Annals of the Rheumatic Diseases最新文献

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Helicobacter pylori upregulates PAD4 expression via stabilising HIF-1α to exacerbate rheumatoid arthritis. 幽门螺杆菌通过稳定 HIF-1α 上调 PAD4 的表达,从而加剧类风湿性关节炎。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2023-225306
Hui Wu, Hanmei Yuan, Jin Zhang, Taojun He, Yilin Deng, Ying Chen, Yunqi Zhang, Weisan Chen, Chao Wu
{"title":"<i>Helicobacter pylori</i> upregulates PAD4 expression via stabilising HIF-1α to exacerbate rheumatoid arthritis.","authors":"Hui Wu, Hanmei Yuan, Jin Zhang, Taojun He, Yilin Deng, Ying Chen, Yunqi Zhang, Weisan Chen, Chao Wu","doi":"10.1136/ard-2023-225306","DOIUrl":"10.1136/ard-2023-225306","url":null,"abstract":"<p><strong>Objective: </strong><i>Helicobacter pylori</i> infection has been reported to aggravate rheumatoid arthritis (RA), but the relevant mechanism remains unclear. This study aimed to investigate the underlying pathogenic mechanism of <i>H. pylori</i> infection in the progression of RA.</p><p><strong>Methods: </strong>The Disease Activity Score (DAS-28) and serum anticitrullinated protein antibody (ACPA) levels were compared between <i>H. pylori</i>-negative and <i>H. pylori</i>-positive patients with RA. MH7A cells were stimulated with polyclonal ACPA purified from the peripheral blood of patients with RA. The citrullination levels were assessed by western blot in GES-1 cells and sera. ChIP, luciferase reporter assays, mass spectrometry and ELISA were applied to explore the molecular mechanism of <i>H. pylori</i> infection in RA progression.</p><p><strong>Results: </strong>The DAS-28 and ACPA levels of patients with RA in the <i>H. pylori</i>-positive group were significantly higher than those in the <i>H. pylori</i>-negative group. Polyclonal ACPA derived from <i>H. pylori</i>-positive patients promoted cell proliferation and induced secretion of IL-6 and IL-8. For the first time, we found that <i>H. pylori</i> infection induces cellular protein citrullination by upregulating protein arginine deiminase type 4 (PAD4). Furthermore, we confirmed a direct functional binding of hypoxia-inducible factor 1α on the <i>PADI4</i> gene promoter. We demonstrated that PAD4 interacts with and citrullinates keratin 1 (K1), and serum and synovial fluid levels of anti-Cit-K1 antibody were markedly increased in <i>H. pylori</i>-infected patients with RA.</p><p><strong>Conclusion: </strong>Our findings reveal a novel mechanism by which <i>H. pylori</i> infection contributes to RA progression. Therapeutic interventions targeting <i>H. pylori</i> may be a viable strategy for the management of RA.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1666-1676"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141896613","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}
引用次数: 0
Efficacy and safety of therapies for Still's disease and macrophage activation syndrome (MAS): a systematic review informing the EULAR/PReS guidelines for the management of Still's disease. 治疗斯蒂尔病和巨噬细胞活化综合征(MAS)的疗效和安全性:为EULAR/PReS斯蒂尔病治疗指南提供信息的系统性综述。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225854
Sara Bindoli, Arianna De Matteis, Stéphane Mitrovic, Bruno Fautrel, Loreto Carmona, Fabrizio De Benedetti
{"title":"Efficacy and safety of therapies for Still's disease and macrophage activation syndrome (MAS): a systematic review informing the EULAR/PReS guidelines for the management of Still's disease.","authors":"Sara Bindoli, Arianna De Matteis, Stéphane Mitrovic, Bruno Fautrel, Loreto Carmona, Fabrizio De Benedetti","doi":"10.1136/ard-2024-225854","DOIUrl":"10.1136/ard-2024-225854","url":null,"abstract":"<p><strong>Objectives: </strong>To analyse the efficacy and safety of treatments for Still's disease and macrophage activation syndrome (MAS).