Search Results (84)

Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are systemic inflammatory diseases deeply rooted in age-related immunosenescence and inflammaging. Conventional long-term glucocorticoid (GC) therapy poses significant metabolic and infectious risks for older adults, necessitating safer alternatives. This review critically evaluates the pathophysiological rationale and clinical efficacy of small-molecule drugs, including Janus kinase inhibitors (JAKi) and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), as steroid-sparing treatments for PMR and GCA. By selectively inhibiting intracellular networks like the JAK-STAT pathway and nucleotide biosynthesis, these agents aim to attenuate maladaptive inflammation. Clinical evidence highlights that JAK inhibitors, particularly upadacitinib for GCA and tofacitinib or baricitinib for PMR, demonstrate the potential to induce remission and significantly reduce the required GC burden in a subset of patients. Although methotrexate remains the primary csDMARD, its modest overall efficacy suggests it should be reserved for patients with definitive contraindications or restricted access to JAK inhibitors. Furthermore, novel therapies like clofutriben demonstrate potential in reversing GC-induced morbidities without compromising disease control. Ultimately, integrating targeted small-molecule immunomodulators establishes a crucial therapeutic paradigm that attempts to maximize clinical remission while safeguarding the physiological integrity of geriatric patients against severe GC toxicities. Full article

Background/Objectives: Latent tuberculosis infection (LTBI) is a persistent immune response to Mycobacterium tuberculosis antigens in the absence of clinically active tuberculosis. It is now established that progression from LTBI to active tuberculosis is directly associated with immune dysregulation, which frequently occurs in immune-mediated diseases requiring treatment with immunosuppressive agents. The aim of this study was to identify LTBI in patients with rheumatological diseases receiving immunosuppressive therapy using contemporary immunodiagnostic methods. Materials and Methods: A retrospective, prospective, group-control study was conducted, analyzing the results of immunodiagnostics in patients with rheumatological diseases on immunosuppressive therapy and without established contact with tuberculosis patients (n = 44; main group). The control group consisted of healthy individuals (n = 51) with no history of tuberculosis contact, clinical or radiological manifestations of the disease, or signs of chronic pathology exacerbation. Both groups were predominantly female (72.7% in the main group and 62.8% in the control group). The mean age in the patient group was 49.1 years (95% CI [44.77; 53.43]). Rheumatoid arthritis was diagnosed in 29.6% (13) of patients (95% CI [16.06; 43.03]). Articular syndrome was observed in at least 72.7% (32) of patients (95% CI [59.57; 85.89]). In 54.6% (24) of cases (95% CI [39.83; 69.26]), patients received biologic immunosuppressive therapy as basic treatment. In 15.9% (7) of cases (95% CI [5.10; 26.72]), patients received conventional synthetic disease-modifying antirheumatic drugs (DMARDs). Of these, 71.43% (5) (95% CI [35.24; 92.44]) underwent comprehensive examination to exclude active tuberculosis prior to biologic therapy initiation. For immunodiagnostics, all subjects underwent an interferon-gamma release assay (IGRA) and/or testing with a recombinant tuberculosis antigen (ATR) sample, with dynamic assessment of test results. All patients with positive immunodiagnostic results underwent multidetector computed tomography of the chest organs. The level of LTBI in the comparison groups was defined as the percentage of positive immunological test results at a significance level of p < 0.05. Statistical data processing was performed using Microsoft Excel 2019. Results: In the main group, positive immunodiagnostic results were recorded in 20.5% (9) of cases (95% CI [8.54; 32.37]), which is significantly higher than in the control group of healthy individuals (5.8% (3), 95% CI [1.41; 16.54]). This reflects statistically significant differences in immunological test results between groups receiving and not receiving immunosuppressive therapy (χ² = 4.545, p = 0.034). Dynamic evaluation of the ATR sample revealed positive results in 21.7% (5) of cases (95% CI [4.88; 38.60]), with four out of five patients demonstrating positive conversion. In the third assessment, positivity was observed in 33.33% (5) of cases (95% CI [9.48; 57.19]), which was higher than in the first (χ² = 1.025, p = 0.312) and second assessments (χ² = 0.629, p = 0.428), although these differences were not statistically significant. Notably, in two out of five patients, the ATR test result changed from negative to positive. Conclusions: In patients with rheumatological diseases receiving immunosuppressive therapy, LTBI was detected in 20.5%, which is significantly higher than in healthy individuals (5.8%, p = 0.034). Furthermore, there was an increase in the proportion of positive tests over time (up to 21.7% and 33.3% on immunotherapy), suggesting an increasing risk of progression to active tuberculosis infection. Full article

