Pub Date : 2024-11-18DOI: 10.1038/s41584-024-01192-8
George C. Tsokos
During the past year, four studies have reported ten mutations in UNC93B1, which encodes the Toll-like receptor (TLR) chaperone protein UNC93B1. All variants increased TLR7 and TLR8 signalling and caused systemic lupus erythematosus in young individuals, and highlight the therapeutic potential of targeting TLR7 and TLR8 in this disease.
{"title":"The emergence of SLE-causing UNC93B1 variants in 2024","authors":"George C. Tsokos","doi":"10.1038/s41584-024-01192-8","DOIUrl":"https://doi.org/10.1038/s41584-024-01192-8","url":null,"abstract":"During the past year, four studies have reported ten mutations in UNC93B1, which encodes the Toll-like receptor (TLR) chaperone protein UNC93B1. All variants increased TLR7 and TLR8 signalling and caused systemic lupus erythematosus in young individuals, and highlight the therapeutic potential of targeting TLR7 and TLR8 in this disease.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"168 1","pages":""},"PeriodicalIF":33.7,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142665369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-10DOI: 10.1038/s41584-023-01056-7
Jessica McHugh
Methotrexate reduces pain and stiffness in hand osteoarthritis with synovitis, according to the results of a new randomized controlled trial.
一项新的随机对照试验结果表明，甲氨蝶呤可减轻伴有滑膜炎的手部骨关节炎患者的疼痛和僵硬感。
{"title":"Methotrexate improves pain in hand OA","authors":"Jessica McHugh","doi":"10.1038/s41584-023-01056-7","DOIUrl":"10.1038/s41584-023-01056-7","url":null,"abstract":"Methotrexate reduces pain and stiffness in hand osteoarthritis with synovitis, according to the results of a new randomized controlled trial.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"20 1","pages":"3-3"},"PeriodicalIF":33.7,"publicationDate":"2023-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72210033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-09DOI: 10.1038/s41584-023-01045-w
Alexander G. S. Oldroyd, Jeffrey P. Callen, Hector Chinoy, Lorinda Chung, David Fiorentino, Patrick Gordon, Pedro M. Machado, Neil McHugh, Albert Selva-O’Callaghan, Jens Schmidt, Sarah L. Tansley, Ruth Ann Vleugels, Victoria P. Werth, International Myositis Assessment and Clinical Studies Group Cancer Screening Expert Group, Rohit Aggarwal
Adult-onset idiopathic inflammatory myopathy (IIM) is associated with an increased cancer risk within the 3 years preceding and following IIM onset. Evidence- and consensus-based recommendations for IIM-associated cancer screening can potentially improve outcomes. This International Guideline for IIM-Associated Cancer Screening provides recommendations addressing IIM-associated cancer risk stratification, cancer screening modalities and screening frequency. The international Expert Group formed a total of 18 recommendations via a modified Delphi approach using a series of online surveys. First, the recommendations enable an individual patient’s IIM-associated cancer risk to be stratified into standard, moderate or high risk according to the IIM subtype, autoantibody status and clinical features. Second, the recommendations outline a ‘basic’ screening panel (including chest radiography and preliminary laboratory tests) and an ‘enhanced’ screening panel (including CT and tumour markers). Third, the recommendations advise on the timing and frequency of screening via basic and enhanced panels, according to risk status. The recommendations also advise consideration of upper or lower gastrointestinal endoscopy, nasoendoscopy and 18F-FDG PET–CT scanning in specific patient populations. These recommendations are aimed at facilitating earlier IIM-associated cancer detection, especially in those who are at a high risk, thus potentially improving outcomes, including survival. In this Evidence-Based Guideline article, an international, multidisciplinary group of experts presents evidence-based consensus recommendations on screening for cancer in patients with adult-onset idiopathic inflammatory myopathy, addressing cancer risk stratification, screening modalities and screening frequency.