</p><p><strong>Methods: </strong>Medline, Embase and Cochrane Library were searched for clinical trials (randomised, randomised controlled trial (RCT), controlled and clinical controlled trial (CCT)), observational studies (retrospective, longitudinal observational retrospective (LOR), prospective and longitudinal observational prospective (LOP)) and systematic reviews (SRs), in which the populations studied were patients with Still's disease and MAS. The intervention was any pharmacological treatment (approved or under evaluation) versus any comparator drug or placebo, and as outcomes, any relevant efficacy and safety event. The risk of bias (RoB) was assessed with the Cochrane RoB and AMSTAR-2 (Assessing the Methodological Quality of Systematic Reviews-2, version 2) for SRs.</p><p><strong>Results: </strong>128 full texts were included: 25 RCTs, 1 CCT, 11 SRs published after 2013 and 91 LOP/LOR studies. In Still's disease, interleukin (IL)-1 inhibitors (IL-1i) and IL-6R inhibitors (IL-6i) were the most studied drugs. Two meta-analyses on RCTs showed an OR, to achieve an ARC50 response rate, of 6.02 (95% CI 2.24 to 21.36) and 8.08 (95% CI 1.89 to 34.57) for IL-1i and IL-6Ri, respectively. Retrospective studies showed that early initiation of IL-1i or IL-6i was associated with high rates of clinically inactive disease. In MAS, GCs were employed in all patients, often associated with ciclosporin and/or anakinra. Rates of complete response were reported, with a range from 53% to 100%. Emapalumab was the only drug tested in a CCT, with a complete response of 93%.</p><p><strong>Conclusion: </strong>IL-1i and IL-6Ri show the highest level of efficacy in the treatment of Still's disease. For MAS, IL-1 and interferon-γ inhibition appear to be effective on a background of high-dose glucocorticoids.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1731-1747"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339933","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}
引用次数: 0
Acod1-mediated inhibition of aerobic glycolysis suppresses osteoclast differentiation and attenuates bone erosion in arthritis. Acod1 介导的有氧糖酵解抑制破骨细胞分化并减轻关节炎的骨侵蚀。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2023-224774
Katerina Kachler, Darja Andreev, Shreeya Thapa, Dmytro Royzman, Andreas Gießl, Shobika Karuppusamy, Mireia Llerins Perez, Mengdan Liu, Jörg Hofmann, Arne Gessner, Xianyi Meng, Simon Rauber, Alexander Steinkasserer, Martin Fromm, Georg Schett, Aline Bozec
{"title":"Acod1-mediated inhibition of aerobic glycolysis suppresses osteoclast differentiation and attenuates bone erosion in arthritis.","authors":"Katerina Kachler, Darja Andreev, Shreeya Thapa, Dmytro Royzman, Andreas Gießl, Shobika Karuppusamy, Mireia Llerins Perez, Mengdan Liu, Jörg Hofmann, Arne Gessner, Xianyi Meng, Simon Rauber, Alexander Steinkasserer, Martin Fromm, Georg Schett, Aline Bozec","doi":"10.1136/ard-2023-224774","DOIUrl":"10.1136/ard-2023-224774","url":null,"abstract":"<p><strong>Objectives: </strong>Metabolic changes are crucially involved in osteoclast development and may contribute to bone degradation in rheumatoid arthritis (RA). The enzyme aconitate decarboxylase 1 (Acod1) is known to link the cellular function of monocyte-derived macrophages to their metabolic status. As osteoclasts derive from the monocyte lineage, we hypothesised a role for Acod1 and its metabolite itaconate in osteoclast differentiation and arthritis-associated bone loss.</p><p><strong>Methods: </strong>Itaconate levels were measured in human peripheral blood mononuclear cells (PBMCs) of patients with RA and healthy controls by mass spectrometry. Human and murine osteoclasts were treated with the itaconate derivative 4-octyl-itaconate (4-OI) in vitro. We examined the impact of Acod1-deficiency and 4-OI treatment on bone erosion in mice using K/BxN serum-induced arthritis and human TNF transgenic (hTNFtg) mice. SCENITH and extracellular flux analyses were used to evaluate the metabolic activity of osteoclasts and osteoclast progenitors. Acod1-dependent and itaconate-dependent changes in the osteoclast transcriptome were identified by RNA sequencing. CRISPR/Cas9 gene editing was used to investigate the role of hypoxia-inducible factor (Hif)-1α in Acod1-mediated regulation of osteoclast development.