Pub Date : 2024-07-01Epub Date: 2024-05-01DOI: 10.1097/BOR.0000000000001023
Philip J Mease
Purpose of review: Pain is the most common and often most troublesome feature of chronic autoimmune diseases such as psoriatic arthritis (PsA) and axial spondyloarthritis (AxSpA). A predominant concept is that the main source of pain is from disease-induced tissue inflammation and structural damage, activating peripheral nerve fibers which relay to the central nervous system. This mechanism is nociceptive pain and the presumption has been that controlling inflammation will be sufficient to reduce this form of pain. However, despite control of inflammation, patients may still have significant residual pain.
Recent findings: We are learning that there are additional pain mechanisms, neuropathic and nociplastic, that are often operative in patients with rheumatologic conditions, that can significantly influence pain experience, quantitation of disease activity, and may benefit from therapeutic approaches distinct from immunotherapy. Neuropathic pain arises from diseased or damaged nerve tissue and nociplastic pain reflects sensitization of the central nervous system due to multiple genetic, neurobiologic, neural network dysregulation, and psychosocial factors. Pain arising from these mechanisms influence assessment of disease activity and thus needs to be factored into decision-making about immunotherapy efficacy.
Summary: This review addresses the importance of accurately assessing the complex mechanisms of pain experience in patients with PsA and AxSpA to more appropriately manage immunomodulatory, neuromodulatory, and nonpharmacologic therapies.
{"title":"Navigating the complexity of pain in psoriatic arthritis and axial spondyloarthritis.","authors":"Philip J Mease","doi":"10.1097/BOR.0000000000001023","DOIUrl":"10.1097/BOR.0000000000001023","url":null,"abstract":"<p><strong>Purpose of review: </strong>Pain is the most common and often most troublesome feature of chronic autoimmune diseases such as psoriatic arthritis (PsA) and axial spondyloarthritis (AxSpA). A predominant concept is that the main source of pain is from disease-induced tissue inflammation and structural damage, activating peripheral nerve fibers which relay to the central nervous system. This mechanism is nociceptive pain and the presumption has been that controlling inflammation will be sufficient to reduce this form of pain. However, despite control of inflammation, patients may still have significant residual pain.</p><p><strong>Recent findings: </strong>We are learning that there are additional pain mechanisms, neuropathic and nociplastic, that are often operative in patients with rheumatologic conditions, that can significantly influence pain experience, quantitation of disease activity, and may benefit from therapeutic approaches distinct from immunotherapy. Neuropathic pain arises from diseased or damaged nerve tissue and nociplastic pain reflects sensitization of the central nervous system due to multiple genetic, neurobiologic, neural network dysregulation, and psychosocial factors. Pain arising from these mechanisms influence assessment of disease activity and thus needs to be factored into decision-making about immunotherapy efficacy.</p><p><strong>Summary: </strong>This review addresses the importance of accurately assessing the complex mechanisms of pain experience in patients with PsA and AxSpA to more appropriately manage immunomodulatory, neuromodulatory, and nonpharmacologic therapies.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"282-288"},"PeriodicalIF":5.1,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140864333","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}
Pub Date : 2024-07-01Epub Date: 2024-03-27DOI: 10.1097/BOR.0000000000001015
Lisa C Adams, Keno K Bressem, Denis Poddubnyy
Purpose of review: To evaluate the current applications and prospects of artificial intelligence and machine learning in diagnosing and managing axial spondyloarthritis (axSpA), focusing on their role in medical imaging, predictive modelling, and patient monitoring.
Recent findings: Artificial intelligence, particularly deep learning, is showing promise in diagnosing axSpA assisting with X-ray, computed tomography (CT) and MRI analyses, with some models matching or outperforming radiologists in detecting sacroiliitis and markers. Moreover, it is increasingly being used in predictive modelling of disease progression and personalized treatment, and could aid risk assessment, treatment response and clinical subtype identification. Variable study designs, sample sizes and the predominance of retrospective, single-centre studies still limit the generalizability of results.
