Current Rheumatology Reports最新文献

Purpose of review: We aimed to introduce recent finding of imaging studies used in axial spondyloarthritis (axSpA).

Recent findings: Using low-dose whole spine CT (CT syndesmophyte score [CTSS]) improved diagnostic accuracy for evaluating spinal structural progression than previous method (modified Stoke Ankylosing Spondylitis Spinal Score [mSASSS]) in axSpA. The novel definition of positive finding of sacroiliac joint (SIJ) and spine magnetic resonance imaging (MRI) enabled to diagnose axSpA earlier than plain radiography. In addition, novel MRI protocol such as volumetric interpolated breath-hold examination improved detection rate of structural change of axial joints in axSpA, Nuclear medicine imaging showed potential for diagnosis and predicting progression of axSpA. Ultrasonography guided injection is useful for controlling local joint pain of axSpA. AxSpA is characterised by pain and inflammation of axial joints such as the SIJ and spine. Detection of active inflammatory lesions using MRI has expanded the subtypes of axSpA to include non-radiographic axSpA (nr-axSpA). In addition, many other imaging techniques have improved, and can now detect structural and early inflammatory lesions of the axial joints. In addition, a method for quantitative measurement of syndesmophytes by CTSS has been developed; this method is more accurate and sensitive than the mSASSS for detecting spinal structural damage. Here, we discuss the current knowledge and clinical advances in computed tomography, MRI, nuclear medicine imaging, and ultrasonography as imaging methods for axSpA.

Purpose of the review: This narrative review aims to discuss the most recent studies regarding the risk of cardiovascular disease (CVD) in women with psoriasis, psoriatic arthritis (PsA) and spondyloarthritis (SpA). In addition, the potential of menopause to modulate/increase CVD risk in women with these diseases will also be explored. It is of major interest to gain more understanding into this topic because it can have meaningful implications for screening and treatment of CVD risk in these women.

Recent findings: Literature shows that psoriasis, PsA, SpA and menopause itself cause higher CVD risks and higher CVD prevalence. This is predominantly explained by the increase of chronic systemic inflammation. No existing literature conclusively demonstrates or studies specifically whether the menopause amplifies this effect caused by psoriasis, PsA, or SpA.

Conclusion: Differences in pathophysiology of psoriasis, SpA and PsA versus the menopausal transition could suggest that menopause may increase the risk of CVD. However, the hypothesis that menopause represents an additional CV risk factor in women with psoriasis, PsA and SpA still needs to be thoroughly investigated and more clinical studies are required for further understanding and conclusions.

Purpose of review: We aim to describe the immunoassays that have been used for myositis autoantibody discovery with a focus on newer methods. We describe recently identified myositis autoantibodies that do not yet form part of routine clinical testing, highlighting what is known about their associated clinical phenotype and potential clues as to their presence.

Recent findings: Novel approaches to autoantibody detection have been employed in recent years including chemiluminescent immunoassay, phage immunoprecipitation-sequencing and modifications to the more traditional immunoprecipitation technique. This has led to the discovery of novel autoantibodies, including novel anti-aminoacyl-tRNA synthetase autoantibodies and autoantibodies which modify cancer risk for patients with anti-TIF1ɣ associated dermatomyositis. New approaches to novel autoantibody detection have facilitated autoantibody discovery and will enable the identification of autoantibodies to a broader range of autoantigens. Challenges remain in translating this knowledge into accessible testing particularly given the rarity of most recently discovered autoantibodies.

Purpose: To summarize advances in research on the epidemiology, pathogenesis, diagnosis, and treatment of Kawasaki Disease (KD), a systemic inflammatory illness of unknown etiology that affects children globally.

Recent findings: The epidemiology of KD was affected by the COVID-19 pandemic and advances in molecular immunology and machine learning have enabled research into its pathogenesis. There is ongoing research into agents that can be used to intensify initial treatment and accumulating evidence supporting the use of certain rescue regimens for refractory disease over others. There is promise surrounding a new coronary artery aneurysm prediction model. Research into the post-acute morbidity of KD continues. The COVID-19 pandemic temporarily reduced the incidence of KD. The NLRP3 inflammasome plays a key role in KD pathogenesis. Intensified initial treatment benefits high-risk patients, yet no intensification regimen shows superiority over another. Corticosteroids, infliximab, or combination therapy with IVIg plus another agent may be superior rescue regimens compared to IVIg alone for refractory KD. The Son score, developed in North America, predicted coronary artery lesions in Japanese and Italian cohorts. Patients with a history of KD may carry long-term physical and emotional burdens that persist into adulthood yet appear to have typical neurocognitive development. Successful transition to adult healthcare presents a challenge.

Purpose of the review: Reactive arthritis (ReA) is an inflammatory joint condition triggered by an infection elsewhere in the body, and this review aims to provide a comprehensive synthesis of recent studies including case reports and case series to determine whether biologics are a treatment option.

