Current Rheumatology Reports最新文献

Purpose of review: We present information on the burden of vaccine-preventable diseases in people with rheumatoid arthritis (RA), the latest evidence on vaccine immunogenicity in disease-modifying antirheumatic drug (DMARD) users, and expert and guideline-based immunization recommendations. We focus on infections with the highest morbidity and mortality, and those relevant due to new developments or current outbreaks.

Recent findings: Following the license expansion for two respiratory syncytial virus (RSV) vaccines, GSK's Arexvy and Pfizer's Abrysvo, the Advisory Committee for Immunization Practices (ACIP) expanded the recommendation for vaccination in adults at increased risk of severe RSV disease. In the spring of 2025, the Center for Disease Control lowered the cutoff for immunization in high-risk groups from ≥ 60 to ≥ 50 years. There are new 2024-2025 SARS-CoV-2 vaccines and updated ACIP recommendations for SARS-CoV-2 immunization that address new viral strains and the known waning immunity from vaccines. All individuals who are moderately to severely immunocompromised (including those with RA) should receive at least one additional vaccine dose compared to the general population. The ACIP has updated its recommendations for pneumococcal immunization, aiming to lower pneumococcal disease incidence in adults. Following the approval of the 21-valent pneumococcal conjugate vaccine, designed to target the serotypes commonly affecting adults, the cutoff for vaccination in the general population changed from ≥ 65 to ≥ 50 years. Recommendations for vaccination in RA patients (everyone age ≥ 18 years) remain unchanged. Vaccine recommendations for RA patients constantly evolve as new DMARDs and vaccines are developed, and our understanding of their interaction with DMARDs vis a vis immunogenicity improves. It is essential to stay current with the latest recommendations from the ACIP and rheumatologic society guidelines.

Purpose of review: Spondyloarthritis animal models such as the HLA-B27 transgenic rat, SKG mouse and cytokine overexpression models have proven useful for testing hypotheses regarding pathogenesis. Recent developments in the field from human studies have shifted attention to HLA-B2705 restricted CD8+ T cell clonotype expansion and the "arthritogenic peptide" theory. Since human and rodent MHC and T cell compartments differ, translatability comes into question. In this review, we will discuss the advantages and caveats of several spondyloarthritis rodent models. We will review classic studies and more recent reports providing insight into pathologic T cells outside the canonical paradigm of MHC Class I-CD8+ T cell interaction.

Recent findings: Animal models have revealed requisite "ingredients' for a spondyloarthritis phenotype, including inflammatory mediators and lymphoid cell types. Most of these models highlight the role of Th17 cells and other IL-17 producing cells. Indeed, the IL-23 minicircle model directly led to the identification of IL-17 producing γδ T cells in typical spondyloarthritis anatomic locations. In addition to identifying lymphocyte players, animal models have elucidated T cell regulation, including innate immune (e.g. neutrophil) T cell crosstalk and gut-joint trafficking. Current studies are also beginning to clarify roles for innate lymphocytic cells such as MAIT and iNKT cells. Animal model studies have provided vital insight into T cell pathogenic mechanisms outside canonical MHC Class I-CD8 interaction. Many of these findings have been replicated in human subjects. Furthermore, work from animal models directly supported the development of IL17 and IL23 targeting therapeutics, attesting to their relevance.

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Purpose of review: This review article examines the evolving evidence on cancer recurrence and new malignancy risk associated with disease-modifying antirheumatic drugs (DMARDs), including TNF inhibitors, rituximab, IL-6 inhibitors, and JAK inhibitors, in patients with rheumatoid arthritis and a prior malignancy.

Recent findings: Conventional synthetic DMARDs are generally considered safe in patients with a history of cancer, with earlier concerns about skin and hematologic malignancies largely disproven. Hydroxychloroquine, sulfasalazine, and leflunomide similarly show no consistent cancer risk. Biologic DMARDs, including TNF inhibitors, rituximab, and abatacept, have not been linked to increased cancer recurrence, though caution is advised in patients with a history of skin cancer. Despite supportive evidence, bDMARD use has declined following cancer diagnoses. JAK inhibitors, however, have shown increased risk of lung cancer in older patients with cardiovascular risk factors, prompting cautious use until more data is available. Although large population clinical trials are lacking, current evidence does not demonstrate any increased risk with initiation of csDMARDs, TNF inhibitors, and rituximab in RA patients with a history of cancer. Abatacept and IL-6 inhibitors may also be reasonable options but require further data. JAK inhibitors should be used cautiously until more reliable data becomes available. These findings support cautious but not prohibitive use of bDMARDs in RA patients with a history of cancer, emphasizing individualized risk assessment and shared decision-making. Further high-quality, prospective studies are needed to guide therapy in this complex clinical population.

Purpose of review: Despite the availability of effective pharmacotherapy to lower serum urate (SUA) levels and consequently reduce the likelihood of flares, gout remains a poorly managed condition. Quality of care assessments are of paramount importance in evaluating the performance of health systems and providers in managing gout, spanning patient (micro), provider or team (meso), and organizational or system-wide (macro) levels. This review focuses on the conceptual underpinnings on how quality of care in gout management is defined and assessed, highlighting methodological challenges, study approaches and contemporary findings.

Recent findings: We illustrate the advantages and pitfalls on the use of quality indicators as the reference by which gout clinical care is deemed to be "optimal". We further introduce pertinent processes/intermediaries of gout care under a conceptual framework for quality assessment. Overall, quality of gout care requires significant improvement, with widespread deficiencies across key parameters including urate lowering therapy (ULT) adherence (micro-level), SUA monitoring (meso-level) and treatment to target SUA levels on a population basis (macro-level). There are large care gaps across processes, intermediaries and outcomes of gout care. Since accurate quality assessment forms the foundational pillar of subsequent quality improvement, this review serves as a reference to advance quality of gout care assessments. Further initiatives are required to enhance ULT adherence, in particular, which is a key intermediary step to optimal gout care and yet remains suboptimal on a population level. The integration of Learning Health Systems is emerging as a promising platform for improving the quality of gout care.

