International Journal of Rheumatic Diseases最新文献

{"title":"Anterior Chest Wall Prominence in a Patient With Chronic Inflammatory Back Pain","authors":"Mauricio Restrepo-Escobar, Édgar Peñaranda-Parada","doi":"10.1111/1756-185x.70898","DOIUrl":"10.1111/1756-185x.70898","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074444","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":"Distinct Clinical Implications of Anti-Topoisomerase I Antibody Positivity and Antibody Titers in Systemic Sclerosis","authors":"Rahul Dey, Sanghamitra Machhua, Yashwant Kumar, Shefali Khanna Sharma","doi":"10.1111/1756-185x.70894","DOIUrl":"10.1111/1756-185x.70894","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074648","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":"Short-Interval Discordance Between Fatigue and Joint Counts in Rheumatoid Arthritis","authors":"Yidi Huang, Lü Liu, Hangwei Wan, Cunxiang Xie, Hailong Wang","doi":"10.1111/1756-185x.70887","DOIUrl":"10.1111/1756-185x.70887","url":null,"abstract":"<p>Fatigue is a core patient-reported outcome in rheumatoid arthritis (RA), but it is only partly explained by inflammatory markers and joint examination [<span>1-3</span>]. Most longitudinal studies have assessed fatigue over several weeks or months [<span>4, 5</span>]. We examined change in fatigue visual analogue scale (VAS) at the second routine assessment, which often occurred within days, and evaluated whether a decrease in fatigue occurred in parallel with changes in swollen joint count (SJC) and tender joint count (TJC).</p><p>We conducted a retrospective single-centre study of hospitalized patients with RA using a de-identified routine-care database from the Department of Rheumatology, Dongzhimen Hospital, Beijing University of Chinese Medicine. Records included in the analysis spanned 12 May 2022 to 18 December 2024. Eligible inpatient records were identified consecutively, and all records meeting the study-specific criteria were included without sampling. Patients were eligible if RA was diagnosed according to the 2010 ACR/EULAR criteria or confirmed by a rheumatologist and fatigue VAS was recorded at baseline and at the second assessment [<span>6</span>]. Baseline was the assessment used for cohort entry, and the second assessment was the next recorded routine-care assessment after baseline. Each patient contributed one assessment pair. Reporting followed STROBE guidance [<span>7</span>]. Fatigue was recorded on a 0–10 VAS, with 0 indicating no fatigue and 10 extreme fatigue. SJC and TJC were obtained from routine 28-joint examinations covering the bilateral shoulders, elbows, wrists, metacarpophalangeal joints, proximal interphalangeal joints and knees. A fatigue decrease was defined as a reduction of at least 1 point on the 0–10 fatigue VAS, consistent with published estimates of minimally important improvement in RA [<span>8</span>]. Because a ≥ 1-point decrease was not possible from a baseline fatigue VAS of 0, the primary fatigue-responder analysis was restricted to patients with baseline fatigue VAS ≥ 1 (<i>n</i> = 189). The 30 patients with baseline fatigue VAS = 0 were retained in the full-cohort analyses and classified as having no ≥ 1-point decrease. The four-pattern fatigue–joint count classification used the full cohort (<i>N</i> = 219). The primary joint-count comparator was any decrease in SJC or TJC. Sensitivity analyses required simultaneous SJC and TJC decrease, at least 20% reduction in either count, or at least 20% reduction in both counts. Continuous paired outcomes were summarized at both assessments and as within-patient change (second assessment minus baseline) and were compared using the Wilcoxon signed-rank test. Paired CRP and ESR analyses used complete paired observations only; missing laboratory values were not imputed. Binary proportions were reported with Wilson 95% confidence intervals. Exploratory logistic regression models were fitted separately for each candidate predictor. Models for disease-activity","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074578","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":"Beyond Pressure Pain Thresholds: Making Exercise-Induced Hypoalgesia Actionable in Knee Osteoarthritis","authors":"Jingjing Yang, Yi Yue, Mingming Li","doi":"10.1111/1756-185x.70892","DOIUrl":"10.1111/1756-185x.70892","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074575","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":"Fibromyalgia and Autoantibodies","authors":"Lekshmi Minikumari Rahulan,&nbsp;Able Lawrence","doi":"10.1111/1756-185x.70884","DOIUrl":"10.1111/1756-185x.70884","url":null,"abstract":"<p>Fibromyalgia syndrome (FMS) is a clinical syndrome defined by chronic widespread pain accompanied by non-restorative sleep, cognitive difficulties colloquially termed “fibrofog,” profound fatigue, and a range of somatic and autonomic symptoms [<span>1</span>]. For more than three decades, the dominant explanatory model has centered on central sensitization; heightened excitability and reduced inhibition within central nociceptive pathways [<span>2</span>]. While this framework successfully accounts for many clinical observations, including temporal summation, secondary hyperalgesia and the frequent presence of comorbidities such as migraine and irritable bowel syndrome, it leaves important peripheral findings unexplained and has limited the development of mechanism-based therapies.