Current opinion in rheumatology最新文献

{"title":"Myositis autoantibodies: from new specificities to new paradigms.","authors":"Andrea Aguilar-Vazquez, Angeles S Galindo-Feria","doi":"10.1097/BOR.0000000000001195","DOIUrl":"https://doi.org/10.1097/BOR.0000000000001195","url":null,"abstract":"<p><strong>Purpose of review: </strong>Myositis-specific autoantibodies have long been used to classify patients into clinically meaningful subsets; however, recent studies show that the field is moving beyond the simple question of which autoantibody is present. This review examines how emerging specificities, epitope architecture, autoantibody coexistence, pathogenic mechanisms, and detection platforms are reshaping the interpretation of myositis serology.</p><p><strong>Recent findings: </strong>Recent work has expanded the autoantibody repertoire through the identification of additional autoantibody specificities, multiprotein antigenic complexes, and transcriptional regulators. At the same time, epitope-level studies reveal that patients sharing the same autoantibody specificity may recognize different antigenic regions, with potential implications for phenotype, prognosis, and assay interpretation. Evidence also challenges the view of myositis autoantibodies as passive biomarkers: selected specificities may mediate complement-dependent muscle injury, amplify inflammatory circuits, or interfere with intracellular antigen function. Meanwhile, new detection platforms have not only improved discovery but also exposed limitations related to conformational epitopes, cross-reactivity, false seronegativity, and assay standardization.</p><p><strong>Summary: </strong>Novelty in myositis autoantibodies should be understood not only as new targets but also as new paradigms linking antigen structure, immune mechanisms, detection methods, and clinical actionability.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":"38 6","pages":"456-469"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105452","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":"Erosive gout: update on mechanisms, impact and treatment.","authors":"Nicola Dalbeth, Lisa K Stamp","doi":"10.1097/BOR.0000000000001180","DOIUrl":"10.1097/BOR.0000000000001180","url":null,"abstract":"<p><strong>Purpose of review: </strong>Erosive gout refers to the presence of at least one gouty bone erosion in a person with gout. This review provides an update on the update on mechanisms, impact, and treatment of erosive gout.</p><p><strong>Recent findings: </strong>Erosive gout is usually the consequence of long-standing tophaceous disease. However, bone erosions in association with tophi can be detected on ultrasound before onset of clinical symptoms in some people with asymptomatic hyperuricaemia. SPP1 (osteopontin)-expressing macrophages have been implicated in pathogenesis of tophaceous gout and SPP1-mediated cellular interactions may influence bone remodelling in the context of erosive gout. In addition to joint deformity, people with erosive gout experience more frequent gout flares and have low rates of disease remission, even with intensive urate-lowering therapy. Oral urate-lowering therapy using a treat to target serum urate approach can prevent progression of erosive gout, and small serial imaging studies have demonstrated infilling of monosodium urate crystal-related bone erosion in pegloticase responders.</p><p><strong>Summary: </strong>Erosive gout is a consequence of tophaceous gout and causes joint deformity which is difficult to reverse once established. Collectively, these findings provide a rationale for urate-lowering therapy for people with gout to prevent the consequences of tophaceous gout including joint damage.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"395-400"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548160","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":"Artificial intelligence for lung disease quantification in systemic sclerosis-associated interstitial lung disease and other connective tissue disease-associated interstitial lung disease.","authors":"Alexander Poellinger, Erika Spada, Aurélie Pahud de Mortanges","doi":"10.1097/BOR.0000000000001201","DOIUrl":"10.1097/BOR.0000000000001201","url":null,"abstract":"<p><strong>Purpose of review: </strong>Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is the leading cause of disease-related mortality in systemic sclerosis and the connective tissue disease-associated ILD (CTD-ILD) in which artificial intelligence imaging has advanced most rapidly. Visual high-resolution CT (HRCT) scoring is reader-dependent and limits clinical decision-making. This review summarizes clinically relevant artificial intelligence and radiomics publications from approximately the last 18 months, focusing on quantification, diagnosis and classification, response assessment, and prognosis.