Background: Pulmonary fibrosis (PF) is a major global health issue associated with substantial morbidity across all age groups. One of the important etiological factors contributing to PF is drug-induced lung injury, which can result from both direct and indirect damage to the pulmonary parenchyma caused by various pharmacological agents, including chemotherapeutics, antirheumatic drugs, cardiovascular medications, and certain antimicrobial agents. The aim of our study was to assess the structure of antibacterials involved in drug-induced PF (DIPF) and analyze signals of DIPF, calculating the reporting odds ratio (ROR) and proportional reporting ratio (PRR) using spontaneous reports (SRs) extracted from the Russian National Pharmacovigilance database. Methods: A retrospective, descriptive pharmacoepidemiological analysis of SRs from the AIS database for the period 1 April 2019–31 March 2025 was conducted. Results: A total of 130 SRs with data on DIPF associated with antibacterial agents were identified, with patients’ mean age of 59.1 ± 14.46 years. Death was reported in 65 SRs (50%) with a mean age of 53.0 ± 13.66 years. Next, antibacterials were identified as leaders: sulfamethoxazole (used alone or in combination with trimethoprim, 20.7% (n = 50)), azithromycin (18.2%, n = 44), levofloxacin (12.4%, n = 30), doxycycline (11.6%, n = 28), and cefuroxime (10.7%, n = 26). Disproportionality analysis performed with PRR and ROR calculation revealed the strongest association with DIPF for cefuroxime (PRR = 15.11, 95% confidence interval, CI: 10.25–22.27; ROR = 15.31, 95% confidence interval, CI: 10.33–22.68). Conclusions: Cefuroxime was revealed as a drug with an unexpected but robust safety signal for DIPF, warranting heightened clinical awareness and further investigation. The observed associations between antibacterial agents and DIPF should be interpreted with caution, as they may reflect protopathic bias (antibiotics prescribed for early symptoms of unrecognized pulmonary fibrosis) or context-dependent biological effects rather than true pro-fibrotic drug properties. Our findings do not establish causality but rather generate safety signals that warrant validation through prospective studies with detailed clinical phenotyping and mechanistic investigations using human cell lines. Full article

Psoriatic arthritis (PsA) is a systemic autoimmune inflammatory disease affecting both the joints and the skin, with the potential involvement of multiple organ systems. A hallmark feature of PsA is enthesitis—inflammation at the sites where tendons and ligaments insert into bone—which arises from a combination of mechanical stress and immune-mediated inflammation. Another defining characteristic of the disease is the paradoxical coexistence of bone erosion and new bone formation, distinguishing it from other inflammatory arthritides. The therapeutic landscape of PsA has evolved considerably over time. Non-steroidal anti-inflammatory drugs (NSAIDs) remain a cornerstone of symptom management, while conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), such as methotrexate, are widely used to control disease progression. The introduction of biologic agents has revolutionized PsA management, with TNF inhibitors, IL-17 inhibitors, and IL-23 inhibitors demonstrating efficacy across a broad range of clinical manifestations. More recently, targeted synthetic small molecules—including JAK inhibitors and TYK2 inhibitors—have expanded the armamentarium of available therapies. The overarching goals of treatment in PsA include the suppression of the underlying inflammatory process and the prevention of structural joint damage. The impact of each therapeutic option on cutaneous psoriasis is an additional and important consideration that guides individualized treatment options. Full article

