POS0529 ANTI-TNF AND METHOTREXATE PROTECT AGAINST RHEUMATOID ARTHRITIS ATHEROSCLEROSIS
Authors: Rojas-Giménez M. , Puche Larrubia M. Á. , Gómez García I. , Calvo Gutierrez J. , Ábalos-Aguilera M. C. , Escudero Contreras A. 
Published: May 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>0.001),RF(r=0.16, p=0.05) homocysteine (r=0.5, p<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<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

VariablesRA n=146Epidemiological characteristics and comorbiditiesAge (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/m2), median (IQR)26.8 (23.4-29.7)Clinical-laboratory characteristicsDisease 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 treatmentSynthetic 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