International Journal of Rheumatic Diseases最新文献

{"title":"Scavenger receptor-A is a sensitive disease activity biomarker in ESR and CRP normal rheumatoid arthritis","authors":"Shixiong Cao,&nbsp;Xu Liu,&nbsp;Yang Xie,&nbsp;Fanlei Hu,&nbsp;Zhanguo Li,&nbsp;Yin Su,&nbsp;Li Luo,&nbsp;Xiaolin Sun","doi":"10.1111/1756-185X.15404","DOIUrl":"10.1111/1756-185X.15404","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Identification of rheumatoid arthritis (RA) patients in active disease with normal ESR and CRP is a challenge in disease activity assessment. The objective of this study was to evaluate the performance and clinical significance of Scavenger receptor-A (SRA) as a disease activity biomarker in RA, especially in ESR and CRP normal patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>One hundred and sixty-two RA (40 discovery cohort; 122 validation cohort), 20 osteoarthritis (OA), and 36 healthy controls (HCs) were recruited. Ten disease activity markers were evaluated by Bio-Plex Pro Human Cytokine Assay in the discovery cohort. SRA levels were measured by enzyme-linked immunosorbent assay (ELISA) in the validation cohort. The association between SRA and clinical phenotypes was also analyzed. ROC analysis was performed for disease activity prediction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>SRA was found to be correlated with disease activity in the discovery cohort. The serum SRA level was verified by ELISA in the validation cohort, and was found to be correlated with disease activity index in RA patients, including DAS28-ESR (<i>r</i> = .477, <i>p</i> &lt; .001), swollen joint counts, and tender joint counts; as well as inflammation markers, including ESR and CRP. In ESR and CRP normal RA, there was a strong correlation between SRA and DAS28-ESR (<span></span><math>\u0000 <semantics>\u0000 <mrow>\u0000 <msup>\u0000 <mi>χ</mi>\u0000 <mn>2</mn>\u0000 </msup>\u0000 </mrow>\u0000 <annotation>$$ {chi}^2 $$</annotation>\u0000 </semantics></math> = 4.564, <i>p</i> = .003). In addition, area under the ROC of SRA was higher than AUC_ESR and AUC_CRP in ESR and CRP normal RA patients, suggesting that serum SRA could be more sensitive than ESR and CRP for disease activity assessment in this group of patients. In the low DAS28-ESR (≤3.2) group, the AUC of SRA for disease activity measurement was higher than that of ESR and CRP, indicating that SRA was also more sensitive than ESR and CRP in low-disease activity RA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>SRA was correlated with RA disease activity and may be a sensitive serum biomarker for disease activity evaluation, especially in ESR and CRP normal patients, as well as in the low-disease activity group. SRA could be a promising marker for disease activity assessment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: ISG15 Deficiency and a Glimpse Into Autoimmunity","authors":"Lujayn Akbar,&nbsp;Bashayer Alawam,&nbsp;Meshal Alhassan,&nbsp;Sarah Yousef Faisal,&nbsp;Mohammed Ahmed Al-Omari,&nbsp;Sulaiman Mohammed Al-Mayouf","doi":"10.1111/1756-185X.15420","DOIUrl":"https://doi.org/10.1111/1756-185X.15420","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142685286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of an Osteoporosis Refracture Prevention Program—A Comparison of Two Australian Rural Centers Using Population Database Linkage","authors":"Peter K. K. Wong,&nbsp;Aedan Roberts,&nbsp;Tracey Ho,&nbsp;Sandy Fraser,&nbsp;Julia Thompson,&nbsp;Jennifer Williamson,&nbsp;Elizabeth Hay","doi":"10.1111/1756-185X.15421","DOIUrl":"https://doi.org/10.1111/1756-185X.15421","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The causal role of immune cells in primary Sjögren's syndrome: A two-sample Mendelian randomization","authors":"Yang Liu,&nbsp;Jie Kang,&nbsp;Yazhen Su,&nbsp;Xiuying Fan,&nbsp;Dan Ma,&nbsp;Zewen Wu,&nbsp;Xueyan Gong,&nbsp;Junkang Zhao,&nbsp;Liyun Zhang","doi":"10.1111/1756-185X.15350","DOIUrl":"https://doi.org/10.1111/1756-185X.15350","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by the destruction of exocrine glands primarily via T-cell-mediated B-cell over-activation and cytokine production. This leads to pronounced dryness of the mouth and eyes and can result in multi-systemic involvement affecting the kidneys, lungs, and blood. In recent years, there has been increasing attention on the role of immune cells in pSS. However, studies investigating the causal role of immune cells in pSS have been relatively limited.