POS0529 ANTI-TNF AND METHOTREXATE PROTECT AGAINST RHEUMATOID ARTHRITIS ATHEROSCLEROSIS
Authors: M. Rojas-Giménez, M. Á. Puche Larrubia, I. Gómez García, J. Calvo Gutierrez, M. C. Ábalos-Aguilera, A. Escudero Contreras
Journal: Annals of the Rheumatic Diseases (2021)

Objectives: To analyze the effect of differents anti-rheumatic treatments on the carotid intima-medial thickness (cIMT) in patients with Rheumatoid Arthritis (RA). Methods: Controlled cross-sectional observational study of a cohort of patients with RA. 146 patients with RA (ACR/EULAR2010).cIMT was measured by semi-automatic carotid ultrasound.Other variables: atheroma plaques, bilateral plaques, DAS28-VSG, lipid metabolism, apoB, apoA1, apoB/apoA1, uric acid, homocysteine. Biological or conventional synthetic disease-modifying antirheumatic drug therapy (bDMARDs/csDMARDs), glucocorticoids. Descriptive, bivariate, Spearman’s test and multivariate model were constructed to identify factors associated with cIMT. Results: The baseline characteristics are shown in Table 1.Significant positive correlation was found between cIMT and apoB ( r =0.22; p =0.014), apoB/apoA1 ( r =0.18; p =0.044), cholesterol( r =0.23; p =0.006),triglycerides( r =0,21, p =0.013),uric acid( r =0.26; p =0.009),age( r =0.65, p &gt;0.001),RF (r =0.16, p =0.05) homocysteine ( r =0.5, p &lt;0.001), BMI ( r =0.19, p =0.023),CRP( r =0.18, p =0.032) and negative correlation with anti-TNFα treatment time( r =-0.20, p =0.02).Patients receiving bDMARDs alone or combined with csDMARDs had less cIMT than those taking only csDMARDs[median (IQR): 0.54 (0.50-0.63), 0.57(0.53-0.65) and 0.65(0.53-0.75); p=0.046].The factors associated with cIMT were age(ß= 0.007, p &lt;0.001),anti-tnf-α treatment ever(ß= -0.06, p =0.027) and methotrexate treatment ever(ß= -0.07, p =0,08). Table 1. Baseline characteristics Variables RA n=146 Epidemiological characteristics and comorbidities Age (years), mean (SD) 55.9 (13.1) Female sex; n (%) 112 (76.7) Smoker, n (%) 30 (21.6) Arterial hypertension, n (%) 45 (30.8) Diabetes mellitus, n (%) 5 (3.4) Previous Cardiovascular disease, n (%) 10 (14.6) Hyperlipidemia, n (%) 46 (31.5) BMI (kg/m 2 ), median (IQR) 26.8 (23.4-29.7) Clinical-laboratory characteristics Disease duration, years, median (IQR) 6.77 (2.2-14.2) Erosions, n (%) 53 (36.6) RF positive, n (%) 119 (81.55) ACPA positive, n (%) 123 (84.2) CRP (mg/dl), median (IQR) 4.8 (1.6-11.5) ESR (mm/h), median (IQR) 12 (6-24) DAS28 at protocol, median (IQR) 2.8 (2.1-3.7) HAQ, mean (SD) 0.78 (0.6) ApoB (mg/dl), mean (SD) 86.8 (21.8) ApoA1 (mg/dl), mean (SD) 149.8 (32.7) Cholesterol (mg/dl), mean (SD) 198.7 (37.3) cLDL (mg/dl), mean (SD) 119.3 (30.3) cHDL (mg/dl), median (IQR) 56 (47-70) Triglycerides (mg/dl), median (RIQ) 92 (73-121) Homocisteyne (mg/dl), median (RIQ) 2.08 (1.7-2.8) cIMT mean (mm), median (IQR) 0.6 (0.53-0.7) Atherosclerotic plaques, n (%) 51 (34.9) Bilateral plaques, n (%) 22 (15.1) Anti-rheumatic treatment Synthetic DMARDs ever, n (%) 146 (100) Methotrexate ever, n (%) 132 (90.4) Time with methotrexate (years), median (IQR) 4.4 (1.04-9.5) Leflunomide ever, n (%) 83 (56.8) Sulfasalazine ever, n (%) 13 (8.9) Hydroxychloroquine ever, n (%) 99 (67.8) Biological DMARDs ever, n (%) 76 (52.05) Anti TNFα ever, n (%) 47 (32.2) Time with antiTNF-α (years), mean (SD) 1.18 (2.8) Jak inhibitor ever, n (%) 10 (6.8) Anti-IL-6 ever, n (%) 28 (19.2) Rituximab ever, n (%) 15 (10.3) Glucocorticoids at protocol, n (%) 82 (56.5) Glucocorticoids dose at protocol (mg), median (IQR) 5 (0-5) Abbreviations: RF: rheumatoid factor; ACPA: anti-citrullinated peptide antibodies, cIMT: carotid intima media thickness; ApoB: apolipoprotein B, ApoA1: apolipoprotein A1, LDL: low-density lipoprotein; HDL: high-density lipoprotein; DAS28: 28-joint Disease Activity Score; HAQ: Health Assessment Questionnaire; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate; IL-6: interleukin 6; Anti TNF, anti–tumor necrosis factor Conclusion: biological disease-modifying antirheumatic drug therapy, in particular Anti TNFα, could protect against the development of atherosclerosis in RA Disclosure of Interests: None declared