</p><p><strong>Recent findings: </strong>The field has moved from visual-score emulation toward outcome-oriented quantitative imaging biomarkers. In SSc-ILD, deep-learning usual interstitial pneumonia (UIP) probability stratifies FVC decline and long-term survival, while whole-chest quantitative imaging biomarkers extend risk prediction beyond lung involvement alone. Automated SSc-specific segmentation, explainable Goh-equivalent scoring, slice-reduced radiomics, and open datasets have strengthened the methodological base. Parallel work in CTD-ILD, RA-ILD, and IIM-ILD shows that artificial intelligence-derived HRCT parameters correlate with DLCO/TLC, predict mortality, and support disease-pattern classification. In broader fibrosing ILD, qCT definitions of progressive pulmonary fibrosis and clinically meaningful CT thresholds provide the most important conceptual advance for future SSc-ILD trials.</p><p><strong>Summary: </strong>Artificial intelligence-based CT quantification is becoming a credible adjunct for rheumatology and radiology practice, but the most defensible deployment model is human-in-the-loop decision support. Prospective multicenter validation, protocol harmonization, calibration, version control, and integration into multidisciplinary discussion remain essential before artificial intelligence outputs can be used as treatment-triggering biomarkers.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"387-394"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911110","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":"Systemic effects of gout flares beyond the joints.","authors":"Edoardo Cipolletta, Mamas A Mamas, Abhishek Abhishek","doi":"10.1097/BOR.0000000000001183","DOIUrl":"10.1097/BOR.0000000000001183","url":null,"abstract":"<p><strong>Purpose of review: </strong>A gout flare is an episode of intense inflammation caused by the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome and production of interleukin (IL)-1β. This pathway is involved in pathogenesis of cardiovascular events and provides a plausible mechanism linking gout flares to cardiovascular diseases.</p><p><strong>Recent findings: </strong>Gout flares are associated with a transient increased risk of cardiovascular events (myocardial infarction, stroke, and cardiovascular death), venous thromboembolism, and tachyarrhythmia in the subsequent 30-60  days - a finding comparable to that observed after other acute inflammatory states, such as influenza and pneumonia.Treat-to-target urate-lowering therapy lowered the risk of major adverse cardiovascular events in an emulated target trial. It also reduced systemic inflammation in observational studies. Additionally, gout flare prophylaxis with colchicine was associated with lower rates of major adverse cardiovascular events in a nationwide cohort study without evidence of residual confounding.</p><p><strong>Summary: </strong>Patients with gout are at a high risk of cardiovascular diseases. Recent data suggest that patients presenting with gout flares warrant heightened vigilance for cardiovascular events, venous thromboembolism, and tachyarrhythmia over the following 30-60 days. Treating gout to the target serum urate level could prevent cardiovascular events and renal function decline. Gout flare prophylaxis with colchicine may have a similar effect.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"412-419"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789480","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":"Updates on idiopathic inflammatory myopathies: partnering with patients, making progress.","authors":"Angeles Galindo-Feria, Marie Hudson, Didem Saygin","doi":"10.1097/BOR.0000000000001190","DOIUrl":"https://doi.org/10.1097/BOR.0000000000001190","url":null,"abstract":"","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":"38 6","pages":"420-422"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105492","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":"Advanced imaging in systemic sclerosis: distinguishing activity from damage across organ systems.","authors":"Alana Haussmann, Elizabeth R Volkmann","doi":"10.1097/BOR.0000000000001182","DOIUrl":"10.1097/BOR.0000000000001182","url":null,"abstract":"<p><strong>Purpose of review: </strong>A central challenge in systemic sclerosis (SSc) is the inability to distinguish active, potentially reversible disease, from damage, irreversible fibrosis. Current imaging modalities, including high-resolution computed tomography (HRCT) and echocardiography, predominantly capture structural damage and cannot resolve this distinction. This review outlines next generation imaging modalities for SSc with focus on quantitative machine learning algorithms and molecular imaging.