{"title":"International Guideline for Idiopathic Inflammatory Myopathy-Associated Cancer Screening: an International Myositis Assessment and Clinical Studies Group (IMACS) initiative","authors":"Alexander G. S. Oldroyd, Jeffrey P. Callen, Hector Chinoy, Lorinda Chung, David Fiorentino, Patrick Gordon, Pedro M. Machado, Neil McHugh, Albert Selva-O’Callaghan, Jens Schmidt, Sarah L. Tansley, Ruth Ann Vleugels, Victoria P. Werth, International Myositis Assessment and Clinical Studies Group Cancer Screening Expert Group, Rohit Aggarwal","doi":"10.1038/s41584-023-01045-w","DOIUrl":"10.1038/s41584-023-01045-w","url":null,"abstract":"Adult-onset idiopathic inflammatory myopathy (IIM) is associated with an increased cancer risk within the 3 years preceding and following IIM onset. Evidence- and consensus-based recommendations for IIM-associated cancer screening can potentially improve outcomes. This International Guideline for IIM-Associated Cancer Screening provides recommendations addressing IIM-associated cancer risk stratification, cancer screening modalities and screening frequency. The international Expert Group formed a total of 18 recommendations via a modified Delphi approach using a series of online surveys. First, the recommendations enable an individual patient’s IIM-associated cancer risk to be stratified into standard, moderate or high risk according to the IIM subtype, autoantibody status and clinical features. Second, the recommendations outline a ‘basic’ screening panel (including chest radiography and preliminary laboratory tests) and an ‘enhanced’ screening panel (including CT and tumour markers). Third, the recommendations advise on the timing and frequency of screening via basic and enhanced panels, according to risk status. The recommendations also advise consideration of upper or lower gastrointestinal endoscopy, nasoendoscopy and 18F-FDG PET–CT scanning in specific patient populations. These recommendations are aimed at facilitating earlier IIM-associated cancer detection, especially in those who are at a high risk, thus potentially improving outcomes, including survival. In this Evidence-Based Guideline article, an international, multidisciplinary group of experts presents evidence-based consensus recommendations on screening for cancer in patients with adult-onset idiopathic inflammatory myopathy, addressing cancer risk stratification, screening modalities and screening frequency.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"805-817"},"PeriodicalIF":33.7,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41584-023-01045-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71524443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-03DOI: 10.1038/s41584-023-01037-w
James Brock, Neil Basu, Johannes C. M. Schlachetzki, Georg Schett, Iain B. McInnes, Jonathan Cavanagh
Depression is a common and disabling comorbidity in rheumatoid arthritis that not only decreases the likelihood of remission and treatment adherence but also increases the risk of disability and mortality in patients with rheumatoid arthritis. Compelling data that link immune mechanisms to major depressive disorder indicate possible common mechanisms that drive the pathology of the two conditions. Preclinical evidence suggests that pro-inflammatory cytokines, which are prevalent in rheumatoid arthritis, have various effects on monoaminergic neurotransmission, neurotrophic factors and measures of synaptic plasticity. Neuroimaging studies provide insight into the consequences of inflammation on the brain (for example, on neural connectivity), and clinical trial data highlight the beneficial effects of immune modulation on comorbid depression. Major depressive disorder occurs more frequently in patients with rheumatoid arthritis than in the general population, and major depressive disorder also increases the risk of a future diagnosis of rheumatoid arthritis, further highlighting the link between rheumatoid arthritis and major depressive disorder. This Review focuses on interactions between peripheral and central immunobiological mechanisms in the context of both rheumatoid arthritis and major depressive disorder. Understanding these mechanisms will provide a basis for future therapeutic development, not least in depression. Depression is a common comorbidity in rheumatoid arthritis, and shared immune mechanisms link the two conditions. This Review explores potential peripheral and central interactions between the immune system and brain, the understanding of which could aid in the development of novel therapeutics.