Summary: Artificial intelligence technologies have significant potential to advance the diagnosis and treatment of axSpA, providing more accurate, efficient and personalized healthcare solutions. However, their integration into clinical practice requires rigorous validation, ethical and legal considerations, and comprehensive training for healthcare professionals. Future advances in artificial intelligence could complement clinical expertise and improve patient care through improved diagnostic accuracy and tailored therapeutic strategies, but the challenge remains to ensure that these technologies are validated in prospective multicentre trials and ethically integrated into patient care.
综述的目的:评估人工智能和机器学习在诊断和管理轴性脊柱关节炎(axSpA)方面的当前应用和前景,重点关注它们在医学成像、预测建模和患者监测方面的作用:人工智能,尤其是深度学习,在辅助 X 光、计算机断层扫描(CT)和核磁共振成像分析诊断 axSpA 方面大有可为,一些模型在检测骶髂关节炎和标记物方面与放射科医生不相上下,甚至更胜一筹。此外,它还越来越多地用于疾病进展和个性化治疗的预测建模,并有助于风险评估、治疗反应和临床亚型识别。小结:人工智能技术在推动轴索硬化症的诊断和治疗方面具有巨大潜力,可提供更准确、高效和个性化的医疗解决方案。然而,将其融入临床实践需要严格的验证、伦理和法律方面的考虑,以及对医疗保健专业人员的全面培训。人工智能的未来发展可以补充临床专业知识,并通过提高诊断准确性和量身定制的治疗策略来改善患者护理,但如何确保这些技术在前瞻性多中心试验中得到验证,并符合伦理要求地融入患者护理中,仍然是一项挑战。
{"title":"Artificial intelligence and machine learning in axial spondyloarthritis.","authors":"Lisa C Adams, Keno K Bressem, Denis Poddubnyy","doi":"10.1097/BOR.0000000000001015","DOIUrl":"10.1097/BOR.0000000000001015","url":null,"abstract":"<p><strong>Purpose of review: </strong>To evaluate the current applications and prospects of artificial intelligence and machine learning in diagnosing and managing axial spondyloarthritis (axSpA), focusing on their role in medical imaging, predictive modelling, and patient monitoring.</p><p><strong>Recent findings: </strong>Artificial intelligence, particularly deep learning, is showing promise in diagnosing axSpA assisting with X-ray, computed tomography (CT) and MRI analyses, with some models matching or outperforming radiologists in detecting sacroiliitis and markers. Moreover, it is increasingly being used in predictive modelling of disease progression and personalized treatment, and could aid risk assessment, treatment response and clinical subtype identification. Variable study designs, sample sizes and the predominance of retrospective, single-centre studies still limit the generalizability of results.</p><p><strong>Summary: </strong>Artificial intelligence technologies have significant potential to advance the diagnosis and treatment of axSpA, providing more accurate, efficient and personalized healthcare solutions. However, their integration into clinical practice requires rigorous validation, ethical and legal considerations, and comprehensive training for healthcare professionals. Future advances in artificial intelligence could complement clinical expertise and improve patient care through improved diagnostic accuracy and tailored therapeutic strategies, but the challenge remains to ensure that these technologies are validated in prospective multicentre trials and ethically integrated into patient care.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"267-273"},"PeriodicalIF":5.1,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140293083","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}
Pub Date : 2024-05-03DOI: 10.1097/bor.0000000000001024
Charles Sutherland, Angelo L Gaffo
Gout flares are a paramount component of disease burden inflicted by gout onto the patient. Furthermore, they are included in the core domain set for long-term gout studies recognized by Outcome Measures in Rheumatology. Along with a validated classification criterion for gout, gout investigators have turned their efforts into defining and characterizing the gout flare. This brief review will summarize the efforts that have been done to define and characterize a gout flare in clinical studies.
