Why this research is relevant to clinicians today & researchers in the future
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WASHINGTON, D.C.—The ACR Convergence 2024 meeting in Washington, D.C., reflected the continued advancement of science and practical research in the field of rheumatoid arthritis. Highlights this year centered on new RA treatments and new uses of existing treatments; the use of artificial intelligence (AI) and other technologies for predicting treatment response and implementing patient monitoring; plus several important topics related to mitigating infection and cardiovascular risk in rheumatoid arthritis (RA).
Treatment
Vagus Nerve Stimulation Device Effective to Treat RA: Abstract L10, Tesser et al.1
RA is a chronic condition for which many therapies are currently available, but all require patients with RA to take ongoing treatment that is typically lifelong. Exploring an innovative approach to RA, this randomized, double-blind, sham-controlled trial evaluated whether neuroimmune modulation through vagus nerve stimulation (VNS) achieved through a device implanted within the carotid sheath as an outpatient procedure could provide significant therapeutic benefits when combined with stable, background, conventional disease-modifying anti-rheumatic drug (DMARD) therapy.
This provocative study highlights the promise of neuroimmune modulation via vagal nerve stimulation as a novel, effective and well-tolerated treatment for patients RA who have had an inadequate response to conventional therapies. For patients who respond well, the opportunity can be framed as an innovative approach to control a patient’s disease through a 60-second night-time pulse delivered while asleep without the need for ongoing conventional, biologic or targeted therapies and with a minimal risk of side effects and no evidence for immunosuppression.
Although not yet approved by the U.S. Food & Drug Administration (FDA), VNS may be a new therapeutic avenue to reduce the reliance of some patients with RA on ongoing pharmacologic treatment while achieving meaningful disease control and structural protection.
Abatacept No Better Than Adalimumab in Early, Seropositive RA: Abstract 2671, Weinblatt et al.2
The optimal treatment selection for individuals living with RA remains elusive. Based on post hoc evaluations of prior RA trials (e.g., AMPLE) or small prospective studies (e.g., EARLY AMPLE), autoantibody positivity (anti-CCP2 and RF), with or without the presence of the shared epitope (SE) HLA risk allele, has been hypothesized to predict enhanced response to abatacept (ABA) over adalimumab (ADA) in patients with early RA who have an inadequate response to methotrexate. AMPLIFIED was a phase 3, randomized trial evaluating the superiority of ABA vs. ADA in such patients receiving background methotrexate.
AMPLIFIED enrolled 338 RA patients, ~65% SE+. Treatment groups had comparable baseline characteristics, and most (95.9%) completed the 24-week treatment period. The trial did not meet its primary end point: ACR50 rates in the SE+ subset were nearly identical (59% ABA vs. 60% ADA; P=0.9). DAS28 (CRP) remission rates (44% ABA vs. 47% ADA) and ACR responses over time were also comparable. Although ABA showed a more pronounced reduction in autoantibody titers (anti-CCP2: −196 vs. −109 U/mL; RF: −121 vs. −27 IU/mL), other clinical response measures and PROs (secondary outcomes) were similar between groups.
The AMPLIFIED trial did not validate shared epitope nor autoantibody positivity as predictors of enhanced response to ABA compared with ADA in patients with early RA receiving background methotrexate. Although ABA demonstrated a greater reduction in autoantibody titers, this did not translate to superior clinical efficacy for any outcome.
The quest to identify and predict which patients with RA are most likely to respond to which RA therapy remains ongoing.
For What Types of Patients May Methotrexate Help Prevent RA? Abstract 2672, Dumoulin et al.,3 & Abstract 2675, Claassen et al.4
Given the appearance of pathogenic autoantibodies years before the development of clinical manifestations of RA, the opportunity to prevent RA is enticing. Several trials have tested various prevention strategies, including use of hydroxychloroquine, rituximab and abatacept. Although hydroxychloroquine has been shown to be ineffective for RA prevention, rituximab and abatacept do appear to delay the onset of RA, but only while these biologics are continued. However, providing ongoing biologic treatment in at-risk patients who lack clinical signs of inflammatory arthritis may be unacceptable to many patients and providers. Thus, the need exists to identify which patients are most at risk and would, therefore, benefit most from preventive treatment. Although anti-citrullinated protein antibodies (ACPAs) may be useful to identify patients at higher risk for developing RA, prevention is particularly challenging in ACPA-negative patients given the low expected rates of progression to RA.