{"title":"Immune mechanisms of depression in rheumatoid arthritis","authors":"James Brock, Neil Basu, Johannes C. M. Schlachetzki, Georg Schett, Iain B. McInnes, Jonathan Cavanagh","doi":"10.1038/s41584-023-01037-w","DOIUrl":"10.1038/s41584-023-01037-w","url":null,"abstract":"Depression is a common and disabling comorbidity in rheumatoid arthritis that not only decreases the likelihood of remission and treatment adherence but also increases the risk of disability and mortality in patients with rheumatoid arthritis. Compelling data that link immune mechanisms to major depressive disorder indicate possible common mechanisms that drive the pathology of the two conditions. Preclinical evidence suggests that pro-inflammatory cytokines, which are prevalent in rheumatoid arthritis, have various effects on monoaminergic neurotransmission, neurotrophic factors and measures of synaptic plasticity. Neuroimaging studies provide insight into the consequences of inflammation on the brain (for example, on neural connectivity), and clinical trial data highlight the beneficial effects of immune modulation on comorbid depression. Major depressive disorder occurs more frequently in patients with rheumatoid arthritis than in the general population, and major depressive disorder also increases the risk of a future diagnosis of rheumatoid arthritis, further highlighting the link between rheumatoid arthritis and major depressive disorder. This Review focuses on interactions between peripheral and central immunobiological mechanisms in the context of both rheumatoid arthritis and major depressive disorder. Understanding these mechanisms will provide a basis for future therapeutic development, not least in depression. Depression is a common comorbidity in rheumatoid arthritis, and shared immune mechanisms link the two conditions. This Review explores potential peripheral and central interactions between the immune system and brain, the understanding of which could aid in the development of novel therapeutics.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"790-804"},"PeriodicalIF":33.7,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71483781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-03DOI: 10.1038/s41584-023-01044-x
Vasiliki Liakouli, Antonio Ciancio, Francesco Del Galdo, Roberto Giacomelli, Francesco Ciccia
Systemic sclerosis (SSc), or scleroderma, is a rare, complex, systemic autoimmune disease of unknown aetiology, characterized by high morbidity and mortality often resulting from cardiopulmonary complications such as interstitial lung disease and pulmonary arterial hypertension. Despite substantial progress in unravelling the pathways involved in the pathogenesis of SSc and the increasing number of therapeutic targets tested in clinical trials, there is still no cure for this disease, although several proposed treatments might limit the involvement of specific organs, thereby slowing the natural history of the disease. A specific focus of recent research has been to address the plethora of unmet needs regarding the global management of SSc-related interstitial lung disease, including its pathogenesis, early diagnosis, risk stratification of patients, appropriate treatment regimens and monitoring of treatment response, as well as the definition of progression and predictors of progression and mortality. More refined stratification of patients on the basis of clinical features, molecular signatures, identification of subpopulations with distinct clinical trajectories and implementation of outcome measures for future clinical trials could also improve therapeutic management strategies, helping to avoid poor outcomes related to lung involvement. Interstitial lung disease (ILD) in patients with systemic sclerosis (SSc) is associated with considerable morbidity and mortality. In this Review, various unmet needs in the management of SSc–ILD are discussed, and solutions are proposed to help improve outcomes for these patients.
