tbuckley/cabot-search huggingface dataset:
AB1445 RETHINKING PREDICTORS: SJOGREN’S SYNDROME AS A POSITIVE PREDICTOR OF RITUXIMAB EFFECTIVENESS IN RHEUMATOID ARTHRITIS
Authors: T. Beirão, M. Diz Lopes, C. Gomes, I. Santos, M. Bernardes, L. Costa
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Rheumatoid arthritis (RA) is a chronic inflammatory rheumatic condition that often requires targeted therapies like rituximab. Understanding baseline predictors of response is crucial for optimizing treatment outcomes. This retrospective study aims to investigate various patient characteristics, baseline patient-reported outcomes, laboratory levels, and immunological markers as potential predictors of rituximab response in RA. <h3>Objectives:</h3> The primary objective is to identify baseline factors associated with rituximab response in RA patients in a real-life setting. <h3>Methods:</h3> A monocentric retrospective study between 2008 and 2023 was conducted. RA patients receiving rituximab were included. Patients below age 18 were excluded. Patient characteristics, disease-related variables, baseline patient-reported outcomes, and laboratory parameters were collected. The study employed statistical tests, including chi-square tests and t-tests, to compare variables between patients with and without a response to rituximab. <h3>Results:</h3> Out of 745 RA patients, 98 met the study inclusion criteria. Among the notable findings (see Table 1), we observed a significantly higher response rate to rituximab in RA patients with secondary Sjogren`s syndrome (p=0.011). Baseline patient-reported outcomes (HAQ and PG-VAS), DG-VAS, disease activity scores (DAS, CDAI, SDAI), 28 TJC and 28 SJC were significantly higher in the responder group (p&lt;0.001). Baseline serum levels of immunoglobulin A (p=0.036) and 25(OH)vitamin D3 (p=0.028), and erythrocyte sedimentation rate (ESR) (p=0.003) also displayed significant associations with rituximab response. Moreover, baseline serum levels of immunoglobulin G and CRP were numerically higher in the rituximab responder group (p=0.080 and p=0.084, respectively). <h3>Conclusion:</h3> This retrospective study provides valuable insights into baseline predictors of rituximab response in RA. Secondary Sjogren`s syndrome, higher baseline disease activity, and specific laboratory parameters such as serum immunoglobulin A and ESR emerge as potential indicators of a favorable response to rituximab treatment. These findings contribute to the ongoing efforts to personalize RA treatment strategies and enhance therapeutic effectiveness with rituximab. Further prospective studies are warranted to validate and expand upon these observations, fostering more precise and individualized management approaches in RA patients undergoing rituximab therapy. <h3>REFERENCES:</h3> [1] Rituximab and tocilizumab for the treatment of rheumatoid arthritis. Nicolás González-Vacarezza1, Alicia Alemán 1, Graciela González 1, Ana Pérez 1. Int J Technol Assess Health Care. 2014 Jul;30(3):282-8. DOI: 10.1017/S0266462314000221. Epub 2014 Jul 28. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB0659 ASSOCIATION OF PLASMA ATHEROGENIC INDEX WITH CAROTID INTIMA-MEDIA HYPERPLASIA IN PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: V. Gonzalez-Gonzalez, D. A. Galarza-Delgado, I. J. Colunga-Pedraza, J. R. Azpiri-Lopez, R. I. Arvizu-Rivera, J. A. Cardenas-de la Garza, M. F. Elizondo-Benitez, A. L. Guajardo-Aldaco
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> The atherogenic index of plasma (AIP) is a novel marker to identify cardiovascular disease. Recently, it was reported that AIP is related to long-term cardiovascular disease risk in women with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). <h3>Objectives:</h3> To evaluate if RA-patients with high AIP present a higher prevalence of carotid plaque in comparison to patients with RA and low AIP. <h3>Methods:</h3> A cross-sectional and comparative study including RA-patients aged 40 to 75 who fulfilled the ACR/EULAR 2010 classification criteria for RA. Patients with previous cardiovascular disease were excluded. Carotid ultrasound was performed on all study participants. The presence of carotid plaque (CP) was defined as diffuse carotid