Rheumatoid arthritis (RA) is a systemic autoimmune disease that can involve the ocular surface and deeper ocular tissues, leading to a spectrum of ophthalmic manifestations ranging from dry eye disease to vision-threatening inflammation, such as scleritis and peripheral ulcerative keratitis (PUK). This paper presents the results of a narrative review conducted using PubMed and Google Scholar from database inception to March 2026. Eligible publications describing clinical features and management of RA-associated ocular disease were synthesized, and no unpublished data were included. According to the literature, dry eye disease (DED) is the most frequent ocular manifestation of RA, and it is primarily managed with lubrication and topical anti-inflammatory therapies, including cyclosporine and lifitegrast. Additional options for refractory disease include neurostimulation and evaporation-targeted therapy. Scleritis and PUK are less common but represent severe inflammatory complications that generally require systemic immunosuppression. Conventional management includes systemic corticosteroids and steroid-sparing agents such as methotrexate (MTX), azathioprine (AZA), cyclophosphamide (CYC), and mycophenolate mofetil (MMF) in aggressive cases. Escalation to biologic disease-modifying antirheumatic drugs (bDMARDs), specifically tumor necrosis factor-alpha (TNF-α) inhibitors and rituximab (RTX), is supported for refractory scleritis and corneal melt, although evidence is largely observational. Among anti-TNF agents, monoclonal antibodies, such as infliximab and adalimumab, appear more effective than etanercept for ocular inflammation. Rituximab is preferred for vasculitis-associated or refractory disease, and Janus Kinase (JAK) inhibitors represent an emerging option requiring careful safety monitoring. Evidence for DED therapies includes randomized controlled trials (RCTs), whereas data for RA-associated scleritis and PUK are largely derived from registries, case series, and case reports. Prospective studies with standardized ocular outcomes are needed to refine treatment algorithms and compare the effectiveness of biologic versus targeted synthetic agents. Full article

Background: Continuity of care for rheumatoid arthritis patients within regional networks enables stable long-term clinical data collection, despite chronic rheumatologist shortages in Japan. We determined 5-year drug survival and discontinuation reasons for eight biological disease-modifying antirheumatic drugs (bDMARDs) using a regional multicenter registry. Methods: We retrospectively analyzed 1182 patients initiating their first (naïve, n = 784) or subsequent (switch, n = 398) bDMARD between May 2001 and August 2022 across five institutions. The primary endpoint (5-year drug survival) and secondary endpoints (discontinuation risk factors and cumulative incidence of reasons) were evaluated using Kaplan–Meier curves, Cox proportional hazards, and Fine & Gray models. Results: Baseline characteristics varied significantly among bDMARDs. Five-year drug survival in the naïve cohort ranged from tocilizumab (50.8%) to golimumab (22.6%); in the switch cohort, from abatacept (42.6%) to infliximab (10.0%). In multivariable Cox analysis of naïve patients, male sex (hazard ratio [HR] = 1.49, 95% confidence interval [CI] = 1.09–2.02), lower baseline 28-joint Disease Activity Score with erythrocyte sedimentation rate (DAS28-ESR) (HR = 0.90, 95% CI = 0.82–0.99), and absence of methotrexate co-therapy (HR = 0.73, 95% CI = 0.55–0.97) predicted discontinuation. The lower baseline DAS28-ESR association potentially reflects successful courses toward intentional cessation following remission. Discontinuations were attributed to inadequate response (27.1%), non-adverse events (25.3%), and adverse events (17.3%). Conclusions: Tocilizumab and abatacept demonstrated the highest retention rates in biologic-naïve and switch cohorts, respectively. Early, individualized drug selection and dose optimization are crucial to maximizing long-term bDMARD effectiveness before switching. Full article

The perioperative management of biologic and immunomodulatory therapies in patients undergoing orthopedic surgery poses a clinical challenge, primarily due to the increased risk of postoperative infections. Biologic agents, particularly TNF inhibitors and interleukin-targeting drugs, may impair host immune responses, potentially increasing the risk of surgical site infections (SSIs), delayed wound healing, and systemic infections. However, abrupt discontinuation of these therapies can lead to disease flare-ups, which themselves may complicate recovery and rehabilitation. In addition, discontinuation of biologics can lead to drug tolerance and unresponsiveness when they are restarted and thereby need switching to another biologic. Recent studies suggest that the infection risk is particularly elevated with ongoing biologic therapy during major surgeries, especially in procedures involving prosthetic implants. Guidelines generally recommend withholding biological disease-modifying antirheumatic drugs (bDMARDs) for at least one dosing cycle prior to surgery, when feasible, while maintaining non-biologic DMARDs in most cases. The decision must be individualized, taking into account the pharmacokinetics of each drug, the type of surgery, the patient’s comorbidities, and the activity of the underlying disease. Close coordination among rheumatologists, orthopedic surgeons, and infectious disease specialists is essential to minimize perioperative complications and optimize patient outcomes. Full article