Given its low cost and familiarity to rheumatologists, the use of methotrexate to prevent clinical RA would be an attractive option, if found efficacious. New results out to four years from the TREAT EARLIER trial addressed this by stratifying participants with ACPA-negative, clinically suspect arthralgias (CSA) on the basis of their predicted risk of RA development and evaluated the efficacy of a one-year course of methotrexate in reducing the incidence of RA.
The trial enrolled 236 participants, including 182 ACPA-negative and 54 ACPA-positive individuals with CSA and subclinical joint inflammation, and randomized participants to methotrexate or placebo. Among ACPA-negative participants, 36% were classified as being at increased risk (25–70% predicted risk), and 64% as being at low risk (<25% predicted risk) of developing RA.
In the increased-risk group, RA developed in 8.6% of the methotrexate-treated arm vs. 29.0% of the placebo arm (HR 0.27; 95% CI 0.07–0.99). The low-risk group had no significant difference in RA development between treatment and placebo arms (7.5% vs. 9.5%, HR 0.79; 95% CI 0.22–2.80). ACPA-negative, increased-risk participants receiving methotrexate experienced persistent improvements in subclinical joint inflammation, physical functioning and grip strength, which were not observed in low-risk participants. Patients who responded best had baseline MRI abnormalities (≥2 locations of tenosynovitis, or ≥1 location of tenosynovitis and >2 locations of osteitis), and the positive predictive value of treatment in these patients approximately 80%.
These new findings provide evidence that a one-year course of methotrexate can prevent ACPA-negative RA in individuals with CSA who are at increased risk of developing RA. MRI abnormalities appear to identify those with the greatest benefit.
Improved Fertility Associated with a Treat-to-Target Strategy: Abstract 1647, Quaack et al.5
Women living with RA face higher rates of infertility and adverse pregnancy outcomes for a variety of disease- and treatment-related reasons. The Preconception Counseling in Active RA (PreCARA) study implemented a treat-to-target approach, emphasizing the use of sulfasalazine, hydroxychloroquine, and, when needed, tumor necrosis factor (TNF) inhibitors or lower-dose prednisone, avoiding non-steroidal anti-rheumatic drugs (NSAIDs) and higher-dose prednisone. The objective of this study was to ascertain whether a treat-to-target approach improved fertility by shortening the time to pregnancy compared with a similar RA cohort that did not adopt treat to target (the pregnancy-induced amerlioaration of RA [PARA] cohort).
PreCARA included 215 patients, and PARA enrolled 245 patients. Patients in the PreCARA cohort achieved lower preconception disease activity (median DAS28CRP[3] 2.33 vs. 3.84 in PARA). Medication use during the preconception period also differed significantly; only 3% of PreCARA patients remained untreated compared with 36% in PARA. TNF inhibitor use was more prevalent in PreCARA (53%) than PARA (3%), and use of higher-dose prednisone (>7.5 mg/day) was notably reduced (23% in PreCARA vs. 48% in PARA). Through up to five years of follow-up, most patients in both cohorts were able to conceive, and the median time to pregnancy was significantly shorter in PreCARA (84 days) than PARA (196 days). Prolonged time to pregnancy (>12 months) was observed in 23% of PreCARA patients compared with 42% in PARA.
This treat-to-target strategy significantly reduced time to pregnancy by optimizing disease activity, minimizing use of NSAIDs and higher-dose prednisone, and using biologics (i.e., TNF inhibitors) judiciously. The treat-to-target approach provides further evidence of the importance of a tailored, yet protocolized, RA management to enhance fertility outcomes in women living with RA.
Artificial Intelligence
Choose the Best First—Predicting RA Treatment Response Using Cell-Free DNA: Abstract 2280, Taylor et al.6
In light of the evidence gap described above that seeks to predict which RA patients are most likely to respond to specific RA treatments, numerous approaches seek to elucidate biomarkers that may predict treatment response. Synovial biopsies have provided insights into RA-specific inflammatory pathways, but invasive sampling limits their clinical utility. The PRIMA-102 study sought to use active, chromatin cell-free DNA (cfDNA) to identify blood-based transcriptomic signals that predict response to targeted therapies, such as TNFα inhibitors and Janus kinase (JAK) inhibitors.