intima-media thickness (cIMT) ≥1.2 mm or focal thickness ≥0.5 mm. Subclinical atherosclerosis was defined as the presence of CP or an increased cIMT (≥0.8mm). AIP was defined by log (TG/HDL-C) mg/dL, and level ≥0.21 was considered a high AIP. Patients were divided into two groups according to AIP levels. The distribution between groups was assessed with the Kolmogorov-Smirnov test. Comparisons with Chi-square or Fisher's exact test and Student's t-test or Mann Whitney's U-test, accordingly. A <i>p</i>-value of ≤0.05 was considered statistically significant. <h3>Results:</h3> A total of 144 patients with RA were included, most patients were women (n=133, 94%). There was no difference between sex, traditional cardiovascular risk factors, disease activity, or disease duration between patients with high AIP and those RA-patients with low AIP (Table 1). Prevalence of CP (37.5% vs 25.0%, <i>p</i>=0.106) and overall subclinical atherosclerosis (58.3% vs 62.5%, <i>p</i>=0.609) was similar between groups (Table 1). However, the prevalence of increased cIMT was higher in RA-patients with high AIP (29.2% vs 54.2%, <i>p</i>=0.002). <h3>Conclusion:</h3> The prevalence of increased cIMT was higher in RA-patients and high atherogenic index of plasma (AIP). AIP could potentially be a useful marker for the early identification of patients with increased cIMT. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB0728 AUTOIMMUNITY: ROLE OF ANTITHYROID ANTIBODIES IN RHEUMATOID ARTHRITIS
Authors: S. Rahmouni, E. Razgallah, M. Mrad, E. Bouallegue, K. Zouaoui, M. Abbes, S. Boussaid, S. Rekik, A. Bahlous, H. Sahli, M. Elleuch
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Rheumatoid arthritis (RA) is an autoimmune disorder that represents the most common rheumatic disease. Whereas, autoimmune thyroid disease is the most common organ-specific autoimmune disease (AITD). Recently, many studies have suggested a relationship between these two diseases [1]. <h3>Objectives:</h3> In our study we aimed to determine whether RA is associated with a higher risk of developing thyroid autoimmune diseases and study their influence on the progression of RA. <h3>Methods:</h3> We conducted a cross-sectional case-control study involving female patients with RA and a group of healthy controls (HC). AITD was defined by the presence of anti-thyroid antibodies (ATA): anti-thyroid peroxidase antibodies (TPOa), and/or anti-thyroglobulin antibodies (TGA), and/or anti-thyroid-stimulating hormone receptor antibodies (TSHra). RA patients were then divided into two groups: patients without AITD TAD and G1 with AITD. <h3>Results:</h3> Fifty-eight female patients with RA were included and 58 HC with mean age (52 ± 14.2 years vs 52.14 ± 14.77 years, p=1). The presence of ATA was significantly higher in RA patients (Table 1). We didn't find statistically significant differences in terms of AITD. (Table 2). <b>Table 2.</b> Comparison of thyroid autoimmune disorder between the two groups There was no difference between the RA with or without ATA regarding the following: The disease duration (G0: 12.35 years [6.28; 14.35] vs G1: 9.80 years [2.42; 19.17], p=0.878), serological biomarkers (ACPA: G0: 61% vs G1: 67%, p=0.757, FR: G0:75%, G1: 100%, p=0.096), the presence of erosion (G0 65% vs G1 78%, p=0.703), disease activity (DAS28 CRP, G0: 4.04 [3.02-5.26], G1: 3.79 [1.96-5.28], p=0.334), functional impairment (HAQ: G0:1.63 [1.2-1.75], G1: 1.34; [0.97-1.5]; p=0,321) and the presence of extra-articular manifestations (G0: 24%, G1: 11%, p=0.668). <h3>Conclusion:</h3> In our study, AITD was found in 16% of RA patients. Patients with RA had higher serum concentrations of TPOa, TGA, and TSHra, however, this did not influence the characteristics of the disease. <h3>REFERENCES:</h3> [1] Liu YJ, Miao HB, Lin S, Chen Z. Association between rheumatoid arthritis and thyroid dysfunction: A meta-analysis and systematic review. Front Endocrinol (Lausanne). 2022 Oct 13; <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB1437 NON-PDL1 BLOCKING PD1 AGONISTIC ANTIBODIES MAY INDUCE PRO-INFLAMMATORY CYTOKINES PRODUCTION IN VITRO
Authors: Y. Orlovsky, L. Y. Hao, M. Swiecki, S. Cole, S. Dutta, I. White