Background: Pharmacovigilance is a critical component of patient safety, particularly among older adults with chronic diseases who are frequently exposed to polypharmacy. In Kosovo, adverse drug reactions (ADRs) reported by patients remain insufficiently recognized within the healthcare system. Polypharmacy, limited access to pharmaceutical counseling, and self-medication practices may contribute to increased medication-related harm. Capturing ADRs directly from patients provides valuable insight into medication safety challenges and communication gaps in clinical care. Objective: To assess the frequency, characteristics, and reporting behavior of adverse drug reactions among adults aged 60–75 years with chronic diseases in Kosovo, and to identify factors associated with awareness and reporting practices. Methods: A multicenter cross-sectional study was conducted between January and September 2025 in four major cities in Kosovo (Prishtina, Prizren, Peja, and Gjilan). A total of 1024 patients receiving continuous therapy for at least one chronic condition were surveyed using a structured questionnaire covering demographic characteristics, drug exposure, ADR experience, and reporting behavior. Statistical analyses included descriptive statistics, chi-square testing, and multivariable logistic regression to identify predictors of ADR reporting. Results: Overall, 47.3% of participants reported experiencing at least one ADR in the preceding 12 months. Among those, 39.5% reported the event to a healthcare professional, whereas 60.5% did not seek professional advice. The most frequently implicated drug classes were antihypertensives (32.8%), analgesics and non-steroidal anti-inflammatory drugs (27.4%), and antirheumatic agents (14.6%), with mainly gastrointestinal (24.1%) and cardiovascular (18.9%) manifestations. Approximately 19.8% of participants reported discontinuing medication due to adverse effects. Female patients were more likely to report ADRs compared to males (p < 0.01). Lack of prior counseling about potential side effects was independently associated with lower reporting (OR = 2.17; 95% CI: 1.41–3.33). Patients using more than six medications had a higher prevalence of ADRs (61.2%). Conclusion: Adverse drug reactions were frequently reported by older patients, while formal reporting to healthcare professionals remained limited. Strengthening patient education, improving patient–provider communication, and integrating clinical pharmacists into primary care may enhance pharmacovigilance practices and medication safety. Full article

Background: Immunomodulatory therapies, including biologic and targeted synthetic disease-modifying antirheumatic drugs (DMARDs) have reshaped the treatment of autoimmune diseases. They alter host defenses, but the current landscape of associated infectious risk is not fully defined. Objective: A scoping review of recent literature was conducted to characterize infectious complications associated with modern immunomodulatory biologic agents, summarize current pathogen patterns, and highlight recommendations for prevention and early recognition in clinical practice. Methods: Following PRISMA-ScR guidelines, a systematic search was performed on Scopus, Science Direct, and PubMed for studies published since 2023. Inclusion criteria focused on adult human subjects, exposure to immunomodulatory therapy, and reported infectious outcomes. Studies focusing exclusively on antineoplastic agents without established use in autoimmune diseases were excluded. After screening 1046 unique records, 16 studies were included in the final review. Findings: High-dose glucocorticoids remain a primary driver of serious infections across autoimmune diseases. Newer agents present mechanism-specific risk profiles. JAK inhibitors are associated with herpes zoster, while TNF-α inhibitors are linked to opportunistic bacterial infections and reactivation of granulomatous infections. B-cell depletion with rituximab correlates with hypogammaglobulinemia and its associated infections, whereas belimumab may offer a lower infection risk in non-renal SLE. Recent post hoc analyses (2023–2025) quantify the elevated risk of herpes zoster with JAK inhibitors compared to TNF inhibitors, particularly in older populations. Conclusions: The infectious risk associated with biologic and targeted DMARDs varies by mechanism. While glucocorticoids remain a primary driver of serious infections, newer data highlights specific vulnerabilities with JAK inhibitors (herpes zoster) and B-cell depletion (hypogammaglobulinemia) that require targeted risk stratification. This review shows the urgent need for individualized risk stratification, targeted prophylaxis (e.g., for Pneumocystis or zoster), and pre-therapy screening to balance therapeutic efficacy with patient safety. Full article