At the time of abstract submission, 237 RA patients had been enrolled and results for 35 patients with RA treated with TNF or JAK inhibitors were reported. Active chromatin profiling identified differentially regulated active chromatin elements (DRACEs) associated with treatment response. Pathway enrichment analysis revealed diverse synovial inflammatory signals, including pro-inflammatory mediators (IL-32, IL-33), chemokine activity (CXCL9, CXCL1), vascular endothelial cell markers (ERG), central memory T cell signals, and lymphoid and myeloid subgroup subpopulation markers. These findings closely mirrored molecular patterns previously observed in synovial biopsy studies, confirming the cfDNA assay’s ability to detect tissue-specific signals through a non-invasive method (i.e., liquid biopsy).
Based on the promising results suggested by this work, cell-free DNA offers potential insights into synovial-specific molecular signatures predictive of treatment response in RA using only a blood test that does not require invasive tissue sampling.
The ongoing study with a larger sample size reported at ACR Convergence 2024 aims to refine and validate a new blood-based test, potentially transforming how targeted therapies are selected for RA patients.
Robotic Ultrasound to Assess RA? No Human Needed: Abstract L20, Aplin et al.7
Considering the ongoing and future workforce shortage of rheumatology providers in the U.S. and abroad, new technology-based approaches, including automated imaging and AI-driven analysis in RA, may offer promise to optimize screening and diagnostic evaluation.
A late-breaking abstract evaluated the precision of ARTHUR, an automated ultrasound scanning system, coupled with DIANA, an AI system that analyzes images to grade synovial hypertrophy (SH) and Doppler activity per the global OMERACT-EULAR synovitis score (GLOESS). The performance of ARTHUR and DIANA was compared with musculoskeletal ultrasound scans performed and graded by a rheumatologist, both compared with ground truth established by an independent expert evaluator.
ARTHUR successfully scanned 85.45% of joints (564/660). For synovial hypertrophy assessment, ARTHUR+DIANA demonstrated a percent exact agreement (PEA) of 49.0% and a percent close agreement (PCA) of 91.2% with ground truth. Binary agreement (healthy vs. disease) was 80.0%. For Doppler activity, PEA and PCA were 62.6% and 94.4%, respectively, with binary agreement of 88.1%. The rheumatologist showed comparable results: PEA of 51.5% for synovial hypertrophy and 63.7% for Doppler, with PCA exceeding 94% for both. At the patient level, ARTHUR+DIANA’s binary assessment agreement with the ground truth for synovial hypertrophy (86.7%) and Doppler (83.3%) numerically surpassed the rheumatologist’s agreements (53.3% and 66.7%, respectively).
This AI-based ultrasound system provided accuracy comparable to that of a musculoskeletal ultrasound-trained rheumatologist in assessing synovial hypertrophy and Doppler activity at the joint level, with superior agreement at the patient level. These findings highlight the potential of an automated system to offer efficient, rapid, reproducible and high-quality assessments for patients with RA without the involvement of a healthcare provider at every step, improving accessibility to diagnostic evaluations, and facilitating early and effective disease management.
Assessing RA at Home Using AI + Smartphone Imaging: Abstract 0867, Blanchard et al.,8 & Abstract 0493, Koller et al.9
Given the rationale described above in which rheumatology providers need more efficient ways to monitor disease activity in patients with RA, both traditional assessment tools, such as the Clinical Disease Activity Index (CDAI), and ultrasound rely on in-person visits and specialized diagnostic testing, making them impractical for remote patient monitoring. Patient-reported outcomes (PROs) commonly used in RA (e.g., pain, morning stiffness) may, by themselves, lack reliability or be confounded by concomitant conditions (e.g., fibromyalgia, osteoarthritis), making it impractical to deliver remote care. At ACR Convergence 2024, investigators from Switzerland reported early results from a comprehensive digital remote monitoring platform that integrates objective digital biomarkers, specifically the Finger Fold Index (FFI) for assessing finger joint swelling, with RA-specific PROs.