</p><p><strong>Results: </strong>Itaconate levels in PBMCs from patients with RA were inversely correlated with disease activity. Acod1-deficient mice exhibited increased osteoclast numbers and bone erosion in experimental arthritis while 4-OI treatment alleviated inflammatory bone loss in vivo and inhibited human and murine osteoclast differentiation in vitro. Mechanistically, Acod1 suppressed osteoclast differentiation by inhibiting succinate dehydrogenase-dependent production of reactive oxygen species and Hif1α-mediated induction of aerobic glycolysis.</p><p><strong>Conclusion: </strong>Acod1 and itaconate are crucial regulators of osteoclast differentiation and bone loss in inflammatory arthritis.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1691-1706"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141533453","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}
引用次数: 0
Multiorgan involvement and circulating IgG1 predict hypocomplementaemia in IgG4-related disease. 多器官受累和循环 IgG1 可预测 IgG4 相关疾病的低补体血症。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225846
Guy Katz, Cory Perugino, Zachary S Wallace, Bohang Jiang, Thomas Guy, Grace A McMahon, Isha Jha, Yuqing Zhang, Hang Liu, Ana D Fernandes, Shiv S Pillai, John Patterson Atkinson, Alfred Hyoungju Kim, John H Stone
{"title":"Multiorgan involvement and circulating IgG1 predict hypocomplementaemia in IgG4-related disease.","authors":"Guy Katz, Cory Perugino, Zachary S Wallace, Bohang Jiang, Thomas Guy, Grace A McMahon, Isha Jha, Yuqing Zhang, Hang Liu, Ana D Fernandes, Shiv S Pillai, John Patterson Atkinson, Alfred Hyoungju Kim, John H Stone","doi":"10.1136/ard-2024-225846","DOIUrl":"10.1136/ard-2024-225846","url":null,"abstract":"<p><strong>Objectives: </strong>Hypocomplementaemia is common in patients with IgG4-related disease (IgG4-RD). We aimed to determine the IgG4-RD features associated with hypocomplementaemia and investigate mechanisms of complement activation in this disease.</p><p><strong>Methods: </strong>We performed a single-centre cross-sectional study of 279 patients who fulfilled the IgG4-RD classification criteria, using unadjusted and multivariable-adjusted logistic regression to identify factors associated with hypocomplementaemia.</p><p><strong>Results: </strong>Hypocomplementaemia was observed in 90 (32%) patients. In the unadjusted model, the number of organs involved (OR 1.42, 95% CI 1.23 to 1.63) and involvement of the lymph nodes (OR 3.87, 95% CI 2.19 to 6.86), lungs (OR 3.81, 95% CI 2.10 to 6.89), pancreas (OR 1.66, 95% CI 1.001 to 2.76), liver (OR 2.73, 95% CI 1.17 to 6.36) and kidneys (OR 2.48, 95% CI 1.47 to 4.18) were each associated with hypocomplementaemia. After adjusting for age, sex and number of organs involved, only lymph node (OR 2.59, 95% CI 1.36 to 4.91) and lung (OR 2.56, 95% CI 1.35 to 4.89) involvement remained associated with hypocomplementaemia while the association with renal involvement was attenuated (OR 1.6, 95% CI 0.92 to 2.98). Fibrotic disease manifestations (OR 0.43, 95% CI 0.21 to 0.87) and lacrimal gland involvement (OR 0.53, 95% CI 0.28 to 0.999) were inversely associated with hypocomplementaemia in the adjusted analysis. Hypocomplementaemia was associated with higher concentrations of all IgG subclasses and IgE (all p<0.05). After adjusting for serum IgG1 and IgG3, only IgG1 but not IgG4 remained strongly associated with hypocomplementaemia.</p><p><strong>Conclusions: </strong>Hypocomplementaemia in IgG4-RD is not unique to patients with renal involvement and may reflect the extent of disease. IgG1 independently correlates with hypocomplementaemia in IgG4-RD, but IgG4 does not. Complement activation is likely involved in IgG4-RD pathophysiology.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1773-1780"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854586","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}
引用次数: 0
Early identification of rheumatoid arthritis: does it induce treatment-related cost savings? 类风湿性关节炎的早期识别:是否能节省治疗费用?
