International Journal of Rheumatic Diseases最新文献

{"title":"Case Report: When Lupus Is Not Primary—Paraneoplastic Systemic Lupus Erythematosus Associated With a Duodenal Neuroendocrine Tumor","authors":"Yunus Emre Dalkılıç, Elçin Kadan, Muhammet Çınar","doi":"10.1111/1756-185x.70849","DOIUrl":"https://doi.org/10.1111/1756-185x.70849","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807746","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":"Beyond the Genetic “Silver Bullet”: The Complex Reality of Precision Rheumatology","authors":"Tang-Kai Cheng, James Cheng-Chung Wei","doi":"10.1111/1756-185x.70848","DOIUrl":"https://doi.org/10.1111/1756-185x.70848","url":null,"abstract":"<p>The allure of precision medicine in rheumatology has long been centered on the “genetic switch”—the hope that a simple germline marker could direct clinicians to the perfect biologic, sparing patients months of trial-and-error. However, the recent study by Yap et al. [<span>1</span>] in <i>Arthritis & Rheumatology</i> serves as a necessary reality check. Investigating the well-known HLA-DRB1 Shared Epitope (SE) and Valine at position 11, the authors found no significant evidence that these systemic markers could differentiate response between abatacept and adalimumab.</p><p>Does this negative result signal the failure of precision rheumatology? Far from it. A survey of recent literature in the <i>International Journal of Rheumatic Diseases</i> (2025–2026) reveals that the field is simply maturing. Unlike existing reviews that broadly catalog genomic advancements, this commentary specifically highlights the critical transition from static germline markers to a dynamic, multimodal framework integrating tissue-specific biology, biomechanics, and imaging. Furthermore, to ensure conceptual clarity, we use the term “precision medicine” throughout this manuscript to denote the overarching paradigm of tailored care, which relies on accurate “patient stratification” based on shared pathophysiological mechanisms, rather than mere symptomatic interventions. It is important to note, however, that while these emerging multimodal approaches show great promise, many of the current studies are limited by small sample sizes, cross-sectional designs, and a lack of external validation across diverse populations. Moving forward, larger, prospective cohorts will be necessary to confirm the clinical utility of these novel markers.</p><p>If systemic DNA is the blueprint, the synovium is the active construction site. The failure of germline markers like the Shared Epitope to predict specific drug responses suggests we are looking in the wrong place. Recent work published in the International Journal of Rheumatic Diseases highlights the power of shifting focus to the target organ. The expression of specific gene signatures like BHLHE40 in synovial CD4<sup>+</sup> T cells has been identified as a potential marker for rheumatoid arthritis phenotypes [<span>2</span>]. This offers a level of granularity that systemic markers cannot match, reinforcing that the precision we seek is likely hidden in the cellular dynamics of the joint itself rather than in the patient's static genetic code. Nevertheless, the feasibility of incorporating synovial tissue analysis into routine clinical practice remains uncertain. Significant barriers, including limited tissue accessibility, the lack of standardized sampling procedures, and high procedural costs, must be addressed before synovial biopsies can be widely adopted for everyday patient stratification.</p><p>Precision medicine is frequently conflated with molecular medicine. However, comprehensive patient stratification must also i","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185x.70848","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807747","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":"Biologics, Janus Kinase Inhibitors, and Cancer: The Comparator on Trial","authors":"Shih-Tsung Chang, Teng-Chieh Hsu","doi":"10.1111/1756-185x.70824","DOIUrl":"10.1111/1756-185x.70824","url":null,"abstract":"<p>Whether Janus kinase (JAK) inhibitors raise the risk of malignancy has no single answer, because the estimate depends on the comparator against which they are judged. Concern that immunomodulatory therapy might promote malignancy has shadowed rheumatology for two decades, yet the accumulated evidence yields two different messages. For biologic disease-modifying antirheumatic drugs (bDMARDs), randomized trials and registries, including studies of patients with prior cancer, have been largely reassuring. Early lymphoma signals during tumor necrosis factor inhibitor (TNFi) therapy were difficult to separate from the disease itself, because rheumatoid arthritis (RA) raises lymphoma risk in proportion to inflammatory activity [<span>1</span>]. Once disease-driven confounding was addressed, pooled randomized trials showed no significant excess malignancy with bDMARDs versus conventional synthetic DMARDs (csDMARDs) or placebo [<span>2</span>]. Reassurance extended to patients with prior malignancy, in whom bDMARDs were not associated with new or recurrent cancer [<span>3</span>], and contemporary registry data in patients without prior cancer are concordant: the BIOBADASER III analysis found no increased cancer risk across non-TNFi bDMARDs and targeted synthetic DMARDs compared with TNFi [<span>4</span>].