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this study, we employed a two-way two-sample Mendelian randomization approach to assess the causal relationship between immune cells and pSS. Utilizing publicly available genome-wide association study (GWAS) data, we explored the causal links between 731 immunophenotypically labeled immune cells and the risk of pSS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Through the use of instrumental variables derived from GWAS data and corrected for false discovery rate (FDR), we identified three immune cells with increased levels that were causally associated with pSS risk (FDR &lt; 0.05). These included IgD+ CD38br AC B cells, CD27 on IgD+ CD38− unswitched memory B cells, and Granulocyte % leukocyte. Additionally, three immune cells with reduced levels were found to be causally associated with pSS risk, namely CD4+ CD8dim %lymphocyte, CD4+ CD8dim %leukocyte, and CD28 on activated and secreting regulatory T cells (Tregs). Furthermore, the development of pSS was associated with elevated levels of CD33br HLA DR+ CD14− % CD33br HLA DR+ in myeloid cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study demonstrates that immune responses influence the progression of pSS in a complex pattern. Our findings may provide new insights into the immunology of pSS pathogenesis and more experimental studies should be conducted to further explore the potential mechanisms between identified immune features and pSS risk, which may provide a basis for exploring early intervention methods for pSS and developing targeted therapeutic strategies or even reshaping immune homeostasis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report of Unusual Manifestation of Mevalonate Kinase Deficiency Syndrome Mimicking Juvenile Idiopathic Arthritis With Systemic Onset","authors":"Ludmila V. Bregel,&nbsp;Alla E. Matunova,&nbsp;Qing Zhou,&nbsp;Mikhail M. Kostik","doi":"10.1111/1756-185X.15416","DOIUrl":"10.1111/1756-185X.15416","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JAK Inhibitors and Cardiovascular Disease in Psoriatic Arthritis: Friends or Foe?","authors":"Jenny Lin-Hong Shi,&nbsp;Wei-Yuan Chuang,&nbsp;Lai-Shan Tam","doi":"10.1111/1756-185X.15419","DOIUrl":"10.1111/1756-185X.15419","url":null,"abstract":"&lt;p&gt;Psoriatic arthritis (PsA) is a heterogeneous autoimmune, inflammatory disease, with inflammatory skin, articular and extra-musculoskeletal involvement, [&lt;span&gt;1, 2&lt;/span&gt;]. PsA occurs in about one-third of psoriasis patients [&lt;span&gt;3&lt;/span&gt;]. Dysregulation of several molecules, including proinflammatory interleukins (ILs), interferons (IFNs), growth factors, and colony-stimulating factors (CSF) act as ligands for receptors connected to intracytoplasmic Janus kinases (JAKs). Consequently, JAKs activate signal transducer and activator of transcription (STAT) proteins, which translocate to the nucleus and induce the expression of inflammatory nuclear factor. The JAK/STAT pathways play a central role in the development and pathogenesis of PsA [&lt;span&gt;4, 5&lt;/span&gt;]. Several studies have reported increased activation of JAK1/STAT3/STAT1, which may contribute to the articular inflammatory process characterized by the expansion of Th17 effector cells in the synovial fluid of patients with active PsA [&lt;span&gt;6, 7&lt;/span&gt;]. By targeting these JAK/STAT pathways, JAK inhibitors effectively reduce inflammatory responses [&lt;span&gt;7-9&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;JAK inhibitors, including tofacitinib and upadacitinib, effectively target these pathways to reduce inflammation and improve symptoms in PsA patients. However, emerging evidence has raised concerns regarding the cardiovascular (CV) risks associated with JAK inhibitors. Both clinical trials and post-marketing surveillance have reported higher incidences of thromboembolism and other CV events in patients using these therapies, particularly at higher doses. Given the growing use of JAK inhibitors in PsA management, understanding the underlying mechanisms of CV risk is crucial for optimizing patient safety.&lt;/p&gt;&lt;p&gt;Since the publication of the Oral Surveillance Study [&lt;span&gt;10&lt;/span&gt;], the use of JAK inhibitors has raised concerns regarding the potential increased risk of CV disease (CVD) in PsA patients. All known cytokines and chemokines create a unique network of self-interactions, activation and regulatory loops. Theoretically, inhibition of JAK should translate into reduction of both autoimmune diseases' activity and reduction of prothrombotic risk. However, JAK inhibitors are less specific than biologics due to the inherent redundancy of the JAK/STAT pathway and therefore may display an increase in off-target effects, which may be related to the association of increased Major Adverse Cardiovascular Events (MACE) and Venous Thromboembolism (VTE) observed [&lt;span&gt;11&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The etiology of thrombotic tendency in PsA may also be linked to other mechanisms and causal factors, including antiphospholipid antibodies, hyperhomocysteinemia, and inflammation. JAKs in various combinations bind to cytokine receptors that transmit prothrombotic and proinflammatory signals from a wide range of cytokines. With the exception of IL-10, IFNβ and IFNλ that exert