痛风发作是痛风给患者造成的疾病负担的重要组成部分。此外,痛风发作还被列入《风湿病学结果测量》(Outcome Measures in Rheumatology)认可的痛风长期研究核心领域集。随着痛风分类标准的验证,痛风研究人员已将工作重点转向痛风发作的定义和特征描述。本文将简要回顾在临床研究中定义和描述痛风发作的工作。
{"title":"Investigating gout flares: beyond a definition.","authors":"Charles Sutherland, Angelo L Gaffo","doi":"10.1097/bor.0000000000001024","DOIUrl":"https://doi.org/10.1097/bor.0000000000001024","url":null,"abstract":"Gout flares are a paramount component of disease burden inflicted by gout onto the patient. Furthermore, they are included in the core domain set for long-term gout studies recognized by Outcome Measures in Rheumatology. Along with a validated classification criterion for gout, gout investigators have turned their efforts into defining and characterizing the gout flare. This brief review will summarize the efforts that have been done to define and characterize a gout flare in clinical studies.","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":"2002 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140828421","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}
Pub Date : 2024-05-01Epub Date: 2024-01-02DOI: 10.1097/BOR.0000000000001000
Beth I Wallace, Laura Cooney, David A Fox
Purpose of review: This review will discuss selected emerging molecular targets and associated potential therapeutic agents for rheumatoid arthritis (RA)-directed treatment.
Recent findings: Agents in active development for RA treatment include those targeted to CD40 and CD40 ligand, programmed death protein 1 (PD-1), and granulocyte-macrophage colony-stimulating factor (GM-CSF). Several other molecules with a strong theoretical role in RA pathogenesis and/or demonstrated efficacy in other autoimmune diseases are also being evaluated as potential drug targets in preclinical or translational studies in RA. These targets include interleukin 1 receptor associated kinases 1 and 4 (IRAK1, IRAK4), tyrosine kinase 2 (Tyk2), bradykinin receptor 1 (B1R), OX40 and OX40 ligand.
Summary: Identification of molecular targets for RA treatment remains an active area of investigation, with multiple therapeutic agents in clinical and preclinical development.
{"title":"New molecular targets in the treatment of rheumatoid arthritis.","authors":"Beth I Wallace, Laura Cooney, David A Fox","doi":"10.1097/BOR.0000000000001000","DOIUrl":"10.1097/BOR.0000000000001000","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review will discuss selected emerging molecular targets and associated potential therapeutic agents for rheumatoid arthritis (RA)-directed treatment.</p><p><strong>Recent findings: </strong>Agents in active development for RA treatment include those targeted to CD40 and CD40 ligand, programmed death protein 1 (PD-1), and granulocyte-macrophage colony-stimulating factor (GM-CSF). Several other molecules with a strong theoretical role in RA pathogenesis and/or demonstrated efficacy in other autoimmune diseases are also being evaluated as potential drug targets in preclinical or translational studies in RA. These targets include interleukin 1 receptor associated kinases 1 and 4 (IRAK1, IRAK4), tyrosine kinase 2 (Tyk2), bradykinin receptor 1 (B1R), OX40 and OX40 ligand.</p><p><strong>Summary: </strong>Identification of molecular targets for RA treatment remains an active area of investigation, with multiple therapeutic agents in clinical and preclinical development.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"235-240"},"PeriodicalIF":5.2,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073625","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}
Pub Date : 2024-05-01Epub Date: 2024-02-26DOI: 10.1097/BOR.0000000000001006
Günter Steiner, René E M Toes
Purpose of review: RA is characterized by the presence of autoantibodies among which rheumatoid factors (RFs) and antimodified protein antibodies (AMPA) are serological hallmarks of the disease. In recent years, several novel insights into the biology, immunogenetics and clinical relevance of these autoantibodies have been obtained, which deserve to be discussed in more detail.