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> T cells play an important role in the development and progression of many autoimmune diseases. Inhibition of T cells and their effector mechanisms has therefore been an area of great therapeutic interest. PD1 (CD279) is a CD28/CTLA4 family coinhibitory receptor that is upregulated when cells are activated. Several lines of evidence link the PD1 pathway to autoimmune diseases, including genetics, correlations between PD1 expression and disease severity in patients, and autoimmune-like immune-related adverse events upon antagonizing the PD1 pathway in oncology. Consequently, the activation of the PD1 pathway through agonist antibodies holds promise as a therapeutic approach in autoimmune diseases. Several PD1 agonists have or are currently being tested in rheumatoid arthritis, psoriasis, alopecia areata, and ulcerative colitis clinical trials, with the goal to engage this endogenous regulatory mechanism. However, the molecular mechanism of how PD1 agonistic molecules work remains unclear. <h3>Objectives:</h3> To increase our understanding of PD1 agonist antibodies mechanism of action on PD1 expressing cells by comparing activities of several PD1-agonistic antibodies. <h3>Methods:</h3> Selected PD1 agonistic antibodies were profiled for binding affinity and ability to interfere with endogenous receptor-ligand interaction through biochemical assays. The functional effects of different PD1 agonistic antibodies were studied in vitro by assessing proliferation capacity and cytokine levels using human T cells. <h3>Results:</h3> Antibodies that block PD1 receptor-ligand interaction led to enhanced lymphocyte activation and increased cytokine production as expected. Further, some, but not all, PD1 agonistic molecules that do not block PD1 receptor-ligand interaction exhibited potential enhancement of proinflammatory cytokine production. <h3>Conclusion:</h3> Our data indicate that PD1 antibodies may become antagonistic under specific situations, leading to an increased inflammatory load in the local environment. Additional analyses will be helpful to further elucidate the molecular mechanism of how agonistic antibodies function, and their propensity to become antagonistic under particular conditions. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> Yevgeniya Orlovsky Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine, Ling-Yang Hao Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine, Melissa Swiecki Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine, Suzanne Cole Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine, Supratik Dutta Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine, Ian White Johnson and Johnson Innovative Medicine, Johnson and Johnson Innovative Medicine.
AB0653 IMPACT OF TSDMARD, TOFACITINIB, ON ENDOTHELIAL FUNCTION IN RA AND ITS ASSOCIATION WITH CELLULAR RATIOS
Authors: A. Syngle, I. Verma, K. Chauhan
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in RA.<sup>1</sup> Endothelial dysfunction (ED), resulting from chronic inflammation and leading to accelerated atherosclerosis, is the key promoter of CVD<sup>2</sup>. ED is the barometer of CV health. <h3>Objectives:</h3> In this study, we aimed to investigate the impact of tofacitinib on endothelial dysfunction in RA and association of endothelial dysfunction with NLR, PLR and LMR to determine whether these ratios could predict the impact of tofacitinib on CV risk. <h3>Methods:</h3> A total of 74 patients with RA patients (62 females, 12 males; mean age: 54.85 ± 8.39 years; range: 32 to 70 years) fulfilling the 2010 Rheumatoid Arthritis classification criteria with active disease (DAS28&gt;3.2)were treated with Tofacitinib (5mg bd, n=20) for 12 weeks as an adjunct to existing stable antirheumatic drugs. Endothelial function was assessed by FMD using AngioDefender and serum lipids were also estimated at baseline and after 12 weeks of treatment. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte to monocyte (LMR) ratios and platelets were estimated. DAS28, ESR, CRP and HAQ-DI were also assessed at baseline and after 12 weeks of treatment. <h3>Results:</h3> After 12 weeks treatment with tofacitinib, FMD significantly improved (7.14± 2.48 to 8.22 ± 2.80, p=0.001). ESR, CRP, DAS-28, HAQ-DI and PLR improved significantly after 12 weeks of treatment (Table 1). However, there was no statistical significant improvent in NLR, LMR and platelets and serum lipids (Table 1). At baseline, a significant negative Pearson correlation was observed between FMD and Age and CRP (Table 2A). However, after 12 weeks treatment with tofacitinib, FMD corelated with age and platelets (Table 2A). DAS-28 significantly correlated with gender, ESR, CRP and FMD (Figure 1) at baseline (Table 2B). However, after 12 weeks treatment, DAS-28 significantly correlated with ESR and CRP level (Table 2B). <h3>Conclusion:</h3> Treatment with tofacitinib improves inflammatory disease activity and endothelial function. However, NLR, LMR and PLR did not significantly correlate with the FMD and disease activity score suggesting that these cellular ratios do not predict the response to tofacitinib therapy in RA. Platelets correlated with FMD after tofacitinib treatment. <h3>REFERENCES:</h3> [1] Gabriel SE. Cardiovascular morbidity and mortality in rheumatoid arthritis. Am J Med. 2008 Oct;121(10 Suppl 1):S9-14. doi: 10.1016/j.amjmed.2008.06.011. PMID: 18926169; PMCID: PMC2858687. [2] Naveed Sattar, David W. McCarey, Hilary Capell and Iain B. McInnes. Explaining How ''High-Grade'' Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis. Circulation 2003; 108: 2957-63. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB0765 DECODING SUCCESSFUL CORTICOSTEROID WITHDRAWAL IN RHEUMATOID ARTHRITIS: INSIGHTS INTO PROGNOSTIC DETERMINANTS
Authors: H. Elhani, N. EL Ouardi, L. Taoubane, H. Toufik, A. Majjad, A. Bezza
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> The withdrawal of corticosteroid therapy in rheumatoid arthritis (RA) patients proves to be a complex process, requiring an individualized and meticulous approach. This study aims to unveil predictive factors that determine the success or failure of corticosteroid withdrawal in RA patients. <h3>Objectives:</h3> The primary objective of this study is to identify and analyze prognostic factors influencing successful corticosteroid withdrawal in rheumatoid arthritis patients undergoing methotrexate therapy, aiming to enhance personalized treatment strategies and improve long-term outcomes in rheumatologic care. <h3>Methods:</h3> This cross-sectional study included 100 patients with RA according to the 2010 ACR/EULAR criteria, all treated with corticosteroid and methotrexate (15-25 mg/week). Patients were classified into two groups: those who successfully withdrew from corticosteroid therapy (G1) and those who failed (G2). <h3>Results:</h3> Data were collected from 100 patients. The median age was 52 [31; 78] years, with 83% being women. Mean CRP at inclusion was 19.5 ± 17.7 mg/L, DAS28-CRP at inclusion was 4.3 ± 1.4, and 28% of patients received at least one Solumedrol IV bolus. Out of the 100 patients in the study, 76% successfully withdrew from corticosteroid therapy, while 24% failed. Patients in group G1 were younger, with an average age of 46 ± 6.6 years, compared to 57 ± 9.6 years for group G2 (p = 0.24), had a shorter duration of corticosteroid treatment (3.9 ± 3.6 months vs. 35.7 ± 37.2 months, p &lt; 0.001), and a lower corticosteroid dose at inclusion (4 ± 1.5 mg, p = 0.002). Multivariate regression analysis results indicated that disease duration (odds ratio [OR] = 0.801, 95% CI 0.729-0.928, p &lt; 0.001) and disease remission (OR = 3.108, 95% CI 1.074-11.475, p = 0.048) were significantly associated factors with the success of corticosteroid withdrawal in RA patients under methotrexate. <h3>Conclusion:</h3> These promising results shed light on the clinical practice of rheumatologists by providing key indicators for identifying patients most likely to succeed in corticosteroid withdrawal. By optimizing treatment, we contribute to improving the quality of life for RA patients and more efficiently managing this condition. This scientific advancement also paves the way for targeted and personalized therapeutic approaches, thereby reducing long-term dependence on corticosteroid therapy in RA patients. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB0767 PLAIN RADIOGRAPHS VS MAGNETIC RESONANCE IMAGING: WHICH DIAGNOSTIC METHOD FOR ANTERIOR ATLANTOAXIAL SUBLUXATIONS IN RHEUMATOID ARTHRITIS?