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225746
Elise van Mulligen, Maureen Rutten-van Mölken, Annette van der Helm-van Mil
{"title":"Early identification of rheumatoid arthritis: does it induce treatment-related cost savings?","authors":"Elise van Mulligen, Maureen Rutten-van Mölken, Annette van der Helm-van Mil","doi":"10.1136/ard-2024-225746","DOIUrl":"10.1136/ard-2024-225746","url":null,"abstract":"<p><strong>Objective: </strong>Early diagnosis and treatment-start is key for rheumatoid arthritis (RA), but the economic effect of an early versus a later diagnosis has never been investigated. We aimed to investigate whether early diagnosis of RA is associated with lower treatment-related costs compared with later diagnosis.</p><p><strong>Methods: </strong>Patients with RA consecutively included in the Leiden Early Arthritis Clinic between 2011 and 2017 were studied (n=431). Symptom duration was defined as the time between symptom onset and first presentation at the outpatient clinic; early treatment start was defined as symptom duration <12 weeks. Information on disease-modifying anti-rheumatic drug use per patient over 5 years was obtained from prescription data from patient records. Prices were used from 2022 and 2012 (proxy of time of prescription) to study the impact of changes in drug costs. Autoantibody-positive and autoantibody-negative RA were studied separately because differences in disease severity may influence costs.</p><p><strong>Results: </strong>Within autoantibody-negative RA, costs were 316% higher in the late compared with the early group (β=4.16 (95% CI 1.57 to 11.1); €4856 vs €1159). When using 2012 prices, results were similar. For autoantibody-positive RA, costs were 19% higher in the late group (€9418 vs €7934, β=1.19, 0.57 to 2.47). This effect was present but smaller when using 2012 prices. Within patients with autoantibody-positive RA using biologicals, late treatment start was associated with 46% higher costs (β=1.46 (0.91 to 2.33)); higher costs were also seen when using 2012 prices.</p><p><strong>Conclusion: </strong>When RA is detected within 12 weeks after symptom onset, treatment-related costs were lower in both autoantibody-negative and autoantibody-positive RA. This study is the first to report how early diagnosis and treatment start impact treatment-related costs.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1647-1656"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632465","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}
引用次数: 0
Paul Hunter Plotz (1937-2024): renaissance rheumatologist, human rights advocate and mensch. 保罗-亨特-普洛茨(Paul Hunter Plotz,1937-2024 年):文艺复兴时期的风湿病学家、人权倡导者和人道主义者。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-226596
Frederick W Miller, John J O'Shea, Daniel L Kastner
{"title":"Paul Hunter Plotz (1937-2024): renaissance rheumatologist, human rights advocate and mensch.","authors":"Frederick W Miller, John J O'Shea, Daniel L Kastner","doi":"10.1136/ard-2024-226596","DOIUrl":"10.1136/ard-2024-226596","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1644-1646"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339937","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}
引用次数: 0
SerpinA3N limits cartilage destruction in osteoarthritis by inhibiting macrophage-derived leucocyte elastase. SerpinA3N 通过抑制巨噬细胞衍生的白细胞弹性蛋白酶来限制骨关节炎中软骨的破坏。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225645