Recent findings: RFs from RA patients seem to target distinct epitopes which appear to be quite specific for RA. Determination of immunoglobulin A (IgA) isotypes of RF and anticitrullinated protein antibodies (ACPA) may provide prognostic information because their presence is associated with reduced therapeutic responses to TNF inhibitors. Furthermore, IgA levels are increased in RA patients and IgA immune complexes are more potent than immunoglobulin G (IgG) complexes in inducing NET formation. Concerning AMPAs, investigations on variable domain glycosylation (VDG) revealed effects on antigen binding and activation of autoreactive B cells. Studies on pathogenetic involvement of ACPA suggest Janus-faced roles: on the one hand, ACPA may be involved in joint destruction and pain perception while on the other hand protective anti-inflammatory effects may be attributed to a subset of ACPAs.
Summary: The autoimmune response in RA is extremely complex and still far from being fully understood. Antibodies are not only valuable diagnostic biomarkers but also seem to play pivotal roles in the pathophysiology of RA.
综述的目的:RA的特点是存在自身抗体,其中类风湿因子(RFs)和抗修饰蛋白抗体(AMPA)是该病的血清学标志。近年来,人们对这些自身抗体的生物学、免疫遗传学和临床意义有了一些新的认识,值得对其进行更详细的讨论:最近的发现:RA 患者的 RF 似乎针对不同的表位,而这些表位似乎对 RA 有相当的特异性。RF和抗瓜氨酸蛋白抗体(ACPA)的免疫球蛋白A(IgA)异型的测定可提供预后信息,因为它们的存在与TNF抑制剂治疗反应的降低有关。此外,RA 患者的 IgA 水平升高,IgA 免疫复合物比免疫球蛋白 G(IgG)复合物更能诱导 NET 的形成。关于 AMPAs,对可变结构域糖基化(VDG)的研究显示了其对抗原结合和自身反应性 B 细胞活化的影响。对ACPA致病作用的研究表明,ACPA扮演着 "亚努斯"(Janus-faced)的角色:一方面,ACPA可能参与关节破坏和疼痛感知,另一方面,ACPA亚群可能具有保护性抗炎作用。抗体不仅是有价值的诊断生物标志物,而且似乎在RA的病理生理学中起着关键作用。
{"title":"Autoantibodies in rheumatoid arthritis - rheumatoid factor, anticitrullinated protein antibodies and beyond.","authors":"Günter Steiner, René E M Toes","doi":"10.1097/BOR.0000000000001006","DOIUrl":"10.1097/BOR.0000000000001006","url":null,"abstract":"<p><strong>Purpose of review: </strong>RA is characterized by the presence of autoantibodies among which rheumatoid factors (RFs) and antimodified protein antibodies (AMPA) are serological hallmarks of the disease. In recent years, several novel insights into the biology, immunogenetics and clinical relevance of these autoantibodies have been obtained, which deserve to be discussed in more detail.</p><p><strong>Recent findings: </strong>RFs from RA patients seem to target distinct epitopes which appear to be quite specific for RA. Determination of immunoglobulin A (IgA) isotypes of RF and anticitrullinated protein antibodies (ACPA) may provide prognostic information because their presence is associated with reduced therapeutic responses to TNF inhibitors. Furthermore, IgA levels are increased in RA patients and IgA immune complexes are more potent than immunoglobulin G (IgG) complexes in inducing NET formation. Concerning AMPAs, investigations on variable domain glycosylation (VDG) revealed effects on antigen binding and activation of autoreactive B cells. Studies on pathogenetic involvement of ACPA suggest Janus-faced roles: on the one hand, ACPA may be involved in joint destruction and pain perception while on the other hand protective anti-inflammatory effects may be attributed to a subset of ACPAs.</p><p><strong>Summary: </strong>The autoimmune response in RA is extremely complex and still far from being fully understood. Antibodies are not only valuable diagnostic biomarkers but also seem to play pivotal roles in the pathophysiology of RA.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"217-224"},"PeriodicalIF":5.2,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971266","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}
Pub Date : 2024-05-01Epub Date: 2024-02-29DOI: 10.1097/BOR.0000000000001008
Yuting Qin, Jianyang Ma, Carola G Vinuesa
Purpose of review: This review aims to provide an overview of the genes and molecular pathways involved in monogenic lupus, the implications for genome diagnosis, and the potential therapies targeting these molecular mechanisms.