Authors: S. Rahmouni, M. Dhifallah, K. Zouaoui, M. Abbes, S. Boussaid, H. Sahli, S. Rekik, M. Elleuch
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Cervical involvement is common in rheumatoid arthritis (RA). The most common abnormality is atlantoaxial subluxations (AAS) [1]. <h3>Objectives:</h3> Our objective was to study the contribution of dynamic standard radiographs and magnetic resonance imaging (MRI) for the diagnosis of anterior atlantoaxial subluxations (AAAS) in RA and to determine the correlation between these two diagnostic tools. <h3>Methods:</h3> We included patients with RA according to the American College of Rheumatology (ACR) criteria. Sociodemographic data, clinical presentation, and radiological features were collected. The diagnosis of anterior AAS (AAAS) was based on measuring the atlantoaxial interval (ADI) ≥ 3 mm on standard radiographs (in neutral and flexion positions) and/or on MRI. ADI was defined as the distance between the posteroinferior aspect of the anterior arch of C1 and the most anterior aspect of the dens [2]. <h3>Results:</h3> We collected data from 53 patients. The female-to-male ratio was 6.57. The mean age was 56 ± 11.24 years. The mean disease duration was 122.16 ± 97.68 months. The mean DAS28CRP was 5.37 ± 1.42. Functional complaints related to AAS were cervical pain in 22 cases (41.5%), cervical-brachial neuralgia in 12 cases (22.6%), vertigo in 5 cases (9.4%), cervical stiffness in 9 cases (17%), and pyramidal syndrome in 3 cases (5.6%). Spinal cord compression was noted in 2 patients. On radiography, 20 patients (37.7%) had AAAS. The mean ADI was 3.04 mm [2-11] in flexion and 2.08 mm [1-10] in the neutral position. On MRI, the mean ADI value was 2.87 mm [1-11]. Thirteen patients (29.5%) had the ADI greater than 3 mm, confirming AAAS. Standard radiographs diagnosed AAAS 1.15 times more than MRI. In our series, a significant difference was found between standard radiographs and MRI in measuring ADI (p=0.017). <h3>Conclusion:</h3> In contrast with previous literature data [3], our study demonstrated the superiority of plain radiographs over MRI. However, it is important to emphasize the complementarity of both diagnostic methods in effective detecting of AAAS. <h3>REFERENCES:</h3> [1] Ellatif M,et al. Update on imaging of the cervical spine in rheumatoid arthritis. Skeletal Radiol. 2022 Aug;51(8):1535-1551. doi: 10.1007/s00256-022-04012-w. Epub 2022 Feb 10. PMID: 35146552. [2] Bundschuh C, Modic MT, Kearney F, et al.. Rheumatoid arthritis of the cervical spine: surface-coil MR imaging. AJR Am J Roentgenol 1988;151:181–87 [3] Joaquim AF, Ghizoni E, Tedeschi H, Appenzeller S, Riew KD. Radiological evaluation of cervical spine involvement in rheumatoid arthritis. Neurosurg Focus. 2015;38(4):1-7. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB0763 VIRAL INFECTIONS AMONG PATIENTS RECEIVING BIOLOGICS FOR RHEUMATIC DISEASES
Authors: S. Bouden, O. Saidane, L. Rouached, A. Ben Tekaya, I. Mahmoud, R. Tekaya, L. Abdelmoula
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Biologics are widely used to treat chronic inflammatory rheumatic diseases such as rheumatoid arthritis (RA) and spondyloarthritis (SpA). Among the side effects, several studies have reported an increased risk of opportunistic infections such as tuberculosis, parasitic and viral infections. <h3>Objectives:</h3> To assess the prevalence of viral infections among RA or SpA patients treated with biologics. <h3>Methods:</h3> A single-center retrospective study was conducted. Patients diagnosed with RA or spA between 2016 and 2023 and treated with biologics were included. Clinical and treatment-related data, including viral complications, were studied. <h3>Results:</h3> One hundred eighty-five patients were included. 81 men and 104 women. The mean age was 46 years (22-75 years). 98 were diagnosed with RA and 87 with SpA (54 ankylosing spondylitis, 21 inflammatory bowel disease-associated spondyloarthritis and 12 psoriatic arthritis). 69 patients were treated with infliximab (37%), 31 with certolizumab (17%), 30 with etanercept (16%), 21 with adalimumab (11%), 19 with rituximab (10%) and 15 with tocilizumab (9%). Twelve episodes of viral infections were reported (6%): six cases of herpes zoster, three cases of herpes simplex infection and three cases of reactivated hepatitis B. Nine patients were treated by TNF alpha inhibitors: six Infliximab and 3 Etanercept. Three patients were treated by Rituximab. These infections were diagnosed after an average of 36 months from the start of treatment with biotherapies (6-60 months). The occurrence of viral infections was significantly more frequent among TNF alpha inhibitors (p=0.03). The six cases of herpes zoster were cured after discontinuation of the biologic and initiation of Aciclovir. The three herpes simplex infection was controlled with Aciclovir, and Infliximab treatment has been resumed 2 weeks after. The three cases of hepatitis B reactivation were controlled by antiviral treatment. <h3>Conclusion:</h3> Biological therapies, especially TNF alpha inhibitors, may lead to an increased risk of viral infections. These infections were reported in 6% of our patients. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>