Using a mobile app in a non-office setting, RA patients were instructed to take dorsal hand photographs using their smartphone camera. The AI-based system used computer vision and convolutional neural networks to calculate the FFI, an objective measure of proximal interphalangeal (PIP) joint swelling and also facilitated collecting PROs. The FFI, calculated as the ratio of pixel length to joint diameter, was analyzed in 327 PIP joints across 109 photographs from 70 patients with RA, including 30 patients with multiple visits. The biomarker’s performance was evaluated at the joint, hand and patient levels, stratified by disease activity stage (active vs. low disease activity) and patient characteristics, such as age and sex.
The mean patient age was 64 years, 80% were women, and 41% of patients were in an active disease state (DAS28-CRP ≥3.2). Significant differences in FFI were observed at the joint level between active and low disease activity groups. Although the FFI at the hand and patient levels showed trends correlating with disease activity, these differences were not statistically significant.
Rheumatologists and RA key opinion leaders (n=10) highlighted the dashboard’s ability to provide detailed, longitudinal visualizations of patient data as a significant benefit. Clinicians noted the integration of objective biomarkers and PROs could enhance remote patient management and enable more precise treatment adjustments.
Preliminary results from patients with RA (n=8) demonstrated high usability and patient engagement, with users expressing motivation to actively manage their disease through regular self-monitoring.
Although still early in development, the possibility for patients to measure their RA disease activity at home using a smartphone app by taking pictures of the dorsum of the hands to detect joint swelling represents a novel and promising solution for addressing the challenges of assessing RA disease activity in resource-limited and remote settings.
Infections & Vaccination in RA
At Time of Vaccination, Hold MTX; Don’t Hold Abatacept or JAK, TNF or IL-17 Inhibitors: Abstract 2676, Morel et al.10; Abstract 2612, Medeiros-Ribeiro et al.11; & Abstract 1718, Mudano et al.12
Serious infections are among the most common, yet potentially preventable, sources of morbidity in patients with RA. The risk of infection may be prevented by appropriate vaccination, yet several immunomodulatory medications used by patients with RA have been shown to blunt vaccine responses. The possibility that one might temporarily hold certain immunomodulatory medications and, thereby, boost vaccine response holds promise to maximize the benefit of vaccination. Several abstracts presented at ACR Convergence 2024 provided new results about this possibility.
The first abstract on this topic describes delayed use of methotrexate for one month at the time that patients were preparing to start or restart methotrexate (after at least a three-month gap, in those previously treated). Among the 276 patients with RA enrolled (mean disease duration 0.1–0.2 years), those randomized to delay methotrexate one month had a better humoral vaccine response than those starting methotrexate immediately (odds ratio 2.4, 95% CI 1.2–4.9) both at one month and one year (odds ratio 1.9, 95% CI 1.1–3.6). Disease activity was slightly greater in the short term, as expected, but not different by one year.
Continuing that same theme, a trial conducted by investigators out of Brazil randomized patients to a two-week cessation (i.e., a methotrexate hold) or continuation of methotrexate at the time that RA patients received each of the two doses of the herpes zoster subunit vaccine (Shingrix). Similar to the results presented above, those randomized to a methotrexate hold had higher post-vaccination geometric mean titers (GMT) than those who continued methotrexate without interruption (10.4, 95% CI 7.9–13.8 vs. 5.8, 95% Ci 4.2–8.1, P=0.012). Flare rates were 9.4% vs. 7.0% and not significantly different between groups.
Finally, the results from the COVID vaccine response (COVER) platform trial that implemented a master protocol and randomized patients to temporary cessation or continuation of various medications for RA or spondyloarthritis (SpA), including TNF inhibitors, abatacept, JAK inhibitors and IL-17 (in patients with SpA). More than 800 patients were randomized, and the top-line findings showed that although baseline use of abatacept and JAK inhibitors blunted vaccine response compared with TNF inhibitors and IL-17 treatment, temporarily holding any of these medications for two weeks did not meaningfully boost immune response. Moreover, flare rates in the patients randomized to hold treatment were appreciably higher (approximately double), particularly for JAK inhibitor-treated patients.