Recent findings: To date, more than 30 genes have been identified as contributors to monogenic lupus. These genes are primarily related to complement deficiency, activation of the type I interferon (IFN) pathway, disruption of B-cell and T-cell tolerance and metabolic pathways, which reveal the multifaceted nature of systemic lupus erythematosus (SLE) pathogenesis.
Summary: In-depth study of the causes of monogenic lupus can provide valuable insights into of pathogenic mechanisms of SLE, facilitate the identification of effective biomarkers, and aid in developing therapeutic strategies.
{"title":"Monogenic lupus: insights into disease pathogenesis and therapeutic opportunities.","authors":"Yuting Qin, Jianyang Ma, Carola G Vinuesa","doi":"10.1097/BOR.0000000000001008","DOIUrl":"10.1097/BOR.0000000000001008","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review aims to provide an overview of the genes and molecular pathways involved in monogenic lupus, the implications for genome diagnosis, and the potential therapies targeting these molecular mechanisms.</p><p><strong>Recent findings: </strong>To date, more than 30 genes have been identified as contributors to monogenic lupus. These genes are primarily related to complement deficiency, activation of the type I interferon (IFN) pathway, disruption of B-cell and T-cell tolerance and metabolic pathways, which reveal the multifaceted nature of systemic lupus erythematosus (SLE) pathogenesis.</p><p><strong>Summary: </strong>In-depth study of the causes of monogenic lupus can provide valuable insights into of pathogenic mechanisms of SLE, facilitate the identification of effective biomarkers, and aid in developing therapeutic strategies.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"191-200"},"PeriodicalIF":5.2,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7616038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139989573","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}
Pub Date : 2024-05-01Epub Date: 2024-03-05DOI: 10.1097/BOR.0000000000001013
Kevin D Deane
Purpose of review: This review discusses updates in the prediction and prevention of future rheumatoid arthritis (RA).
Recent findings: In individuals with musculoskeletal symptoms and elevated antibodies to citrullinated proteins (ACPA) without clinical inflammatory arthritis (IA), a 'simple' score has a positive predictive value (PPV) of ∼28% for clinical IA/RA within 1 year, and a comprehensive score (including ultrasound) has a PPV of ∼71% for clinical RA within 5 years. Controlled clinical trials in individuals at-risk for future RA have been performed using corticosteroids, rituximab, atorvastatin, methotrexate, hydroxychloroquine and abatacept. Abatacept modestly reduced rates of incident clinical RA and imaging inflammation within the trials, rituximab delayed clinical IA, and methotrexate improved function, symptoms and imaging inflammation. Vitamin D with or without omega 3 fatty acids reduced incidence of autoimmune diseases, including RA. While not proven in controlled clinical trials, observational studies suggest exercise, weight loss and smoking cessation may reduce progression to clinical RA.
Summary: Prediction and prevention of RA is advancing although there are no currently approved interventions for prevention. Future studies should include deeper evaluation of the pathophysiology of RA development to improve prediction and identify key pathways to target in future clinical trials, as well as develop infrastructure to support prevention-related research.