{"title":"Systemic sclerosis interstitial lung disease: unmet needs and potential solutions","authors":"Vasiliki Liakouli, Antonio Ciancio, Francesco Del Galdo, Roberto Giacomelli, Francesco Ciccia","doi":"10.1038/s41584-023-01044-x","DOIUrl":"10.1038/s41584-023-01044-x","url":null,"abstract":"Systemic sclerosis (SSc), or scleroderma, is a rare, complex, systemic autoimmune disease of unknown aetiology, characterized by high morbidity and mortality often resulting from cardiopulmonary complications such as interstitial lung disease and pulmonary arterial hypertension. Despite substantial progress in unravelling the pathways involved in the pathogenesis of SSc and the increasing number of therapeutic targets tested in clinical trials, there is still no cure for this disease, although several proposed treatments might limit the involvement of specific organs, thereby slowing the natural history of the disease. A specific focus of recent research has been to address the plethora of unmet needs regarding the global management of SSc-related interstitial lung disease, including its pathogenesis, early diagnosis, risk stratification of patients, appropriate treatment regimens and monitoring of treatment response, as well as the definition of progression and predictors of progression and mortality. More refined stratification of patients on the basis of clinical features, molecular signatures, identification of subpopulations with distinct clinical trajectories and implementation of outcome measures for future clinical trials could also improve therapeutic management strategies, helping to avoid poor outcomes related to lung involvement. Interstitial lung disease (ILD) in patients with systemic sclerosis (SSc) is associated with considerable morbidity and mortality. In this Review, various unmet needs in the management of SSc–ILD are discussed, and solutions are proposed to help improve outcomes for these patients.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"20 1","pages":"21-32"},"PeriodicalIF":33.7,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71483782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-03DOI: 10.1038/s41584-023-01042-z
Claas H. Hinze, Dirk Foell, Christoph Kessel
Systemic juvenile idiopathic arthritis (sJIA) is an inflammatory disease with hallmarks of severe systemic inflammation, which can be accompanied by arthritis. Contemporary scientific insights set this paediatric disorder on a continuum with its counterpart, adult-onset Still disease (AOSD). Patients with sJIA are prone to complications, including life-threatening hyperinflammation (macrophage activation syndrome (sJIA-MAS)) and sJIA-associated lung disease (sJIA-LD). Meanwhile, the treatment arsenal in sJIA has expanded markedly. State-of-the-art therapeutic approaches include biologic agents that target the IL-1 and IL-6 pathways. Beyond these, a range of novel agents are on the horizon, some of them already being used on a compassionate use basis, including JAK inhibitors and biologic agents that target IL-18, IFNγ, or IL-1β and IL-18 simultaneously. However, sJIA, sJIA-MAS and sJIA-LD still pose challenging conundrums to rheumatologists treating paediatric and adult patients worldwide. Although national and international consensus treatment plans exist for the treatment of ‘classic’ sJIA, the treatment approaches for early sJIA without arthritis, and for refractory or complicated sJIA, are not well defined. Therefore, in this Review we outline current approaches for the treatment of sJIA and provide an outlook on knowledge gaps. Treatment of ‘classic’ systemic juvenile idiopathic arthritis (sJIA) is evolving markedly, and treatment options for early sJIA without arthritis, and refractory or complicated sJIA are not well defined. This Review outlines current approaches and provides an outlook on knowledge gaps.
{"title":"Treatment of systemic juvenile idiopathic arthritis","authors":"Claas H. Hinze, Dirk Foell, Christoph Kessel","doi":"10.1038/s41584-023-01042-z","DOIUrl":"10.1038/s41584-023-01042-z","url":null,"abstract":"Systemic juvenile idiopathic arthritis (sJIA) is an inflammatory disease with hallmarks of severe systemic inflammation, which can be accompanied by arthritis. Contemporary scientific insights set this paediatric disorder on a continuum with its counterpart, adult-onset Still disease (AOSD). Patients with sJIA are prone to complications, including life-threatening hyperinflammation (macrophage activation syndrome (sJIA-MAS)) and sJIA-associated lung disease (sJIA-LD). Meanwhile, the treatment arsenal in sJIA has expanded markedly. State-of-the-art therapeutic approaches include biologic agents that target the IL-1 and IL-6 pathways. Beyond these, a range of novel agents are on the horizon, some of them already being used on a compassionate use basis, including JAK inhibitors and biologic agents that target IL-18, IFNγ, or IL-1β and IL-18 simultaneously. However, sJIA, sJIA-MAS and sJIA-LD still pose challenging conundrums to rheumatologists treating paediatric and adult patients worldwide. Although national and international consensus treatment plans exist for the treatment of ‘classic’ sJIA, the treatment approaches for early sJIA without arthritis, and for refractory or complicated sJIA, are not well defined. Therefore, in this Review we outline current approaches for the treatment of sJIA and provide an outlook on knowledge gaps. Treatment of ‘classic’ systemic juvenile idiopathic arthritis (sJIA) is evolving markedly, and treatment options for early sJIA without arthritis, and refractory or complicated sJIA are not well defined. This Review outlines current approaches and provides an outlook on knowledge gaps.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"778-789"},"PeriodicalIF":33.7,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71483783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-02DOI: 10.1038/s41584-023-01036-x
Marc Feldmann, Ravinder N. Maini, Enrique R. Soriano, Vibeke Strand, Tsutomu Takeuchi
2023 marks 25 years since the approval of the first biologic drug in rheumatology. In this Viewpoint, five rheumatology researchers discuss how biologic therapy has transformed clinical practice, reflecting on their own experience, past and current challenges and what the future might hold for biologic drugs.