</p><p><strong>Recent findings: </strong>The unifying advance across organ systems is a shift from documenting damage to measuring disease activity directly. Machine-learning-derived quantitative HRCT detects radiological patterns of ILD sensitive to change in SSc-associated interstitial lung disease. Parametric cardiac magnetic resonance mapping resolves diffuse interstitial fibrosis missed by late gadolinium enhancement. Fibroblast activation protein inhibitor PET (FAPI-PET) visualizes active fibrogenesis in lung and myocardium, identifying biologically active disease even before structural distortion occurs. [18F]Sodium fluoride PET detects metabolically active calcinosis. High-frequency ultrasound, elastography, and optical coherence tomography (OCT)-angiography extend objective assessment of cutaneous and microvascular involvement.</p><p><strong>Summary: </strong>Emerging imaging modalities in SSc may enable earlier detection of active disease amenable to treatment modification and yield more sensitive endpoints for SSc clinical trials.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"359-368"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677351","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":"Uncovering scleromyositis: no myth, just missed.","authors":"Océane Landon-Cardinal, Margherita Giannini, Geneviève Gyger, Benjamin Ellezam","doi":"10.1097/BOR.0000000000001187","DOIUrl":"10.1097/BOR.0000000000001187","url":null,"abstract":"<p><strong>Purpose of review: </strong>Scleromyositis (SM), the muscle-specific manifestation of scleroderma, is increasingly recognized as a distinct myositis subset, yet it remains poorly captured by existing classification criteria and absent from therapeutic guidelines. This review provides recent advances in SM with emphasis on challenging presentations and propose a pragmatic diagnostic framework integrating clinical, serological, capillaroscopic, and histopathological data.</p><p><strong>Recent findings: </strong>Recent studies identify capillaropathy as the unifying pathological hallmark of SM across muscle biopsy subtypes. Nailfold videocapillaroscopy reveals a predominantly scleroderma-active or scleroderma-like microangiopathy discriminating SM from potential myositis mimickers. Recent cohort studies demonstrate that SM confers independent mortality burden and substantial cardiac risk warranting immediate cardiac evaluation at diagnosis regardless of autoantibody profile or histological pattern. Pericyte dysfunction may link capillaropathy to fibrosis in SM, while autoantibodies appear to directly disrupt intracellular pathways, contributing to the shared vasculopathic and profibrotic signature that defines SM as a distinct entity.</p><p><strong>Summary: </strong>SM represents a clinically severe and underrecognized disease spectrum that frequently escapes current classification frameworks. Early SM diagnosis requires systematic integration of clinical, serological, capillaroscopic, and histopathological data, with capillaropathy as the unifying thread. Establishing a consensus SM definition and securing clinical trial inclusion remain the most urgent research priorities.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"470-480"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873159","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":"Redefining systemic sclerosis-associated pulmonary hypertension as an immune-mediated vasculopathy across the cardiopulmonary circulation.","authors":"Ai Yaku, Ruben J Mylvaganam, Sanjiv J Shah","doi":"10.1097/BOR.0000000000001202","DOIUrl":"10.1097/BOR.0000000000001202","url":null,"abstract":"<p><strong>Purpose of review: </strong>Systemic sclerosis-associated pulmonary hypertension (SSc-PH) is a heterogeneous, difficult-to-treat condition in which multiple pulmonary hypertension groups frequently overlap. Recent evidence suggests that vascular involvement may contribute to multiple SSc-PH phenotypes. This review highlights recent advances in understanding vascular features and emerging therapeutic strategies beyond vasodilation.</p><p><strong>Recent findings: </strong>Pathological and imaging studies demonstrate that vascular remodeling in SSc-PH extends beyond pulmonary arteries to pulmonary veins, capillaries, and coronary microcirculation, consistent with widespread immune-mediated vascular dysfunction. These features are increasingly recognized across various SSc-PH phenotypes: pulmonary arterial hypertension and pulmonary veno-occlusive disease; pulmonary hypertension associated with left heart disease, most commonly heart failure with preserved ejection fraction (PH-HFpEF); and pulmonary hypertension-associated with interstitial lung disease (PH-ILD); each of which is often accompanied by intrinsic right ventricular (RV) dysfunction. Emerging therapies targeting activin signaling, macrophage-vascular crosstalk, B-cell immunity, and endothelial-to-mesenchymal transition require further study but may be essential to identifying disease-modifying approaches across SSc-PH phenotypes.