综述的目的:本综述讨论了预测和预防未来类风湿性关节炎(RA)的最新进展:在有肌肉骨骼症状和瓜氨酸蛋白抗体(ACPA)升高但无临床炎症性关节炎(IA)的个体中,"简单 "评分对1年内临床IA/RA的阳性预测值(PPV)为28%,综合评分(包括超声波)对5年内临床RA的阳性预测值(PPV)为71%。对未来可能患上 RA 的高危人群进行了对照临床试验,使用了皮质类固醇、利妥昔单抗、阿托伐他汀、甲氨蝶呤、羟氯喹和阿帕他赛。在试验中,阿巴他赛普适度降低了临床 RA 病发率和影像学炎症,利妥昔单抗推迟了临床 IA,而甲氨蝶呤改善了功能、症状和影像学炎症。含有或不含有欧米伽 3 脂肪酸的维生素 D 可降低包括 RA 在内的自身免疫性疾病的发病率。小结:尽管目前还没有获得批准的预防干预措施,但 RA 的预测和预防工作正在取得进展。未来的研究应包括对RA发展的病理生理学进行更深入的评估,以提高预测能力,确定未来临床试验的目标关键途径,以及开发支持预防相关研究的基础设施。
{"title":"Rheumatoid arthritis: prediction of future clinically-apparent disease, and prevention.","authors":"Kevin D Deane","doi":"10.1097/BOR.0000000000001013","DOIUrl":"10.1097/BOR.0000000000001013","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review discusses updates in the prediction and prevention of future rheumatoid arthritis (RA).</p><p><strong>Recent findings: </strong>In individuals with musculoskeletal symptoms and elevated antibodies to citrullinated proteins (ACPA) without clinical inflammatory arthritis (IA), a 'simple' score has a positive predictive value (PPV) of ∼28% for clinical IA/RA within 1 year, and a comprehensive score (including ultrasound) has a PPV of ∼71% for clinical RA within 5 years. Controlled clinical trials in individuals at-risk for future RA have been performed using corticosteroids, rituximab, atorvastatin, methotrexate, hydroxychloroquine and abatacept. Abatacept modestly reduced rates of incident clinical RA and imaging inflammation within the trials, rituximab delayed clinical IA, and methotrexate improved function, symptoms and imaging inflammation. Vitamin D with or without omega 3 fatty acids reduced incidence of autoimmune diseases, including RA. While not proven in controlled clinical trials, observational studies suggest exercise, weight loss and smoking cessation may reduce progression to clinical RA.</p><p><strong>Summary: </strong>Prediction and prevention of RA is advancing although there are no currently approved interventions for prevention. Future studies should include deeper evaluation of the pathophysiology of RA development to improve prediction and identify key pathways to target in future clinical trials, as well as develop infrastructure to support prevention-related research.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"225-234"},"PeriodicalIF":5.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10959682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027629","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}
Pub Date : 2024-05-01Epub Date: 2024-01-31DOI: 10.1097/BOR.0000000000001001
Silvia Sirotti, Robert Terkeltaub, Georgios Filippou
Purpose of review: In 1977, McCarty astutely observed, 'The variety of names suggested for the condition associated with deposits of calcium pyrophosphate dihydrate crystals is exceeded only by the variations of its clinical presentation'. Fast forward to 2024, a standardized nomenclature for calcium pyrophosphate deposition (CPPD) is still lacking. This review aims to delineate the challenges in characterizing CPPD through nomenclature and imaging.
Recent findings: Despite the effort of nomenclature standardization in 2011 by the EULAR, confusion persists in the literature and clinical practice, with pseudo-forms and obscure abbreviations. The Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) has launched a project to redefine CPPD nomenclature and formulate a user-friendly language for effective communication with patients and other stakeholders. Additionally, recent advancements in imaging, have shed light on various aspects of the disorder.
Summary: Almost 60 years from the first description of a clinical manifestation related to calcium pyrophosphate crystals, a common language describing the disorder is still lacking. A redefined CPPD nomenclature, together with lay-friendly terminology, would significantly contribute to the uniformity of CPPD research, enhance public understanding and awareness and improve doctor-patient communication and therefore disease outcomes. Imaging can provide deep insights into CPPD elements, promoting comprehension of this disorder.