{"title":"25 years of biologic DMARDs in rheumatology","authors":"Marc Feldmann, Ravinder N. Maini, Enrique R. Soriano, Vibeke Strand, Tsutomu Takeuchi","doi":"10.1038/s41584-023-01036-x","DOIUrl":"10.1038/s41584-023-01036-x","url":null,"abstract":"2023 marks 25 years since the approval of the first biologic drug in rheumatology. In this Viewpoint, five rheumatology researchers discuss how biologic therapy has transformed clinical practice, reflecting on their own experience, past and current challenges and what the future might hold for biologic drugs.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"761-766"},"PeriodicalIF":33.7,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-02DOI: 10.1038/s41584-023-01055-8
Sarah Onuora
New research shows that the amino acid l-arginine ameliorates arthritis and inhibits inflammatory bone loss by altering energy metabolism in osteoclasts.
新研究表明，氨基酸 L-精氨酸可通过改变破骨细胞的能量代谢，改善关节炎并抑制炎性骨质流失。
{"title":"l-arginine inhibits arthritis and bone loss by reprogramming osteoclast metabolism","authors":"Sarah Onuora","doi":"10.1038/s41584-023-01055-8","DOIUrl":"10.1038/s41584-023-01055-8","url":null,"abstract":"New research shows that the amino acid l-arginine ameliorates arthritis and inhibits inflammatory bone loss by altering energy metabolism in osteoclasts.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"760-760"},"PeriodicalIF":33.7,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-02DOI: 10.1038/s41584-023-01038-9
Dennis McGonagle, Paula David, Tom Macleod, Abdulla Watad
Since the original description of spondyloarthritis 50 years ago, results have demonstrated similarities and differences between ankylosing spondylitis (AS) and axial psoriatic arthritis (PsA). HLA-B27 gene carriage in axial inflammation is linked to peri-fibrocartilaginous sacroiliac joint osteitis, as well as to spinal peri-entheseal osteitis, which is often extensive and which provides a crucial anatomical and immunological differentiation between the AS and PsA phenotypes. Specifically, HLA-B27-related diffuse bone marrow oedema (histologically an osteitis) and bone marrow fatty corners detected via magnetic resonance imaging, as well as radiographic changes such as sacroiliitis, vertebral squaring, corner erosions and Romanus lesions, all indicate initial bone phenotypes in HLA-B27+ axial disease. However, in much of PsA with axial involvement, enthesitis primarily manifests in ligamentous soft tissue as ‘ligamentitis’, with characteristic lesions that include para-syndesmophytes and sacroiliac joint bony sparing. Like axial PsA, diffuse idiopathic skeletal hyperostosis phenotypes, which can be indistinguishable from PsA, exhibit a thoracic and cervical spinal ligamentous soft-tissue tropism, clinically manifesting as syndesmophytosis that is soft-tissue-centric, including paravertebral soft-tissue ossification and sacroiliac soft-ligamentous ossification instead of joint-cavity fusion. The enthesis bone and soft tissues have radically different immune cell and stromal compositions, which probably underpins differential responses to immunomodulatory therapy, especially IL-23 inhibition. In this Perspective, the authors propose that despite the known similarities between ankylosing spondylitis and axial psoriatic arthritis, the localization of inflammation to bone in ankylosing spondylitis and to ligamentous soft tissue in axial axial psoriatic arthritis differentiates these diseases and has important implications for diagnosis, pathology and treatment.