</p><p><strong>Summary: </strong>There is increasing recognition that vascular remodeling across the cardiopulmonary circulation may underlie multiple SSc-PH phenotypes, providing novel insight into SSc-PH disease mechanisms and rationale for the development of therapies targeting vascular remodeling, fibrosis, inflammation, and intrinsic RV dysfunction beyond conventional vasodilator treatment.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"369-377"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879352","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":"Inclusion body myositis: new insights into pathogenesis and therapeutic perspectives.","authors":"François Fer, Olivier Benveniste","doi":"10.1097/BOR.0000000000001198","DOIUrl":"10.1097/BOR.0000000000001198","url":null,"abstract":"<p><strong>Purpose of review: </strong>Inclusion body myositis (IBM) is the most common acquired myopathy in individuals over 50 years of age and remains refractory to conventional immunosuppressive therapies. This review summarizes recent advances in the understanding of IBM pathogenesis and highlights emerging therapeutic strategies.</p><p><strong>Recent findings: </strong>Recent studies have refined the understanding of the interplay between degenerative and immune-mediated mechanisms in IBM. Abnormal protein aggregation, impaired proteostasis, and alterations of the autophagic pathway contribute to muscle fiber degeneration. In parallel, increasing evidence supports a central role for highly differentiated cytotoxic CD8 + T cells invading major histocompatibility complex class I-expressing muscle fibers. Recent immunophenotyping studies have identified expanded populations of terminally differentiated killer cell lectin-like receptor G1-expressing CD8 + T cells in blood and muscle, suggesting a potential role for these cells in sustaining chronic muscle injury. These findings have prompted the development of targeted immunotherapies aimed at selectively modulating pathogenic cytotoxic T-cell populations.</p><p><strong>Summary: </strong>IBM appears to result from a complex interaction between degenerative and immune-mediated pathways. Improved characterization of the immune effector cells involved in muscle injury is opening new avenues for targeted therapies and may ultimately lead to treatments for this condition that currently lacks disease-modifying therapy.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"481-487"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872898","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":"Novel therapies for refractory idiopathic inflammatory myopathy-associated interstitial lung disease.","authors":"Laurence Poirier-Blanchette, Na'ama Avitzur, Eugene Krustev","doi":"10.1097/BOR.0000000000001194","DOIUrl":"10.1097/BOR.0000000000001194","url":null,"abstract":"<p><strong>Purpose of review: </strong>Idiopathic inflammatory myopathies (IIM) are systemic autoimmune rheumatic diseases in which interstitial lung disease (ILD) is a frequent extra-muscular manifestation and a major driver of morbidity and mortality. ILD occurs most commonly in antisynthetase syndrome and anti-melanoma differentiation-associated gene 5 (anti-MDA5) dermatomyositis syndrome, the latter carrying a high risk of rapidly progressive ILD (RP-ILD). Although recent guidelines outline conventional immunosuppressive strategies, a subset of patients progress despite escalation, and the definition of refractory IIM-ILD remains poorly standardized.</p><p><strong>Recent findings: </strong>Because type I and II interferon signaling, other cytokines, and aberrant B-cell activity have been implicated in the pathogenesis of IIM-ILD, novel therapies have been used off-label to target these mechanisms in treatment-resistant disease. This review summarizes emerging off-label and investigational therapies, including Janus kinase inhibitors, direct cytokine inhibitors (anifrolumab, dazukibart, tocilizumab, basiliximab), B-cell- and plasma-cell-targeted approaches (anti-CD20 antibodies, daratumumab, chimeric antigen receptor T-cell therapy, bispecific T-cell engagers), intravenous immunoglobulin, and antifibrotics, and rescue measures.</p><p><strong>Summary: </strong>Across these agents, evidence is confined to case reports, small series, and observational cohorts, with few randomized trials reporting IIM-ILD-specific outcomes. Prospective studies are needed to define patient selection, treatment sequencing and combinations, durability, and safety of novel therapies in IIM-ILD.</p>","PeriodicalId":11145,"journal":{"name":"Current opinion in rheumatology","volume":" ","pages":"499-508"},"PeriodicalIF":5.4,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911138","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}