</p><p>JAK inhibitors reopened the question. In ORAL Surveillance, a regulator-mandated, open-label trial enrolling patients with RA aged 50 years or older with at least one cardiovascular risk factor, tofacitinib failed to meet noninferiority against a TNFi for malignancy, with adjudicated cancers excluding nonmelanoma skin cancer occurring in 4.2% versus 2.9% of patients [<span>5, 6</span>]. Regulatory boxed-warning updates for relevant JAK inhibitors followed [<span>7</span>]. This uncertainty, and the need to interpret cancer signals cautiously rather than as a fixed class label, has been noted previously [<span>8</span>]. Yet subsequent synthesis complicated the headline: a meta-analysis across 78 randomized trials and long-term extension studies spanning joint, skin, and bowel disease found no clear excess malignancy for JAK inhibitors compared with placebo or methotrexate, but a higher incidence when compared with a TNFi [<span>9</span>]. These are three distinct comparisons rather than a single verdict on the class; a non-significant difference against placebo or methotrexate is not proof of equivalence. A larger Bayesian network meta-analysis, spanning 305 randomized trials and long-term extension studies and more than 160 000 participants with rheumatoid arthritis, psoriatic disease, or inflammatory bowel disease, has since reported higher relative estimates for all malignancies, including nonmelanoma skin cancer, with JAK inhibitors versus both a TNFi and standard care, defined as placebo or methotrexate monotherapy; the modeled absolute excess versus a TNFi was negligible in standard-risk populations but clinically meaningful in higher-ri","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701224","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":"Association of Plasma miRNA-7-5p and miRNA-214-5p With Rheumatoid Arthritis Associated Interstitial Lung Disease","authors":"Irem Sahinoğlu,&nbsp;Umit Karakas,&nbsp;Sadettin Uslu,&nbsp;Deniz Kizilirmak,&nbsp;Emre Ali Acar,&nbsp;Filiz Cemre Tasgöz,&nbsp;Mevlüt Kacar,&nbsp;Seref Sülükcü,&nbsp;Merve Türkegün Sengül,&nbsp;Mehmet Emin Erdal,&nbsp;Ozgül Soysal Gündüz","doi":"10.1111/1756-185x.70820","DOIUrl":"10.1111/1756-185x.70820","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Rheumatoid arthritis–associated interstitial lung disease (RA-ILD) is a major extra-articular complication contributing to increased morbidity and mortality. Circulating microRNAs (miRNAs) have emerged as potential non-invasive biomarkers in autoimmune diseases. This study aimed to evaluate whether plasma miRNA-7-5p and miRNA-214-5p are associated with the presence of RA-ILD and with radiological and functional indicators of pulmonary involvement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this cross-sectional study, 58 RA patients (29 RA-ILD, 29 without ILD) and 30 matched healthy controls were included. RA-ILD was diagnosed by multidisciplinary assessment (HRCT and pulmonary function tests). Plasma miRNA levels were measured by qRT-PCR and analyzed using the 2^−ΔΔCT method. Diagnostic performance was evaluated by ROC analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Plasma miRNA-7-5p and miRNA-214-5p levels were significantly higher in RA patients compared with healthy controls (<i>p</i> &lt; 0.05 for both). Among RA patients, both miRNAs were significantly lower in those with ILD (<i>p</i> &lt; 0.05). miRNA-7-5p demonstrated promising discriminatory performance for identifying RA-ILD (AUC = 0.87, 95% CI: 0.760–0.947; <i>p</i> &lt; 0.001), whereas miRNA-214-5p showed modest accuracy (AUC = 0.676, 95% CI: 0.539–0.794; <i>p</i> = 0.01). In multivariable analysis, ILD presence was independently associated with decreased levels of both miRNAs. Neither miRNA correlated significantly with DAS28-CRP, disease duration, nor with radiological or functional severity parameters.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Circulating miRNA-7-5p and miRNA-214-5p are associated with the presence of RA-ILD but do not reflect disease severity in this cohort. Larger prospective studies are required to validate their potential role as adjunctive biomarkers for RA-ILD detection and risk stratification.