Purpose of the review: Behçet's Syndrome (BS) is a multisystemic vasculitis that can affect the heart, leading to pericarditis, myocarditis, intracardiac thrombosis, endomyocardial fibrosis, valvular dysfunction, and coronary artery disease. This review summarizes the clinical presentation, diagnostic challenges, and therapeutic strategies for cardiac involvement in BS.

Recent findings: Advanced imaging techniques have revealed subclinical cardiac involvement in BS. Myocardial dysfunction and fibrosis contribute to heart failure and arrhythmias, while intracardiac thrombi often coexist with pulmonary artery involvement. Coronary artery vasculitis and aneurysms may mimic atherosclerotic disease, complicating diagnosis. Biologic therapies, including TNF-α inhibitors, show promise in refractory cases. Early diagnosis and immunosuppressive therapy are crucial. A multidisciplinary approach is essential to managing cardiac complications and optimizing patient outcomes. Future research should refine screening protocols and explore targeted immunotherapies for BS-related cardiovascular disease.

Purpose of review: Pain is one of the most debilitating sequelae of rheumatoid arthritis. Established and emerging therapies offer effective disease control for many patients, though they often have underwhelming efficacy for pain relief. The uncoupling of pain intensity from disease activity and inflammation presents an ongoing challenge in both our understanding of the pathophysiology and our ability to treat joint pain. The generation of high-parameter, unbiased -omic data sets generated from patient-derived tissues is changing how we think about rheumatoid arthritis pain. In this review, we discuss the peripheral drivers of pain in rheumatoid arthritis-affected joints and their innervating primary afferents. We evaluate how human molecular immunology and neuroscience approaches are helping us unravel the heterogeneity of pain in rheumatoid arthritis and propose future directions to clarify how pain is maintained in the absence of inflammation.

Recent findings: Synovial fibroblasts have emerged as key pronociceptive drivers within the rheumatic joint. Further to the classical proinflammatory mediators known to drive pain, such as cytokines and prostaglandins, bone morphogenetic proteins, ephrin signaling, and netrins appear to be upregulated in both rheumatoid arthritis-affected synovium and the innervating sensory neurons. Resulting adaptations to innervating primary afferents such as synaptogenesis and neurite outgrowth may occur in a sensory neuron subtype-specific manner causing pain that is disproportionate to inflammation. Nociceptor sprouting in the joint may explain why pain tends to persist despite adequate disease control. Future mechanistic work exploring the conditions under which these nociceptors sprout into the joint will provide new therapeutic avenues for ensuring that pain resolves alongside the inflammation associated with rheumatoid arthritis.

Purpose of review: Diagnostic delay remains a critical challenge in axial spondyloarthritis (axSpA). This review highlights key clinical and imaging research from 2024 that addresses this persistent issue, with a focus on the evolving roles of MRI, artificial intelligence (AI), and updated Canadian management recommendations.

Recent findings: Multiple studies published in 2024 emphasized the continued problem of diagnostic delay in axSpA. Studies support the continued use of sacroiliac joint MRI as a central diagnostic tool for axSpA, particularly in patients with chronic back pain and associated conditions like uveitis, psoriasis (PsO), or inflammatory bowel disease. AI-based tools for interpreting sacroiliac joint MRIs demonstrated moderate agreement with expert assessments, offering a potential solution to variability and limited access to expert musculoskeletal radiology. These innovations may support earlier diagnosis and reduce misclassification. Innovative models of care, including patient-initiated telemedicine visits, reduced in-person visit frequency without compromising clinical outcomes in patients with stable axSpA. Updated Canadian treatment guidelines introduced more robust data on Janus kinase (JAK) inhibitors and offered stronger support for tapering biologics in patients with sustained low disease activity or remission, while advising against abrupt discontinuation. This clinical and imaging year in review covers challenges and innovations in axSpA, emphasizing the need for early access to care and the development of tools to support prompt diagnosis and sustained continuity of care.

Purpose of review: This review was written to inform practicing clinical rheumatologists about recent advances in artificial intelligence (AI) based research in rheumatoid arthritis (RA), using accessible and practical language. We highlight developments from 2023 to early 2025 across diagnostic imaging, treatment prediction, drug discovery, and patient-facing tools. Given the increasing clinical interest in AI and its potential to augment care delivery, this article aims to bridge the gap between technical innovation and real-world rheumatology practice.

Recent findings: Several AI models have demonstrated high accuracy in early RA detection using imaging modalities such as thermal imaging and nuclear scans. Predictive models for treatment response have leveraged routinely collected electronic health record (EHR) data, moving closer to practical application in clinical workflows. Patient-facing tools like mobile symptom checkers and large language models (LLMs) such as ChatGPT show promise in enhancing education and engagement, although accuracy and safety remain variable. AI has also shown utility in identifying novel biomarkers and accelerating drug discovery. Despite these advances, as of early 2025, no AI-based tools have received FDA approval for use in rheumatology, in contrast to other specialties. Artificial intelligence holds tremendous promise to enhance clinical care in RA-from early diagnosis to personalized therapy. However, clinical adoption remains limited due to regulatory, technical, and implementation challenges. A streamlined regulatory framework and closer collaboration between clinicians, researchers, and industry partners are urgently needed. With thoughtful integration, AI can serve as a valuable adjunct in addressing clinical complexity and workforce shortages in rheumatology.