</p><p>Diagnostic criteria themselves reveal biological heterogeneity. The 1990 American College of Rheumatology (ACR) classification criteria required the presence of at least 11 of 18 tender points together with widespread pain [<span>3</span>]. The subsequent 2010/2011 criteria, revised in 2016, abandoned the tender-point examination in favor of a widespread pain index (WPI) and a symptom-severity score (SSS) [<span>4</span>]. Patients classified by the two systems only partially overlap [<span>5</span>]. While the majority fulfill both sets of criteria, a non-trivial proportion satisfy only the 1990 or only the 2016 definition. Individuals meeting solely the 2016 criteria more often carry comorbid neuropsychiatric diagnoses including post-traumatic stress disorder, restless-legs syndrome, and chronic fatigue syndrome, suggesting that the 2016 phenotype may capture a more centrally driven or multisystem distress state, whereas the classic 1990 phenotype may be enriched for peripheral nociceptive drivers [<span>5</span>]. Differences in comorbidity do not by themselves establish distinct pain mechanisms; hence, should be regarded as hypothesis-generating. Recognition of this heterogeneity is a prerequisite for interpreting serological and histopathological studies.</p><p><b>Lekshmi Minikumari Rahulan:</b> methodology, visualization, writing – original draft, writing – review and editing. <b>Able Lawrence:</b> conceptualization, methodology, visualization, writing – review and editing, supervision.</p><p>The authors have nothing to report.</p><p>The authors have nothing to report.</p><p>The authors declare no conflicts of interest.</p><p>The authors have nothing to report.</p>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185x.70884","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074570","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":"Development and Characterization of a Fully Human Recombinant MPO-ANCA Monoclonal Antibody as Candidate Quality Control Material","authors":"Meiyu Guo,&nbsp;Yeshuang Yuan,&nbsp;Xuan Zhang,&nbsp;Yudong Liu","doi":"10.1111/1756-185x.70889","DOIUrl":"10.1111/1756-185x.70889","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>MPO-ANCA detection suffers prominent inter-assay variability due to a shortage of standardized, sustainable quality control (QC) materials. Existing patient-pooled sera have limited supply, while chimeric monoclonal antibodies fail to fully mimic human autoantibodies. This study aimed to construct a fully human recombinant MPO-ANCA monoclonal antibody and systematically characterize its analytical performance as a candidate QC material for multi-platform MPO-ANCA immunoassay evaluation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A human anti-MPO scFv phage display library was constructed using peripheral blood mononuclear cells obtained from MPO-ANCA-positive patients. Following antigen-specific biopanning and screening, the candidate clone H042 was selected and converted into a full-length human IgG1 monoclonal antibody. We verified its structural integrity, antigen specificity, pANCA immunofluorescence pattern, quantitative linearity, thermal/freeze–thaw stability, and cross-kit performance across enzyme-linked immunosorbent assay (ELISA), chemiluminescence immunoassay (CLIA), multiplex flow immunoassay, and indirect immunofluorescence assay (IIFA) from multiple mainstream manufacturers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Purified H042 exhibited intact IgG structure, strong MPO binding affinity, and no cross-reactivity with PR3/GBM. It presented typical pANCA staining in IIFA and showed predictable quantitative response. H042 retained &gt; 89% residual activity under accelerated thermal and repeated freeze–thaw stress. Notably, H042 yielded consistent qualitative positivity on all tested kits of four mainstream methodologies without false-negative signals, despite inter-platform signal intensity differences.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The fully human monoclonal antibody H042 demonstrated favorable structural integrity, MPO specificity, and broad detectability across the evaluated commercial assay platforms. These characteristics support its potential as a scalable recombinant candidate QC material and an auxiliary tool for MPO-ANCA assay harmonization and laboratory quality assurance.