Augustin Latourte, Sarah Jaulerry, Alice Combier, Chahrazad Cherifi, Yohan Jouan, Thierry Grange, Julien Daligault, Hang-Korng Ea, Martine Cohen-Solal, Eric Hay, Pascal Richette
{"title":"SerpinA3N limits cartilage destruction in osteoarthritis by inhibiting macrophage-derived leucocyte elastase.","authors":"Augustin Latourte, Sarah Jaulerry, Alice Combier, Chahrazad Cherifi, Yohan Jouan, Thierry Grange, Julien Daligault, Hang-Korng Ea, Martine Cohen-Solal, Eric Hay, Pascal Richette","doi":"10.1136/ard-2024-225645","DOIUrl":"10.1136/ard-2024-225645","url":null,"abstract":"<p><strong>Objectives: </strong>Inflammatory mediators such as interleukin 6 (IL-6) are known to activate catabolic responses in chondrocytes during osteoarthritis (OA). This study aimed to investigate the role of a downstream target gene of IL-6, the serine protease inhibitor SerpinA3N, in the development of cartilage damage in OA.</p><p><strong>Methods: </strong>RNA sequencing was performed in murine primary chondrocytes treated with IL-6, and identified target genes were confirmed in human and murine OA cartilage samples. Male cartilage-specific <i>Serpina3n</i>-deficient mice and control mice underwent meniscectomy (MNX) or sham surgery at 10 weeks of age. Intra-articular injections of SerpinA3N or sivelestat (an inhibitor of leucocyte elastase (LE), a substrate for SerpinA3N) were performed in wild-type mice after MNX. Joint damage was assessed 3-9 weeks after surgery by histology and micro-CT. The effect of sivelestat was assessed in cartilage explants exposed to macrophage-derived conditioned media.</p><p><strong>Results: </strong>RNA sequencing revealed that SerpinA3N is a major target gene of IL-6 in chondrocytes. The expression of SerpinA3N is increased in OA cartilage. Conditional loss of SerpinA3N in chondrocytes aggravated OA in mice, while intra-articular injection of SerpinA3N limited joint damage. Chondrocytes did not produce serine proteases targeted by SerpinA3N. By contrast, macrophages produced LE on IL-6 stimulation. Sivelestat limited the cartilage catabolism induced by conditioned media derived from IL-6-stimulated macrophages. Additionally, an intra-articular injection of sivelestat is protected against OA in the MNX model.</p><p><strong>Conclusions: </strong>SerpinA3N protects cartilage against catabolic factors produced by macrophages, including LE. SerpinA3N and LE represent new therapeutic targets to dampen cartilage damage in OA.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1781-1790"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970470","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}
引用次数: 0
Systemic juvenile idiopathic arthritis and adult-onset Still's disease are the same disease: evidence from systematic reviews and meta-analyses informing the 2023 EULAR/PReS recommendations for the diagnosis and management of Still's disease. 系统性幼年特发性关节炎和成人型斯蒂尔病是同一种疾病:系统回顾和荟萃分析的证据为 2023 年 EULAR/PReS 关于斯蒂尔病诊断和管理的建议提供了参考。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225853
Arianna De Matteis, Sara Bindoli, Fabrizio De Benedetti, Loreto Carmona, Bruno Fautrel, Stéphane Mitrovic