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701289","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":"Association Between Serum Matrix Metalloproteinase-3 Levels and Cognitive Function in Patients With Rheumatoid Arthritis","authors":"Longchuan Xu","doi":"10.1111/1756-185x.70817","DOIUrl":"10.1111/1756-185x.70817","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678717","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":"Genetic Association Between BTN3A1 Polymorphisms and the Risk of Rheumatoid Arthritis in a Chinese Population","authors":"Qingxue Shu,&nbsp;Anfang Huang,&nbsp;Chengsong He","doi":"10.1111/1756-185x.70792","DOIUrl":"10.1111/1756-185x.70792","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>BTN3A1 has been associated with systemic lupus erythematosus (SLE) and psoriasis; however, its relationship with rheumatoid arthritis (RA) risk, particularly regarding BTN3A1 polymorphisms and RA susceptibility remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 390 age- and sex-matched participants, including RA patients and healthy controls, were enrolled. Demographic, laboratory, and clinical data were collected. Five BTN3A1 polymorphisms (rs1796520, rs3857550, rs3208733, rs6912853, rs10456045) were genotyped. Allele and genotype associations between the groups were analyzed, as well as their associations with clinical and laboratory features in RA patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among RA patients, 79.74% were female and 20.26% were male; among controls, 84.36% were female and 15.64% were male. For rs3208733, the frequencies of the CC genotype and C allele differed significantly between RA patients and controls. For rs6912853, the frequency of the TC genotype differed significantly. For rs10456045, the frequencies of the GG, AG, and GG + AG genotypes differed significantly. Regarding clinical and laboratory associations: for rs1796520, antinuclear antibody (ANA)-positive patients showed higher frequencies of the CC + TC genotype and C allele; anti-Rib-positive patients showed a higher frequency of the C allele. RA patients carrying the CC + TC genotype had fewer swollen joints and higher levels of IL-12p70 and IFN-α than TT carriers. For rs6912853, CC + TC carriers had fewer tender joints and higher levels of C-reactive protein (CRP) and IFN-γ than TT carriers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>BTN3A1 gene polymorphisms are associated with RA risk, suggesting future therapeutic exploration of BTN3A1 in RA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673773","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":"Association Between Chikungunya Infection and Rheumatoid Arthritis in Taiwan—A Cross-Sectional Study","authors":"Chang-Yi Yen,&nbsp;Chang-Chi Lin,&nbsp;Ping-Chang Lin,&nbsp;Ching-Yi Tsai,&nbsp;Li-Teh Liu,&nbsp;Chen-Hsuan Lin,&nbsp;Chun-Hong Chen,&nbsp;Chia-Chun Tseng,&nbsp;Hua-Chen Chan,&nbsp;Cheng-Chin Wu,&nbsp;Tsan-Teng Ou,&nbsp;Jih-Jin Tsai,&nbsp;Jeng-Hsien Yen","doi":"10.1111/1756-185x.70784","DOIUrl":"10.1111/1756-185x.70784","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Chikungunya virus (CHIKV) infection might cause chronic chikungunya arthritis resembling rheumatoid arthritis (RA). The purpose of this study is to investigate the potential role of this virus in the pathogenesis of RA in Taiwan, a non-endemic area.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This cross-sectional study enrolled 98 RA patients and 200 healthy controls. Serum CHIKV IgM and IgG were tested using two commercial enzyme-linked immunosorbent assay (ELISA) kits (Abcam and Euroimmun) and an in-house neutralization assay. ELISA-IgM was performed only in patients with RA. ELISA or neutralization positive samples were further tested for CHIKV RNA by reverse-transcription-polymerase chain reaction. Associations between CHIKV seropositivity and various autoantibodies were analyzed. The agreements among these assays were also evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Neutralizing antibodies were detected in 2 of 98 RA patients and in none of the controls (<i>p</i> = 0.107, Fisher's exact test; <i>p</i> = 0.043, chi-square). Both patients were absent from Abcam-IgM and -IgG, as well as Euroimmun-IgM and -IgG testing. There was no association between Abcam-IgM or Euroimmun-IgM and rheumatoid factor, anti-cyclic citrullinated peptide, antinuclear, or anti-extractable nuclear antigen antibodies. Poor agreements were noted between the neutralizing assay and Abcam-IgG or Euroimmun-IgG (<i>κ</i> = 0 and 0, respectively). A similar finding was also found between Abcam-IgM and Euroimmun-IgM (<i>κ</i> = −0.38).