Taken together, results from these three trials indicate that it is advisable to delay methotrexate for one month at the time that patients are newly diagnosed with RA when recommended vaccines should be given, and that methotrexate should be interrupted (for two weeks) at the time of vaccination for already treated patients. However, holding other classes of medications (abatacept, JAK inhibitors, TNF inhibitors and IL-17 inhibitors) at the time of COVID vaccination does not appear warranted and doing so results in increased rates of RA flare.
Cardiovascular & Mortality Risk in RA
Can Statins Mitigate the Excess CVD Risk Associated with JAK Inhibitors? Abstract 1724, Johnson et al.13 & Abstract 1745, Giles et al.14
Patients with RA suffer from excess cardiovascular disease (CVD) mortality, yet predicting the future risk of CVD events for individual patients with RA has proved challenging. Evaluation of population-based CVD risk calculators, including the Framingham risk score and the ACC/AHA pooled cohort risk equation, have proved to be relatively poorly calibrated (i.e., with low accuracy), resulting in a EULAR recommendation to apply an adjustment factor of a 1.5x multiplier to the predicted risk estimated for non-RA patients. This simple approach helps with, but does not resolve, the problem and CVD risk is still misclassified for many RA patients. Based on recently presented data on the accuracy of the newest population-based CVD risk calculator, PREVENT (introduced in the U.S. in late 2023). However, a large study from a large cohort of U.S. veterans found that the PREVENT risk calculator was poorly calibrated and meaningfully underestimated CVD risk for patients with RA, similar to previous general population CVD risk calculators.
Despite these inadequate tools to estimate the risk of CVD for individuals with RA, in 2022, the ORAL Surveillance trial that recruited high CVD risk RA patients (age ≥50 with ≥1 CVD risk factor) identified a higher incidence of major adverse cardiovascular events (MACE) with tofacitinib compared to TNF inhibitors. While this finding appropriately triggered a wave of concerns amongst treating rheumatologists, mitigating the potentially elevated risk of CVD associated with JAK inhibitors and appropriate patient selection has been less well studied. Further, post hoc analyses presented at ACR Convergence 2024 found that only one-third of these high-risk patients with RA received a statin at any time during the trial. Even more importantly for clinicians considering JAK inhibitors for their patients in the contemporary era, additional results from Oral Surveillance presented at ACR Convergence 2024 found the excess risk for major adverse cardiovascular events (MACE) observed among the patients with a history of atherosclerotic cardiovascular disease (ASCVD; overall hazard ratio 1.98, 95% CI 0.95, 4.14) appeared to be solely confined to those not using statins (hazard ratio 4.07, 95% CI 1.21, 13.76). No excess risk for MACE was found for tofacitinib among those receiving statins (HR 1.09, 95% 0.42, 2.85).
These findings suggest the concern about the CVD risk associated with JAK inhibitors may not be present among even high-risk RA patients with a history of ASCVD if they are to receive statins. Although there may be some reticence on the part of rheumatology providers to prescribe statins or other hyperlipidemia treatments themselves, these new data further underscore the importance of use of statins in patients with RA. Specifically, it suggests that the adverse CVD safety profile of JAK inhibitors for high-risk patients may be able to be attenuated if statins are used concomitantly.
Risk of Mortality
Stopping Glucocorticoids Associated with Mortality Benefit: Abstract 2673, Lacaille et al.15
Rheumatology providers and patients with RA continue to have a love-hate relationship with glucocorticoids. Although current guidelines from the ACR conditionally recommend avoiding glucocorticoids, even in the short term (i.e., fewer than three months, conditional recommendation) and the long term (i.e. longer than three months, strong recommendation), many patients with RA are persistently maintained on glucocorticoids. Avoidance or discontinuation of glucocorticoids may confer many benefits including reduced risk for mortality due to cardiovascular events and infections. A longitudinal cohort study was conducted using administrative health data from British Columbia, Canada, capturing incident RA cases between 1996 and 2013 with follow-up until 2018. The cohort included 28,078 glucocorticoid users (55.9% of the total cohort), and use was measured in a time-varying fashion, with a particular focus on time since cessation. Mortality outcomes due to cardiovascular disease and infections were identified via death certificates.