{"title":"Describing calcium pyrophosphate deposition: undoing the tower of Babel!","authors":"Silvia Sirotti, Robert Terkeltaub, Georgios Filippou","doi":"10.1097/BOR.0000000000001001","DOIUrl":"10.1097/BOR.0000000000001001","url":null,"abstract":"<p><strong>Purpose of review: </strong>In 1977, McCarty astutely observed, 'The variety of names suggested for the condition associated with deposits of calcium pyrophosphate dihydrate crystals is exceeded only by the variations of its clinical presentation'. Fast forward to 2024, a standardized nomenclature for calcium pyrophosphate deposition (CPPD) is still lacking. This review aims to delineate the challenges in characterizing CPPD through nomenclature and imaging.</p><p><strong>Recent findings: </strong>Despite the effort of nomenclature standardization in 2011 by the EULAR, confusion persists in the literature and clinical practice, with pseudo-forms and obscure abbreviations. The Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) has launched a project to redefine CPPD nomenclature and formulate a user-friendly language for effective communication with patients and other stakeholders. Additionally, recent advancements in imaging, have shed light on various aspects of the disorder.</p><p><strong>Summary: </strong>Almost 60 years from the first description of a clinical manifestation related to calcium pyrophosphate crystals, a common language describing the disorder is still lacking. A redefined CPPD nomenclature, together with lay-friendly terminology, would significantly contribute to the uniformity of CPPD research, enhance public understanding and awareness and improve doctor-patient communication and therefore disease outcomes. Imaging can provide deep insights into CPPD elements, promoting comprehension of this disorder.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":"36 3","pages":"241-250"},"PeriodicalIF":5.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140184003","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}
Pub Date : 2024-05-01Epub Date: 2024-02-21DOI: 10.1097/BOR.0000000000001009
Hailey Baker, J Kennedy Amaral, Robert T Schoen
Purpose of review: Postinfectious inflammatory arthritis can result from various pathogens, including bacteria, viruses, fungi, and parasites. Prompt identification and treatment of acute infection is vital, but some cases progress to chronic arthritis despite successful treatment of infection. Postinfectious inflammatory arthritis varies from mild, self-limited arthralgia to severe, refractory arthritis, necessitating ongoing disease-modifying treatment. This review explores the spectrum of postinfectious inflammatory arthritis to provide insights into effective management.
Recent findings: Research continues regarding the benefit of antimicrobial therapy, beyond treatment of the acute infection, to diminish the severity of postinfectious inflammatory arthritis. Following treatment of acute infection, most cases are self-limited so treatment is symptomatic. However, a difficult-to-predict fraction of cases develop chronic postinfectious inflammatory arthritis that can be challenging to manage. Recently, as more biologic, and targeted synthetic DMARDs have become available, treatment options have expanded.
Summary: In this article, we use the term 'postinfectious inflammatory arthritis' rather than 'reactive arthritis' because it describes a broader spectrum of diseases and emphasizes the common pathogenesis of a postinfectious inflammatory process. We summarize the conventional therapies and recent management developments for the most frequently encountered postinfectious inflammatory arthritides.
