Georgina R Harvey, Christine MacFadyen, Sarah L Tansley
{"title":"Newer Autoantibodies and Laboratory Assessments in Myositis.","authors":"Georgina R Harvey, Christine MacFadyen, Sarah L Tansley","doi":"10.1007/s11926-024-01171-8","DOIUrl":"10.1007/s11926-024-01171-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":"27 1","pages":"5"},"PeriodicalIF":5.7,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"An Update on Kawasaki Disease.","authors":"Anurag Ratan Goel, Ali Yalcindag","doi":"10.1007/s11926-024-01167-4","DOIUrl":"10.1007/s11926-024-01167-4","url":null,"abstract":"<p><strong>Purpose: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":"27 1","pages":"4"},"PeriodicalIF":5.7,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Treatment of Reactive Arthritis with Biological Agents.","authors":"Avarna Agarwal, Debashis Maikap, Prasanta Padhan","doi":"10.1007/s11926-024-01165-6","DOIUrl":"10.1007/s11926-024-01165-6","url":null,"abstract":"<p><strong>Purpose of the review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":" ","pages":"450-458"},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"How to Distinguish Non-Inflammatory from Inflammatory Pain in RA?","authors":"Sharmila Khot, George Tackley, Ernest Choy","doi":"10.1007/s11926-024-01159-4","DOIUrl":"10.1007/s11926-024-01159-4","url":null,"abstract":"<p><strong>Purpose of the review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":" ","pages":"403-413"},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11527911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Rheumatoid Arthritis-Associated Interstitial Lung Disease (RA-ILD): Update on Prevalence, Risk Factors, Pathogenesis, and Therapy.","authors":"Daniel I Sullivan, Dana P Ascherman","doi":"10.1007/s11926-024-01155-8","DOIUrl":"10.1007/s11926-024-01155-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":" ","pages":"431-449"},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jessica Day, Hani Kushlaf, Stacey Tarvin, Lorenzo Cavagna, Veronica Codullo, Samuel Katsuyuki Shinjo, Xia Lyu, Johannes Knitza, Raouf Hajji, Peter R Blier, Chih Wei Tseng, Simone Appenzeller, Lisa G Rider, Lisa Christopher-Stine, Latika Gupta
{"title":"Telemedicine for the Care of Patients with Idiopathic Inflammatory Myopathies: Experience, Insights and Future Directions from the International Myositis Assessment and Clinical Studies Telemedicine Scientific Interest Group.","authors":"Jessica Day, Hani Kushlaf, Stacey Tarvin, Lorenzo Cavagna, Veronica Codullo, Samuel Katsuyuki Shinjo, Xia Lyu, Johannes Knitza, Raouf Hajji, Peter R Blier, Chih Wei Tseng, Simone Appenzeller, Lisa G Rider, Lisa Christopher-Stine, Latika Gupta","doi":"10.1007/s11926-024-01163-8","DOIUrl":"10.1007/s11926-024-01163-8","url":null,"abstract":"","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":" ","pages":"414-420"},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent Updates on the Pathogenesis of Inflammatory Myopathies.","authors":"Jon Musai, Andrew L Mammen, Iago Pinal-Fernandez","doi":"10.1007/s11926-024-01164-7","DOIUrl":"10.1007/s11926-024-01164-7","url":null,"abstract":"<p><strong>Purpose of review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":" ","pages":"421-430"},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11527972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Immune Checkpoint Inhibitor Associated Rheumatoid Arthritis.","authors":"Luigino Bernabela, Bonnie Bermas","doi":"10.1007/s11926-024-01173-6","DOIUrl":"10.1007/s11926-024-01173-6","url":null,"abstract":"<p><strong>Purpose of this review: </strong>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.</p><p><strong>Recent findings: </strong>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.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":"27 1","pages":"3"},"PeriodicalIF":5.7,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Unveiling the Potential of Probiotics in Osteoarthritis Management.","authors":"Asima Karim","doi":"10.1007/s11926-024-01166-5","DOIUrl":"10.1007/s11926-024-01166-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Osteoarthritis (OA), a highly prevalent degenerative joint disease, is of increasing concern due to its debilitating nature and negative impact on quality of life. Recent investigations have explored the therapeutic potential of probiotics to alleviate OA. This review summarizes the emerging evidence for the potential role of probiotics in managing OA symptoms and disease progression. The link between gut dysbiosis and chronic inflammation, a key player in OA progression is discussed in this review.</p><p><strong>Recent findings: </strong>Probiotics may modulate gut microbiota composition, potentially reducing systemic inflammation and alleviating OA symptoms, including joint pain and function. Possible mechanisms through which probiotics may exert these effects, including dampening inflammatory pathways and enhancing intestinal barrier integrity have been highlighted. Promising results from preclinical and clinical studies investigating the specific beneficial effects of specific probiotic strain(s) for OA management have been highlighted. Finally, limitations in current research and future directions, emphasizing the need for well-designed, large-scale clinical trials to definitively establish the therapeutic potential of probiotics in OA treatment have been discussed.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":"27 1","pages":"2"},"PeriodicalIF":5.7,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Benjamin Klein, Nguyen Thi Kim Nguyen, Rezvan Moallemian, J Michelle Kahlenberg
{"title":"Keratinocytes - Amplifiers of Immune Responses in Systemic Lupus Erythematosus.","authors":"Benjamin Klein, Nguyen Thi Kim Nguyen, Rezvan Moallemian, J Michelle Kahlenberg","doi":"10.1007/s11926-024-01168-3","DOIUrl":"10.1007/s11926-024-01168-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>Epithelial cells have been acknowledged as important players in autoimmune diseases by directing and enhancing inflammatory responses. Here, we summarize recent publications that examine keratinocyte (KC) dysfunction and its contribution to cutaneous and systemic disease in systemic lupus erythematosus patients.</p><p><strong>Recent findings: </strong>Chronic upregulation of type I interferon (IFN) in KCs is a feature of both lesional and nonlesional lupus skin. This IFN rich environment modulates epidermal cell death responses and promotes inflammatory responses to UV light exposure. In addition, newer technologies such as single cell RNA-seq are informing our understanding of lupus-specific intercellular crosstalk and how this contributes to disease. Recent discoveries in KC dysfunction in lupus skin include aberrant IFN responses to environmental stress, enhanced cytokine and chemokine secretion and epigenetic changes leading to increased cell death. Further research will enable precision therapies for lupus treatment.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":"27 1","pages":"1"},"PeriodicalIF":5.7,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}