Proteoglycans and their fragments have potential as diagnostic or theragnostic biomarkers to identify diseases characterized by dysregulated extracellular matrix remodeling, such as juvenile idiopathic arthritis (JIA). Therefore, our study aimed to evaluate the diagnostic utility of plasma proteoglycan profiles, namely, aggrecan, decorin, and biglycan, released from osteoarticular structures into the blood of children with juvenile idiopathic arthritis. These profiles are potential biomarkers of tissue destruction and/or indicators of the efficacy of therapy with the biologic agent etanercept (ETA). This study was conducted on 263 blood samples collected from 25 healthy children and 34 children at various stages of juvenile idiopathic arthritis disease: immediately after diagnosis, following treatment with disease-modifying antirheumatic drugs (DMARD) (methotrexate, sulfasalazine, and prednisone), and during 3, 6, 12, 18, and 24 months of therapy with etanercept. Quantitative levels of aggrecan, biglycan, and decorin were measured using ELISA kits. In children with JIA, plasma aggrecan levels were elevated at diagnosis, decreased after ineffective DMARD therapy, and increased again at 24 months of etanercept treatment despite clinical improvement. By contrast, biglycan levels were similar to those in healthy controls but decreased during etanercept therapy. Decorin levels were initially high in untreated and DMARD-treated patients but returned to normal after 24 months of biologic treatment. After considering these findings and the ROC analysis, we conclude that decorin appears to be a promising biomarker for diagnosing and monitoring etanercept therapy in JIA, and biglycan is a useful biochemical marker for assessing the effectiveness of ETA treatment. Full article

Background: We aimed to investigate the risk for a serious infection in rheumatoid arthritis (RA) patients after tapering the dose of biological/targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs). Methods: This nested case–control study investigated the risk for a serious infection in RA patients who underwent mandatory b/tsDMARDs dose reduction 2.5 years after starting therapy with a single b/tsDMARD in the National Health Insurance Research Database (NHIRD). Cases were those patients who developed a serious infection afterwards. Matched controls were selected from those patients who did not develop a serious infection. We used unconditional logistic regression to analyze the odds ratios (ORs) of b/tsDMARDs dose reduction and discontinuation between cases and controls. Results: RA patients underwent an average dose reduction of 60%. Among a total of 268 cases and 1072 controls, we did not observe a lower risk for a serious infection in those patients who tapered or discontinued b/tsDMARDs. However, those patients who had discontinued b/tsDMARDs had a higher risk for a serious infection when compared with those who had not and had reduced their b/stDMARDs dose reduction below the average (i.e., ≤60%), with an adjusted OR of 1.48 (95%CI: 1.05, 2.09). Conclusions: Dose reduction in b/tsDMARDs in RA patients might not be associated with a lower risk for serious infection. Discontinuation of b/tsDMARDs, however, was likely associated with a higher risk for serious infection. Full article

Psoriatic arthritis (PsA) is a chronic, immune-mediated inflammatory arthritis associated with psoriasis, affecting joints, entheses, and the axial skeleton. While primary care providers and dermatologists frequently encounter psoriasis (PsO), early recognition of PsA remains critical to preventing irreversible joint damage. This paper is written to provide a comprehensive overview of PsA, beginning with a clinical case that highlights diagnostic and therapeutic challenges. In this review, the epidemiology of PsA will be discussed, emphasizing its prevalence and risk factors among patients with PsO. The discussion extends to the underlying pathogenesis, focusing on genetic predisposition, environmental triggers, and key cytokines, including TNF-α, IL-17, and IL-23, that have become targets for advanced therapeutics. The clinical features of PsA are explored in detail, including peripheral and axial arthritis, enthesitis, dactylitis, and extra-articular manifestations. Diagnostic approaches are discussed, with a focus on the Classification Criteria for Psoriatic Arthritis (CASPAR) and Moll & Wright criteria. Additionally, we examine screening tools designed to facilitate early detection in dermatology clinics. Diagnostic modalities, including imaging and serologic markers, are reviewed. Finally, we explore the evolving landscape of PsA treatment, spanning conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), biologic agents (bDMARDs), and targeted synthetic DMARDs (tsDMARDs). Given the increasing availability of cytokine-targeted therapies, an interdisciplinary approach between dermatologists and rheumatologists is essential for optimizing outcomes in PsA patients. Patients with PsA are cared for by rheumatologists, dermatologists, and primary care providers who help manage the comorbidities associated with PsA. By bridging primary care, dermatology, and rheumatology in the care of PsA, this paper aims to enhance understanding of PsA for facilitating early identification and timely intervention for improved patient care. Full article