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038204","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":"Comment on: “Association Between Chikungunya Infection and Rheumatoid Arthritis in Taiwan—A Cross-Sectional Study”","authors":"Licheng Lv,&nbsp;Haoxuan Yan","doi":"10.1111/1756-185x.70893","DOIUrl":"10.1111/1756-185x.70893","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149037749","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 Non-Coding Genome in Dermatomyositis: Alu Element Overexpression as a Potential Driver of the Interferon Signature","authors":"Tang-Kai Cheng,&nbsp;Teng-Chieh Hsu,&nbsp;James Cheng-Chung Wei","doi":"10.1111/1756-185x.70869","DOIUrl":"10.1111/1756-185x.70869","url":null,"abstract":"&lt;p&gt;Dermatomyositis (DM) has long been recognized as a distinct clinicopathological entity within the spectrum of idiopathic inflammatory myopathies (IIMs), primarily characterized by its profound type I interferon (IFN) signature [&lt;span&gt;1&lt;/span&gt;]. As recent discussions on IIM classification have emphasized, conventional clinicopathological categories are increasingly being complemented by serological, genetic, and molecular frameworks that better capture disease heterogeneity [&lt;span&gt;2&lt;/span&gt;]. However, the precise “upstream” trigger for this IFN surge has remained elusive. While viral mimicry has been hypothesized, recent breakthroughs in genomic sequencing—specifically the Telomere-to-Telomere (T2T) reference genome—have shifted our focus toward the “dark matter” of our own DNA: the noncoding genome [&lt;span&gt;3&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;A landmark study reveals that the pathogenic driver in DM may not be an external pathogen, but rather the uncontrolled expression of Alu elements [&lt;span&gt;3&lt;/span&gt;]. These short interspersed elements (SINEs), which occupy approximately 10% of the human genome, have a high propensity to form endogenous double-stranded RNA (dsRNA). Under normal physiological conditions, the enzyme ADAR (adenosine deaminase acting on RNA) “edits” these dsRNA structures—converting adenosine to inosine (A-to-I)—to prevent them from triggering innate immune sensors [&lt;span&gt;4&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;In DM muscle, however, a global elevation of Alu expression—including 577 unique Alu elements—appears to overwhelm the cellular editing capacity. This leads to an accumulation of unedited or insufficiently edited dsRNA that triggers MDA5-mediated inflammation [&lt;span&gt;5&lt;/span&gt;]. MDA5 itself is also a known autoantigen in DM, thereby linking endogenous dsRNA sensing with the characteristic IFN cascade [&lt;span&gt;6&lt;/span&gt;]. This internal “viral mimicry” model provides a compelling explanation for the prominent type I IFN signature of DM, supported by the observation that Alu overexpression appears relatively specific to DM and is not similarly enriched in other myositis subtypes such as inclusion body myositis (IBM) or antisynthetase syndrome (ASyS).&lt;/p&gt;&lt;p&gt;The clinical implications of these genomic findings are substantial but still emerging. The correlation between Alu expression, interferon-stimulated genes, and inflammatory cell signatures suggests that the “Alu editome” may capture an important layer of immune activation in DM and could eventually contribute to molecular subtyping or disease monitoring. Furthermore, the enrichment of edited Alu elements on chromosome 19 highlights a nonrandom genomic architecture that may intensify dsRNA sensing and IFN activation in DM [&lt;span&gt;3&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;However, translating the Alu signature into clinical practice will require validation in larger, longitudinal, and disease-subtype–stratified cohorts. Future studies should carefully account for treatment exposure, disease duration, biopsy site, autoantibody status, and baseline di","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185x.70869","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038239","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":"Case Report: Cryoglobulinemic Vasculitis Relapse With Peripheral Neuropathy During HDV-RNA Positivity Despite HBV-DNA Suppression","authors":"Fuat Albayram,&nbsp;Sezgin Zontul,&nbsp;Servet Yolbaş,&nbsp;Rabia Sağir","doi":"10.1111/1756-185x.70885","DOIUrl":"https://doi.org/10.1111/1756-185x.70885","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149014805","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: Childhood Scleredema Following Streptococcal Infection Mimicking Systemic Sclerosis","authors":"Bablu Kumar Gaur,&nbsp;Shruti Jain,&nbsp;Garima Verma Jain,&nbsp;Bhavna Chopra","doi":"10.1111/1756-185x.70886","DOIUrl":"https://doi.org/10.1111/1756-185x.70886","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 10","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149014804","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}