{"title":"Management of postinfectious inflammatory arthritis.","authors":"Hailey Baker, J Kennedy Amaral, Robert T Schoen","doi":"10.1097/BOR.0000000000001009","DOIUrl":"10.1097/BOR.0000000000001009","url":null,"abstract":"<p><strong>Purpose of review: </strong>Postinfectious inflammatory arthritis can result from various pathogens, including bacteria, viruses, fungi, and parasites. Prompt identification and treatment of acute infection is vital, but some cases progress to chronic arthritis despite successful treatment of infection. Postinfectious inflammatory arthritis varies from mild, self-limited arthralgia to severe, refractory arthritis, necessitating ongoing disease-modifying treatment. This review explores the spectrum of postinfectious inflammatory arthritis to provide insights into effective management.</p><p><strong>Recent findings: </strong>Research continues regarding the benefit of antimicrobial therapy, beyond treatment of the acute infection, to diminish the severity of postinfectious inflammatory arthritis. Following treatment of acute infection, most cases are self-limited so treatment is symptomatic. However, a difficult-to-predict fraction of cases develop chronic postinfectious inflammatory arthritis that can be challenging to manage. Recently, as more biologic, and targeted synthetic DMARDs have become available, treatment options have expanded.</p><p><strong>Summary: </strong>In this article, we use the term 'postinfectious inflammatory arthritis' rather than 'reactive arthritis' because it describes a broader spectrum of diseases and emphasizes the common pathogenesis of a postinfectious inflammatory process. We summarize the conventional therapies and recent management developments for the most frequently encountered postinfectious inflammatory arthritides.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"155-162"},"PeriodicalIF":5.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971267","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}
Pub Date : 2024-05-01Epub Date: 2024-02-23DOI: 10.1097/BOR.0000000000001007
Elena Myasoedova, Eric L Matteson
Purpose of review: To discuss changes in epidemiology, recent advances in understanding of the pathogenesis and management of selected extraarticular manifestations of rheumatoid arthritis (ExRA).
Recent findings: The incidence of ExRA overall and subcutaneous rheumatoid nodules in particular is declining after 2000. These trends reflect improved RA disease activity with early effective immunosuppressive treatments; changing environmental risk factors can be contributing. ExRA continues to carry a two-fold increased mortality risk. RA-associated interstitial lung disease (RA-ILD) is a major contributor to mortality, with no decline in incidence and scant therapeutic options. Individualized risk stratification for RA-ILD based on patient-level risk factors and biomarker profile is evolving with MUC5B as a major genetic risk factor. Clinical trials are underway to evaluate the benefits of novel antifibrotic therapies and targeted therapies for RA-ILD. The risk of cardiovascular disease in RA is generally amendable to treatment with disease-modifying antirheumatic drugs, although cardiovascular risk associated with JAK inhibition is not fully understood.
Summary: Despite reduction in incidence of ExRA overall, the incidence of RA-ILD shows no significant decline and remains a major therapeutic challenge. The use of novel antifibrotics and immunosuppressive drugs shows promise in slowing the progression of RA-ILD.
{"title":"Updates on interstitial lung disease and other selected extra-articular manifestations of rheumatoid arthritis.","authors":"Elena Myasoedova, Eric L Matteson","doi":"10.1097/BOR.0000000000001007","DOIUrl":"10.1097/BOR.0000000000001007","url":null,"abstract":"<p><strong>Purpose of review: </strong>To discuss changes in epidemiology, recent advances in understanding of the pathogenesis and management of selected extraarticular manifestations of rheumatoid arthritis (ExRA).</p><p><strong>Recent findings: </strong>The incidence of ExRA overall and subcutaneous rheumatoid nodules in particular is declining after 2000. These trends reflect improved RA disease activity with early effective immunosuppressive treatments; changing environmental risk factors can be contributing. ExRA continues to carry a two-fold increased mortality risk. RA-associated interstitial lung disease (RA-ILD) is a major contributor to mortality, with no decline in incidence and scant therapeutic options. Individualized risk stratification for RA-ILD based on patient-level risk factors and biomarker profile is evolving with MUC5B as a major genetic risk factor. Clinical trials are underway to evaluate the benefits of novel antifibrotic therapies and targeted therapies for RA-ILD. The risk of cardiovascular disease in RA is generally amendable to treatment with disease-modifying antirheumatic drugs, although cardiovascular risk associated with JAK inhibition is not fully understood.</p><p><strong>Summary: </strong>Despite reduction in incidence of ExRA overall, the incidence of RA-ILD shows no significant decline and remains a major therapeutic challenge. The use of novel antifibrotics and immunosuppressive drugs shows promise in slowing the progression of RA-ILD.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"203-208"},"PeriodicalIF":5.1,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971268","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}