{"title":"Systemic juvenile idiopathic arthritis and adult-onset Still's disease are the same disease: evidence from systematic reviews and meta-analyses informing the 2023 EULAR/PReS recommendations for the diagnosis and management of Still's disease.","authors":"Arianna De Matteis, Sara Bindoli, Fabrizio De Benedetti, Loreto Carmona, Bruno Fautrel, Stéphane Mitrovic","doi":"10.1136/ard-2024-225853","DOIUrl":"10.1136/ard-2024-225853","url":null,"abstract":"<p><strong>Objectives: </strong>To analyse the similarity in clinical manifestations and laboratory findings between systemic juvenile idiopathic arthritis (sJIA) and adult-onset Still's disease (AOSD).</p><p><strong>Methods: </strong>Three systematic reviews (SR) were performed. One included cohort studies comparing sJIA versus AOSD that described clinical and biological manifestations with at least 20 patients in each group (SR1). The second identified studies of biomarkers in both diseases and their diagnostic performance (SR2). The last focused on diagnostic biomarkers for macrophage activation syndrome (MAS, SR3). Medline (PubMed), Embase and Cochrane Library were systematically searched. The risk of bias was assessed with an adapted form of the Hoy scale for prevalence studies in SR1 and the Quality Assessment of Diagnostic Accuracy Studies-2 in SR2 and SR3. We performed meta-analyses of proportions for the qualitative descriptors.</p><p><strong>Results: </strong>Eight studies were included in SR1 (n=1010 participants), 33 in SR2 and 10 in SR3. The pooled prevalence of clinical manifestations did not differ between sJIA and AOSD, except for myalgia, sore throat and weight loss, which were more frequent in AOSD than sJIA because they are likely ascertained incompletely in sJIA, especially in young children. Except for AA amyloidosis, more frequent in sJIA than AOSD, the prevalence of complications did not differ, nor did the prevalence of biological findings. Ferritin, S100 proteins and interleukin-18 (IL-18) were the most frequently used diagnostic biomarkers, with similar diagnostic performance. For MAS diagnosis, novel biomarkers such as IL-18, C-X-C motif ligand 9, adenosine deaminase 2 activity and activated T cells seemed promising.</p><p><strong>Conclusion: </strong>Our results argue for a continuum between sJIA and AOSD.</p><p><strong>Prospero registration number: </strong>CRD42022374240 and CRD42024534021.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1748-1761"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339938","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}
引用次数: 0
Serum from patients with idiopathic inflammatory myopathy induces skeletal muscle weakness. 特发性炎症性肌病患者的血清会诱发骨骼肌无力。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-225912
Cecilia Leijding, Suchada Kaewin, Kristofer M Andreasson, Begum Horuluoglu, Angeles Shunashy Galindo-Feria, Eveline Van Gompel, Maryam Dastmalchi, Stefano Gastaldello, Helene Alexanderson, Ingrid E Lundberg, Daniel C Andersson
{"title":"Serum from patients with idiopathic inflammatory myopathy induces skeletal muscle weakness.","authors":"Cecilia Leijding, Suchada Kaewin, Kristofer M Andreasson, Begum Horuluoglu, Angeles Shunashy Galindo-Feria, Eveline Van Gompel, Maryam Dastmalchi, Stefano Gastaldello, Helene Alexanderson, Ingrid E Lundberg, Daniel C Andersson","doi":"10.1136/ard-2024-225912","DOIUrl":"10.1136/ard-2024-225912","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1796-1797"},"PeriodicalIF":20.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142091709","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}
引用次数: 0
Ruxolitinib as a salvage therapy in adult-onset macrophage activation syndrome: insights from eight cases. 将Ruxolitinib作为成人型巨噬细胞活化综合征的挽救疗法:从八个病例中获得的启示。
IF 20.3 1区 医学
Annals of the Rheumatic Diseases Pub Date : 2024-11-14 DOI: 10.1136/ard-2024-226433
Ziyi Song, Haihong Yao, Yuebo Jin, Xue Li, Yuan Jia, Jing He, Zhanguo Li
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