AB1253 EVALUATION OF CYSTEINE-RICH 61 IN RHEUMATOID ARTHRITIS AS A DIAGNOSTIC MARKER AND PREDICTOR OF ATHEROSCLEROSIS
Authors: H. A. Esaily, D. M. Serag, M. S. Rizk, A. Sonbol, D. Salem
Journal: Annals of the Rheumatic Diseases (2020)

Background: Matricellular protein Cysteine-rich protein 61 (Cyr61) is involved in chronic inflammatory disorders like rheumatoid arthritis (RA) and atherosclerosis. Objectives: This study aimed to assess the value of serum Cyr61 in diagnosis of rheumatoid arthritis, evaluating its correlation with disease activity and its relation to atherosclerosis. Methods: Cross-sectional study included 105 RA patients classified into active and inactive groups according to disease activity score (DAS28) with 50 healthy age and gender-matched controls. Full clinical and laboratory assessment was done including enzyme-linked immunosorbent assay (ELISA) measurement of Cyr61. Bilateral assessment of carotid intima-media thickness (CIMT) was done using high resolution-ultrasonography. Comparison of Cyr61 between RA patients and controls, correlation between Cyr61 and disease activity and CIMT were analyzed with appropriate statistical analyses. Results: Significant elevation of Cyr61 in RA patients compared to controls (235.62±62.5 vs. 73.11±18.2) respectively. The cut off value of Cyr61 was 99.25 pg/ml, with area under the curve (AUC) =0.995, P &lt;0.001, 98 % sensitivity and 95% specificity. Cyr61 was inversely correlated with DAS28 and its components in RA patients (r=- 0.92, r=- 0.94) (p&lt;0.001). There was a significant positive correlation between Cyr61 levels and CIMT in inactive and active RA patients (r=0.88, r=0.47) respectively. Conclusion: Serum Cyr61 as a potential diagnostic biomarker in RA is inversely correlated with disease activity. High Cyr61 in RA is a risk factor for atherosclerosis. Disruption of serum Cyr61 is engaged in the pathogenesis of both rheumatoid arthritis and atherosclerosis which is a clue for a future treatment strategy of RA. References: [1]Smolen JS, Aletaha D, Barton A, Burmester GR, Emery P, Firestein GS, Kavanaugh A, McInnes IB, Solomon DH, Strand V, Yamamoto K (2018) Rheumatoid arthritis. Nature reviews Disease primers 4:18001. doi:10.1038/nrdp.2018.1 [2]Pelechas E, Kaltsonoudis E, Voulgari PV, Drosos AA (2019) Rheumatoid Arthritis. In: Pelechas E, Kaltsonoudis E, Voulgari PV, Drosos AA (eds) Illustrated Handbook of Rheumatic and Musculo-Skeletal Diseases. Springer International Publishing, Cham, pp 45-76. doi:10.1007/978-3-030-03664-5_3 [3]Sparks JA (2019) Rheumatoid Arthritis. Annals of Internal Medicine 170 (1):ITC1-ITC16. doi:10.7326/aitc201901010 [4]Abd El-Monem S, Ali A, Hashaad N, Bendary A, Abd El-Aziz H (2019) Association of rheumatoid arthritis disease activity, severity with electrocardiographic findings, and carotid artery atherosclerosis. Egyptian Rheumatology and Rehabilitation 46 (1):11-20. doi:10.4103/err.err_36_18 [5]Rawla P (2019) Cardiac and vascular complications in rheumatoid arthritis. Reumatologia 57 (1):27-36. doi:10.5114/reum.2019.83236 [6]de Brito Rocha S, Baldo DC, Andrade LEC (2019) Clinical and pathophysiologic relevance of autoantibodies in rheumatoid arthritis. Advances in Rheumatology 59 (1):2. doi:10.1186/s42358-018-0042-8 Disclosure of Interests: None declared