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study was not sufficiently powered to establish a causal association between CHIKV infection and RA development. Poor agreements were noted among different commercial ELISA kits and neutralization assays, underscoring the limitations of the serology assay.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673678","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":"Pregnancy Outcome in a Patient With DADA2 Syndrome on Continued Adalimumab Therapy","authors":"Bhargavi Pridhivi,&nbsp;GSRSNK Naidu,&nbsp;Prateek Bhatia,&nbsp;Pui Y. Lee,&nbsp;Minakshi Rohilla,&nbsp;Aman Sharma","doi":"10.1111/1756-185x.70818","DOIUrl":"10.1111/1756-185x.70818","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669433","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":"Antigen-Specific Tolerization in Rheumatoid Arthritis: Evaluating the Translational Potential of hPAD4 Plasmid Therapy","authors":"Tang-Kai Cheng,&nbsp;Hideto Kameda,&nbsp;James Cheng-Chung Wei","doi":"10.1111/1756-185x.70809","DOIUrl":"10.1111/1756-185x.70809","url":null,"abstract":"&lt;p&gt;The incidence and clinical burden of autoimmune inflammatory diseases, particularly rheumatoid arthritis (RA), continue to rise and place profound strains on global healthcare systems [&lt;span&gt;1&lt;/span&gt;]. Beyond the immediate impacts of chronic joint inflammation, RA significantly elevates the risk of secondary complications, including a marked increase in the development of secondary osteoarthritis, underscoring the urgency of arresting inflammatory cascades before irreversible structural damage occurs [&lt;span&gt;2&lt;/span&gt;]. While the current therapeutic armamentarium—ranging from conventional early aggressive interventions like methotrexate [&lt;span&gt;3&lt;/span&gt;] to targeted biologic agents like adalimumab [&lt;span&gt;4&lt;/span&gt;]—has improved patient outcomes, the field is navigating the complex realities of treating a super-elderly society. Consequently, there is an acute need to transition toward therapies that induce long-term remission without compromising systemic immunocompetence [&lt;span&gt;5&lt;/span&gt;]. A recent study by Pagni et al., published in &lt;i&gt;Arthritis &amp; Rheumatology&lt;/i&gt;, introduces a compelling strategy to meet this need: halting the production of anti-citrullinated protein antibodies (ACPAs) by inducing targeted immune tolerance [&lt;span&gt;6&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The pathophysiological hallmark of RA is the generation of autoantibodies directed against citrullinated proteins. Historically, the “shared epitope binds citrullinated peptide” hypothesis posited that RA-associated HLA-DRB1 molecules preferentially bind these altered peptides, subsequently driving B cell responses. However, because ACPAs recognize up to 100 000 distinct citrullinated peptides, this mechanism would require an implausibly massive repertoire of specific helper T cells. To address this, Pagni et al. advocate for a paradigm-shifting alternative: the hapten/carrier mechanism [&lt;span&gt;6&lt;/span&gt;]. In this model, human peptidyl arginine deiminase 4 (hPAD4) acts as the carrier protein, and the multiple citrullinated proteins serve as haptens. T cell recognition of hPAD4 provides the necessary help for B cells to produce ACPAs. Consequently, inducing tolerance to the single hPAD4 protein presents a mathematically and immunologically feasible target to block responses to thousands of downstream citrullinated antigens [&lt;span&gt;6&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;To intervene precisely at this immune fulcrum, the researchers engineered a multicistronic tolerogenic plasmid encoding hPAD4 alongside three active murine anti-inflammatory cytokines: transforming growth factor (TGF) β1, interleukin (IL) 10, and IL-2 [&lt;span&gt;6&lt;/span&gt;]. Transfecting antigen-presenting cells with this plasmid forces the co-expression of the autoantigen and suppressive signals, theoretically recruiting regulatory T cells to extinguish the hPAD4-reactive T cell response. This highly specific action starkly contrasts with the broad immune modulation seen in traditional treatments like methotrexate or systemic glucocorticoids, which leave patients vu","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669521","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: Leflunomide-Induced Cutaneous Eruption in a Patient With Probable Chemotherapy-Associated Inflammatory Polyarthritis","authors":"Kübra Neslihan Kurt Oktay,&nbsp;Samet Aygun,&nbsp;Elem Yorulmaz,&nbsp;Duygu Geler Kulcu","doi":"10.1111/1756-185x.70805","DOIUrl":"10.1111/1756-185x.70805","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"29 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669503","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}