{"title":"Predominant ligament-centric soft-tissue involvement differentiates axial psoriatic arthritis from ankylosing spondylitis","authors":"Dennis McGonagle, Paula David, Tom Macleod, Abdulla Watad","doi":"10.1038/s41584-023-01038-9","DOIUrl":"10.1038/s41584-023-01038-9","url":null,"abstract":"Since the original description of spondyloarthritis 50 years ago, results have demonstrated similarities and differences between ankylosing spondylitis (AS) and axial psoriatic arthritis (PsA). HLA-B27 gene carriage in axial inflammation is linked to peri-fibrocartilaginous sacroiliac joint osteitis, as well as to spinal peri-entheseal osteitis, which is often extensive and which provides a crucial anatomical and immunological differentiation between the AS and PsA phenotypes. Specifically, HLA-B27-related diffuse bone marrow oedema (histologically an osteitis) and bone marrow fatty corners detected via magnetic resonance imaging, as well as radiographic changes such as sacroiliitis, vertebral squaring, corner erosions and Romanus lesions, all indicate initial bone phenotypes in HLA-B27+ axial disease. However, in much of PsA with axial involvement, enthesitis primarily manifests in ligamentous soft tissue as ‘ligamentitis’, with characteristic lesions that include para-syndesmophytes and sacroiliac joint bony sparing. Like axial PsA, diffuse idiopathic skeletal hyperostosis phenotypes, which can be indistinguishable from PsA, exhibit a thoracic and cervical spinal ligamentous soft-tissue tropism, clinically manifesting as syndesmophytosis that is soft-tissue-centric, including paravertebral soft-tissue ossification and sacroiliac soft-ligamentous ossification instead of joint-cavity fusion. The enthesis bone and soft tissues have radically different immune cell and stromal compositions, which probably underpins differential responses to immunomodulatory therapy, especially IL-23 inhibition. In this Perspective, the authors propose that despite the known similarities between ankylosing spondylitis and axial psoriatic arthritis, the localization of inflammation to bone in ankylosing spondylitis and to ligamentous soft tissue in axial axial psoriatic arthritis differentiates these diseases and has important implications for diagnosis, pathology and treatment.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"818-827"},"PeriodicalIF":33.7,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-10-30DOI: 10.1038/s41584-023-01048-7
Rieke Alten, Max Weinbrecht-Mischkewitz
Biosimilars have an important place in the treatment of rheumatic conditions. The non-inferiority of biosimilars to bio-originators is ensured, but full and effective clinical adoption of these agents nonetheless requires consideration of several important issues, including the need for shared decision-making and a potential nocebo effect.
{"title":"Maximizing the success of biosimilar implementation","authors":"Rieke Alten, Max Weinbrecht-Mischkewitz","doi":"10.1038/s41584-023-01048-7","DOIUrl":"10.1038/s41584-023-01048-7","url":null,"abstract":"Biosimilars have an important place in the treatment of rheumatic conditions. The non-inferiority of biosimilars to bio-originators is ensured, but full and effective clinical adoption of these agents nonetheless requires consideration of several important issues, including the need for shared decision-making and a potential nocebo effect.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"19 12","pages":"757-758"},"PeriodicalIF":33.7,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71413148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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