabolic syndrome were excluded. Twenty healthy individuals, non smokers, matched for age and sex as controls. All patients were subjected to detailed history taking, a complete clinical examination. Laboratory investigations were done included serum resistin and HOMA was calculated, also the SLE disease activity index (SLEDAI 2K) and SLE disease damage index (SLEDDI) were applied and the scores were estimated. The carotid intima media thickness (CIMT) was assessed by carotid doppler ultrasonography. <h3>Results</h3> There was no statistically significant difference in serum resistin between SLE patients and healthy individuals (p=0.804). As regards the correlation with disease parameters Serum resistin show statistically significant correlation correlation with hs-CRP (p=0.027), HDL (p&lt;0.001), and ANA titre (p=0.013), but no significant correlation with HOMA, SLEDAI, SLEDDI, CIMT and different clinical activities. There was a statistically significant difference in CIMT between SLE patients and the controls (P= 0.006). <h3>Conclusion</h3> Although serum resistin is correlated with two of cardiovascular risk factors (HDL, hs-CRP), it doesn't correlate significantly with CIMT in SLE patients. Resistin is correlated to inflammation more than subclinical atherosclerosis. Moreover, SLE patients have higher CIMT than healthy population so SLE is considered a CVD risk factor. <h3>References</h3> [1] Gisterå A, Hansson GK. The immunology of atherosclerosis. Nature Reviews Nephrology. 2017 Jun;13(6):368. [2] Stanic AK, Stein CM, Morgan AC, Fazio S, Linton MF, Wakeland EK, Olsen NJ, Major AS. Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus. Proceedings of the National Academy of Sciences. 2006 May 2;103(18):7018-23. [3] Chu S, Ding W, Li K, Pang Y, Tang C. Plasma resistin associated with myocardium injury in patients with acute coronary syndrome. Circulation Journal. 2008;72(8):1249-53. <h3>Disclosure of Interests</h3> None declared