COVID-19 vaccination has played a pivotal role in mitigating the global health crisis and reducing morbidity and mortality associated with SARS-CoV-2 infection. While its public health benefits are unequivocal, the unprecedented scale of vaccination—reaching billions worldwide—has also enabled the detection of rare autoimmune events, including systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, and Guillain–Barré syndrome. Although such events occur in only a small subset of individuals, often influenced by genetic, environmental, or dosage-related factors, they underscore the importance of understanding immune tolerance mechanisms in vaccination. This review synthesizes clinical observations and immunological findings from the COVID-19 vaccination era, highlighting key mechanisms such as molecular mimicry, adjuvant-induced inflammation, bystander activation, epitope spreading, and polyclonal B cell activation. We also consider how novel vaccine platforms, particularly mRNA-based technologies, may influence immune regulation and self-tolerance. Importantly, we discuss the therapeutic management of vaccine-associated autoimmunity, including the use of corticosteroids, intravenous immunoglobulin (IVIG), plasma exchange, disease-modifying anti-rheumatic drugs (DMARDs), and other immunosuppressive agents, many of which have led to favorable clinical outcomes. By integrating mechanistic insights with treatment strategies, this review emphasizes that the overall benefits of COVID-19 vaccination overwhelmingly outweigh the risks, while advocating for continued surveillance, mechanistic research, and risk stratification to inform safer and more targeted vaccination strategies in future pandemics. Full article

Gout is a form of sterile inflammatory arthritis in which monosodium urate (MSU) crystals deposit and provoke a neutrophil-predominant response, primarily driven by activation of the NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome. Here, we show that auranofin, a Food and Drug Administration (FDA)-approved anti-rheumatic agent, exerts anti-inflammatory effects in both in vitro and in vivo models of gout. Auranofin inhibited NLRP3 inflammasome activation in human THP-1 cells and murine macrophages, leading to reduced cleavage of caspase-1, interleukin-1β (IL-1β), and interleukin-18 (IL-18). In MSU crystal-induced mouse models, auranofin treatment reduced paw swelling, serum cytokine levels, and tissue inflammation. Notably, auranofin suppressed neutrophil migration and decreased expression of C-X-C motif chemokine ligand 1 (CXCL1) in inflamed foot tissue and air-pouch exudates. Mechanistically, auranofin disrupted the interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) axis, a key signaling pathway promoting neutrophil recruitment. Overexpression of IL-33 abolished the anti-inflammatory effects of auranofin, highlighting the central role of IL-33 in gout pathogenesis. Together, our findings suggest that auranofin alleviates MSU-induced inflammation by concurrently inhibiting NLRP3 inflammasome activation and IL-33-mediated neutrophil recruitment, supporting its potential as a dual-action therapeutic candidate for gout. Full article

Background: Rheumatoid arthritis is the most prevalent systemic inflammatory disease, mainly affecting the synovial tissue of small and large joints, also associated with significant extra-articular manifestations. Throughout the progression of the disease, cardiac structures may be affected, including the conducting system, myocardium, endocardium, coronary arteries, and valves, potentially resulting in a higher incidence of cardiac arrhythmias. Methods: We performed a narrative review of the most recent studies that highlight the epidemiology, pathophysiology, diagnosis, and management of arrhythmias occurring in patients with rheumatoid arthritis. Furthermore, we examined the impact of disease-modifying antirheumatic drugs (DMARDs)—including conventional synthetic (csDMARDs), biologic (bDMARDs), and targeted synthetic agents (tsDMARDs)—on cardiac electrophysiology. Results: Cardiac immune cells may influence arrhythmogenesis through non-canonical and inflammatory mechanisms by modifying myocardial tissue architecture or by interacting with cardiomyocytes, potentially altering their electrical function. Conclusions: This review emphasizes the essential role of a multidisciplinary approach integrating rheumatology and cardiology expertise in the screening and management of arrhythmias in patients with rheumatoid arthritis. Full article