anti-thrombotic potential, signaling downstream of these cytokines cre","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.15419","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCR5 mediates rheumatoid arthritis progression by promoting the activation and proliferation of non-classical Th1 cells","authors":"Jinlin Miao,&nbsp;Bei Zhang,&nbsp;Haoyang Sun,&nbsp;Peiyan Zhang,&nbsp;Haomiao Shen,&nbsp;Jiawei Wang,&nbsp;Junfeng Jia,&nbsp;Kui Zhang,&nbsp;Zhaohui Zheng,&nbsp;Ping Zhu","doi":"10.1111/1756-185X.15370","DOIUrl":"https://doi.org/10.1111/1756-185X.15370","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by immune dysegulation, including an immune imbalance due to abnormal activation of non-classical Th1 cells (CD161⁺ Th1). This study investigated the effects of CCR5 on the activation and proliferation of CD161⁺ Th1 and their pathogenicity in patients with RA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study was conducted on 53 patients with RA and 32 age- and sex-matched healthy controls (HC). The cell phenotype was assessed by flow cytometry and the cytokine levels in the supernatant were detected by ELISA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We demonstrate a marked increase in CD161⁺ Th1 cells in the synovial fluid of RA patients. These cells exhibit a hyperactivated and hyperproliferative state alongside elevated CCR5 expression. Furthermore, the levels of CD161⁺ Th1 cells, CD25, and CCR5 in RA synovial fluid show a positive correlation with the disease activity. Additionally, our study reveals that CCR5 facilitates the activation, proliferation, and cytokine production of CD161⁺ Th1 cells through the pZAP70/NFAT signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings contribute to a deeper understanding of RA pathogenesis and uncover a novel mechanism that regulates non-classical CD161⁺ Th1 responses in RA, which may provide a potential therapeutic target.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between proton pump inhibitor and acute gout attacks in patients with acute upper gastrointestinal bleeding combined with gout","authors":"Qiaoli Xu","doi":"10.1111/1756-185X.15403","DOIUrl":"10.1111/1756-185X.15403","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term follow-up of anti-TNF treatment in adult and pediatric DADA2 patients: Insights from real-world data","authors":"Gizem Ayan,&nbsp;Ozge Basaran,&nbsp;Busra Firlatan,&nbsp;Levent Kilic,&nbsp;Yelda Bilginer,&nbsp;Mehmet Alikasifoglu,&nbsp;Omer Karadag,&nbsp;Seza Ozen","doi":"10.1111/1756-185X.15377","DOIUrl":"https://doi.org/10.1111/1756-185X.15377","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background/Purpose</h3>\u0000 \u0000 <p>Our objective was to investigate real-world outcomes and treatment strategies in individuals affected by DADA2 using over 10-year period real-life experience.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This descriptive analysis encompassed all adult/pediatric patients with DADA2 from our Vasculitis Research Center prospective database. Patients on anti-TNF therapy have been specifically examined, analyzing the treatment's duration, indications, and outcomes. Treatment responses were based on physicians' assessments and categorized as full response (symptom-free with normal acute phase reactants) or partial/no response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Totally 32 patients (Adult/Childhood age: 19/13) were analyzed. Anti-TNF agents were prescribed to 27 of the 32 patients. Over a median follow-up of 58 months on anti-TNF therapy, 10 patients (35.7%) exhibited a complete response, predominantly in cases with nervous system or skin involvement. Partial responses were observed in the other 10 patients (35.7%). Currently, 20/ 27 patients remain on anti-TNF treatment. Among the seven who are not on anti-TNF now: five died (four of them with a late diagnosis, one could not continue due to cardiomyopathy), one refused treatment and one had a cure after bone marrow transplantation. We have become aware that four patients increased their dose interval and one returned to the normal interval after an increase in CRP. The first patient was diagnosed in 2013 and over the last 10 years, 6/32 (18.8%) of the patients died.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Anti-TNF treatment is beneficial for vasculitic and inflammatory lesions. The clinical course of patients is diverse, especially if the diagnosis is delayed, with a mortality rate of up to 20% over a 10-year period.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 11","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invited Speaker and Oral Presentation Abstracts","authors":"","doi":"10.1111/1756-185X.15344","DOIUrl":"10.1111/1756-185X.15344","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 S3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.15344","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}