The study identified 2,489 cardiovascular-related deaths and 387 infection-related deaths. Each year of cumulative glucocorticoid use increased mortality risk by 7.5% (cardiovascular disease) and 6.8% (infections), although risk decreased by 1.3% (cardiovascular disease) and 4.9% (infections) per year after glucocorticoid cessation. Importantly, the duration of previous glucocorticoid use influenced the timeline of risk reduction. For patients with prior glucocorticoid use of 6, 12, and 24 months, cardiovascular disease mortality risk decreased to pre-glucocorticoid levels after 1.5, 3.5 and 10 years of cessation, respectively. Similarly, for infection-related mortality, the risk returned to baseline after 2.5, 3.5 and 5.5 years of cessation for 6, 12 and 24 months of prior use. Notably, patients who used glucocorticoids for more than two years (cardiovascular disease) or three years (infections) never returned to pre-glucocorticoid mortality risk levels.
Not only does this study underscore the long-term mortality risks associated with prolonged glucocorticoid use in RA, it also highlights risk that persists long after cessation. Encouragingly, glucocorticoid-associated risk of mortality of cardiovascular disease events and infections did return to baseline after cessation of treatment with glucocorticoid for less than two years, yet it never fully returned to baseline in cases of extended glucocorticoid use.
These findings highlight the importance of minimizing glucocorticoid duration and dosage, aligning with current RA guidelines, to mitigate mortality risks. These data offer hope that discontinuing glucocorticoid therapy confers demonstratable mortality benefit, supporting shared decision making between patients and providers regarding glucocorticoid therapy.
Honorable Mentions
Abstract 2610
Knitza J, Mucke J, Grahammer M, Kuhn S, et al. Treatment concordance of asynchronous virtual visits compared to traditional in-person visits in patients with rheumatoid arthritis: Results of the prospective, multi-center, randomized controlled TELERA trial [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Abstract 1746
Kerschbaumer A, Steiner M, Pruckner P, et al. Global recruiting patterns are associated with placebo response rates in clinical trials of rheumatoid arthritis [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Abstract 1719
Wallace B, Gao Y, Kim H, et al. Cumulative glucocorticoid exposure and major adverse cardiovascular events in a cohort of Veterans with rheumatoid arthritis: A nested case-control study [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Abstract 0799
Wheeler A, Riley T, Baker J, et al. Peripheral biomarker signatures and a genetic risk score improve the identification of RA-ILD beyond clinical risk factors [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Abstract 0800
McDermott G, Juge P, Hayashi K, et al. Associations of rheumatoid arthritis polygenic risk with age at onset, serostatus, and interstitial lung disease [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Abstract 1713
Frideres H, Wichman C, Dong J, et al. Comparisons of non-TNFi biologic and targeted synthetic DMARDs in rheumatoid arthritis-associated interstitial lung disease: A propensity score-matched study using national Veterans Affairs data [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
Jeffrey Curtis, MD, MS, MPH, is the Marguerite Jones Harbert-Gene Ball Endowed professor of medicine, Division of Clinical Immunology & Rheumatology, University of Alabama at Birmingham. A rheumatologist and epidemiologist, Dr. Curtis has research interests in rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis and osteoporosis, as well as methodologic interests in real-world evidence, causal inference, machine learning and artificial intelligence.
Disclosure
Dr. Curtis was the lead author on Abstract 1718 and participated in several other RA-related studies presented at ACR Convergence 2024.
References
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- Weinblatt M, Emery P, Bykerk V, et al. Subcutaneous abatacept vs adalimumab head-to-head comparison in adults with early, dual seropositive rheumatoid arthritis, positive for the shared epitope HLA class II risk alleles, and an inadequate response to methotrexate: Results from a phase 3 trial [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
- Dumoulin Q, Krijbolder D, Visser K, et al. Prevention of the development of rheumatoid arthritis by a 1-year course of methotrexate in ACPA-negative arthralgia patients at increased risk for rheumatoid arthritis: 4 year results of the TREAT EARLIER trial [abstract]. Arthritis Rheumatol. 2024;76(suppl 9).
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