Recent findings: Recent studies indicate that biological agents, including anti-TNF agents (infliximab, adalimumab, etanercept), anti-IL17 (secukinumab), and anti-IL6 (tocilizumab), are effective in treating refractory cases of ReA. Evidence suggests these agents are associated with significant clinical improvement. Notably, the data reveal that these biologics are generally well-tolerated, with a low incidence of major adverse events, which supports their safety profile for use in ReA. Biological agents, including anti-TNF, anti-IL17, and anti-IL6 therapies, can be safely and effectively used in the treatment of ReA when conventional therapies fail. It further emphasizes the need for a well-designed controlled trial to provide scientific basis for better informed clinical decisions in cases not responding to conventional treatment.

Purpose of the review: Managing non-inflammatory pain in rheumatoid arthritis (RA) can be a huge burden for the rheumatologist. Pain that persists despite optimal RA treatment is extremely challenging for patient and physician alike. Here, we outline the latest research relevant to distinguishing non-inflammatory from inflammatory RA pain and review the current understanding of its neurobiology and management.

Recent findings: Nociplastic pain is a recently introduced term by the international pain community. Its definition encompasses the non-inflammatory pain of RA and describes pain that is not driven by inflamed joints or compromised nerves, but that is instead driven by a functional reorganisation of the central nervous system (CNS). Insights from all areas of nociplastic pain research, including fibromyalgia, support a personalised pain management approach for non-inflammatory pain of RA, with evidence-based guidelines favouring use of non-pharmacological interventions. Future developments include novel CNS targeting pharmacotherapeutic approaches to treat nociplastic pain.

Purpose of review: Rheumatoid arthritis is frequently complicated by interstitial lung disease (RA-ILD), an underappreciated contributor to excess morbidity and mortality. The true prevalence of RA-ILD is difficult to define given the variability in diagnostic criteria used. The lack of standardized screening methods, an incomplete understanding of disease pathogenesis, and dearth of validated biomarkers have limited the development of controlled clinical trials for this disease.

Recent findings: Numerous studies have focused on clinical, radiographic, genetic, molecular, and/or serologic markers of disease severity as well as risk of disease progression. In addition to defining valuable clinical biomarkers, these studies have provided insights regarding the pathogenesis of RA-ILD and potential therapeutic targets. Additional studies involving immunomodulatory and/or anti-fibrotic agents have assessed new therapeutic options for different stages of RA-ILD. RA-ILD continues to be a major contributor to the increased morbidity and mortality associated with RA. Advancements in our understanding of disease pathogenesis at a molecular level are necessary to drive the development of more targeted therapy.

Purpose of review: This review aims to provide a comprehensive and updated overview of autoimmune myopathies, with a special focus on the latest advancements in understanding the role of autoantibodies. We will begin by examining the risk factors and triggers associated with myositis. Next, we will delve into recent research on how autoantibodies contribute to disease pathogenesis. Finally, we will explore the latest innovations in treatment strategies and their implications for our understanding of myositis pathogenesis.

Recent findings: Recent research has revealed that myositis-specific autoantibodies can infiltrate muscle cells and disrupt the function of their target autoantigens, playing a crucial role in disease pathogenesis. Significant advances in treatment include CD19 CAR-T cell therapy, JAK-STAT inhibitors, and novel strategies targeting the type 1 interferon pathway in dermatomyositis. Additionally, the ineffectiveness of complement inhibitors in treating immune-mediated necrotizing myositis has challenged established views on disease mechanisms. Autoimmune myopathies are a collection of disorders significantly influenced by specific autoantibodies that drive disease pathogenesis. This review highlights the critical role of autoantibody research in deepening our understanding of these conditions and discusses recent therapeutic advancements targeting key pathogenic pathways.

Purpose of this review: Immune checkpoint inhibitors (ICI) have revolutionized cancer therapy over the past decade. Unfortunately, immune related adverse events (irAEs) are common, including rheumatologic adverse events. These rheumatologic irAEs include de novo rheumatoid arthritis-like presentations or flares of pre-existing rheumatoid arthritis, collectively called ICI-associated rheumatoid arthritis. In this article we review the different mechanisms of disease activity and management approaches including use of conventional (cs) DMARDs and biologic (b) DMARDs in this patient population. Other forms of ICI-induced inflammatory arthritis e.g., PMR-like or Spondylarthritis-type IA, are beyond the scope of this review.

Recent findings: The heterogeneous presentations of inflammatory arthritis in patients receiving immune checkpoint inhibitors has made this a challenging area to study. Nonetheless, recent studies are providing better understanding on the mechanisms of de novo disease and flares in patients with rheumatoid arthritis. About half of patients with pre-existing rheumatoid arthritis flare after receiving checkpoint inhibitors. Persistent arthritis is often encountered in patients receiving combination immune checkpoint inhibitors. Outcomes on overall survival do not differ in rheumatoid arthritis patients receiving checkpoint inhibitors compared to their non-arthritis counterparts. Rheumatologist play a critical role in the management of active rheumatoid arthritis induced by checkpoint inhibitors. Collaboration with oncology colleagues will continue to be a crucial component in providing quality care to these patients. While the use of glucocorticoids is often the first line therapy for active inflammatory arthritic disease, we recommend earlier consideration of DMARDs just as we inverted the treatment pyramid several decades ago, for rheumatoid arthritis.