International Journal of Rheumatic Diseases最新文献

{"title":"Case Report: Ankylosing Spondylitis Complicated With Systemic Lupus Erythematosus","authors":"Li-Fang Yan,&nbsp;Yue-e Zeng,&nbsp;Yan Xu","doi":"10.1111/1756-185X.70275","DOIUrl":"https://doi.org/10.1111/1756-185X.70275","url":null,"abstract":"<div>\u0000 \u0000 <p>Ankylosing spondylitis (AS) is rarely found in conjunction with connective tissue diseases. Moreover, reports on the coexistence of AS with systemic lupus erythematosus (SLE) are few. Here, we describe such a case of coexisting AS and SLE in a 58-year-old male patient. He presented with a 5-year history of pain in the lower spine. Immunological tests showed positive results for antinuclear and Sm antibodies. The human leukocyte antigen B27 was also positive. Here, we report a case where AS coexisted with SLE.</p>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932287","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":"Intractable Thigh Pain due to Active Vasculitis in Femoral Arteries in Takayasu Arteritis","authors":"Sankar Jayaprakash,&nbsp;Nidhi Goel,&nbsp;Harsh Jain,&nbsp;Samvedna Khatri,&nbsp;Archana Yadav,&nbsp;Anilkumar Adidam Venkata Suryakant,&nbsp;Debraj Sen,&nbsp;Ashish Chandwani,&nbsp;Kartik Sivasami,&nbsp;Abhishek Kumar,&nbsp;Vivek Vasdev","doi":"10.1111/1756-185X.70233","DOIUrl":"https://doi.org/10.1111/1756-185X.70233","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932274","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":"Novel and Effective 28-Joint Disease Activity Measure for Rheumatoid Arthritis: The Disease Activity Score 28-Monocyte Chemotactic Protein-1","authors":"Liou Lieh-bang","doi":"10.1111/1756-185X.70267","DOIUrl":"https://doi.org/10.1111/1756-185X.70267","url":null,"abstract":"&lt;p&gt;Remission is widely considered the primary therapeutic goal in rheumatoid arthritis (RA) management, and this target has increasingly become attainable with the advent of biologic treatments. The feasibility of achieving remission can be evaluated using various criteria, including the 28-joint Disease Activity Score (DAS28) index [&lt;span&gt;1&lt;/span&gt;]. However, the 2011 remission criteria established by the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) [&lt;span&gt;2&lt;/span&gt;] were demonstrated to outperform the DAS28-erythrocyte sedimentation rate (ESR) for patient global, physician global, morning stiffness, and functional status assessments [&lt;span&gt;3&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Aletaha and Smolen have argued for abandoning DAS28-based remission criteria [&lt;span&gt;4&lt;/span&gt;], citing the potential for residual joint swelling even when DAS28-ESR scores are &lt; 2.0 [&lt;span&gt;5&lt;/span&gt;] as well as the possibility of residual tissue and molecular abnormalities indicating active disease as valid reasons for doing so [&lt;span&gt;6&lt;/span&gt;]. Nevertheless, we have developed an alternative, clinically useful DAS28-based approach: the DAS28 index supplemented with monocyte chemotactic protein-1 (DAS28-MCP-1) results [&lt;span&gt;7, 8&lt;/span&gt;]. MCP-1 is produced locally by activated monocytes and fibroblasts at the site of inflammation. In addition, a MCP-1 antagonist reduces or prevents arthritis in MRL-lpr mice. It implies that MCP-1 is much involved in arthritic inflammation [&lt;span&gt;7&lt;/span&gt;]. The four cut-off points of DAS28-MCP-1 for the remission, low, moderate, and high disease activity categories are &lt; 2.2, ≤ 3.6, and ≤ 4.8, respectively [&lt;span&gt;9&lt;/span&gt;]. Our findings indicate the high criterion validity of the DAS28-MCP-1, with strong intercorrelations and time–change correlations among various disease activity scores as well as favorable limits of agreement identified through Bland–Altman plots [&lt;span&gt;8&lt;/span&gt;]. Furthermore, DAS28-MCP-1 scores were correlated with Health Assessment Questionnaire-Disability Index (HAQ-DI) scores, similarly to all other disease activity scores [&lt;span&gt;8&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Swollen joint count (SJC) has been demonstrated to be more strongly correlated with the development of bone erosions than ESR and CRP in patients with RA [&lt;span&gt;10&lt;/span&gt;]. The committee that established the 2011 ACR/EULAR remission criteria for RA reported that 10% of patients with a DAS28-ESR score of &lt; 2.6 had ≥ 4 swollen joints and that 1 patient had &gt; 20 swollen joints [&lt;span&gt;11&lt;/span&gt;]. Similarly, our findings revealed that 5.2% of the included patients with RA with a DAS28-ESR score of &lt; 2.6 had ≥ 4 swollen joints, with one patient presenting with 10 swollen joints [&lt;span&gt;12&lt;/span&gt;]. By contrast, none of the patients with RA with a DAS28-CRP score of &lt; 2.5 or a DAS28-MCP-1 score of &lt; 2.2 had ≥ 4 swollen joints [&lt;span&gt;12&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The relationship between MCP-1 levels in blood and SJC has been investigated in both earlier and more rec","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70267","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932273","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":"Systemic Sclerosis-Associated Interstitial Lung Disease: Current Insights and Future Directions","authors":"Ming-Yuan Victor Chao,&nbsp;Po-Cheng Shih,&nbsp;Pui-Ying Leong","doi":"10.1111/1756-185X.70269","DOIUrl":"https://doi.org/10.1111/1756-185X.70269","url":null,"abstract":"&lt;p&gt;Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is a progressive and potentially debilitating pulmonary complication of systemic sclerosis (SSc). It is characterized by inflammatory and fibrotic changes in the lung parenchyma, significantly contributing to morbidity and mortality [&lt;span&gt;1&lt;/span&gt;]. The clinical course of SSc-ILD varies widely, with some patients experiencing rapid disease progression and severe respiratory impairment, while others exhibit a more indolent trajectory. Despite advances in therapeutic interventions, no universally accepted treatment strategy for SSc-ILD exists, necessitating continued research into optimal management approaches.&lt;/p&gt;&lt;p&gt;The pathogenesis of SSc-ILD is complex, involving genetic predisposition, immune dysregulation, vasculopathy, and fibrosis [&lt;span&gt;2&lt;/span&gt;]. Microvascular damage and dysfunction are the earliest morphological and functional indicators of systemic sclerosis (SSc), a progressive connective tissue disease marked by vascular abnormalities and widespread fibrosis, often initially presenting as Raynaud phenomenon [&lt;span&gt;3&lt;/span&gt;]. Key profibrotic mediators include an imbalance in macrophage activation (M1/M2) and T-helper 2 (Th2)-polarized cytokines. Elevated IL-4 and IL-13 (traditionally “allergic” cytokines) with higher circulating mixed M1/M2 monocyte/macrophage cell percentages are associated with SSc-ILD [&lt;span&gt;2, 4, 5&lt;/span&gt;]. IL-6, a pleiotropic cytokine, sustains chronic inflammation and links the early immune response to later fibrosis. These cytokines, together with potent fibrogenic growth factors like transforming growth factor-beta (TGF-β), create a profibrotic lung microenvironment. The interaction between endothelin/VEGF(Vascular Endothelial Growth Factor) signaling from injured vasculature and TGF-β is thought to be a pivotal trigger that converts quiescent fibroblasts into activated myofibroblasts, resulting in excessive extracellular matrix deposition and progressive fibrosis [&lt;span&gt;1, 6&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Although no animal model of SSc-ILD fully replicates all pathological aspects of the disease, bleomycin-induced lung fibrosis remains a valuable tool and is extensively utilized to investigate the pathogenesis of SSc-ILD [&lt;span&gt;7&lt;/span&gt;]. In the bleomycin model, initial lung injury is characterized by type I interferon (IFN) signaling activation, with subsequent TGF-β recognized as a pivotal driver of fibrosis [&lt;span&gt;8&lt;/span&gt;]. As the disease progresses or is intervened upon, Th2 cells drive the formation of alternatively activated profibrogenic macrophages and collagen production [&lt;span&gt;9&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Multiple clinical trials have shaped the management of SSc-ILD. Notably, inclusion criteria and patient characteristics vary across trials, which can impact outcomes and applicability to individual patients. To inform clinical decision-making, we summarize key trials' populations—including ILD patterns on imaging, disease duration, skin involvement, age, an","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925778","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":"Hydroxychloroquine Re-Examined: A Legacy Drug Facing Modern Challenges","authors":"Matthew Jiang,&nbsp;Maninder Mundae","doi":"10.1111/1756-185X.70271","DOIUrl":"https://doi.org/10.1111/1756-185X.70271","url":null,"abstract":"&lt;p&gt;Hydroxychloroquine (HCQ) has in many ways been a pharmacological chameleon, with changing formulations and evolving clinical uses, from its early role as an antimalarial to being a cornerstone treatment in rheumatic disease. Targeted therapies have changed the treatment landscape of these conditions over recent decades. This raises the question of the long-term therapeutic role of HCQ and its limitations, which we will aim to explore some of these questions.&lt;/p&gt;&lt;p&gt;The story of HCQ's origin is somewhat disputed; however, the first claimed use of quinine (from which HCQ is derived) was in the 1600s when bark powder from the Cinchona tree in South America was used to treat febrile illness [&lt;span&gt;1&lt;/span&gt;] was then widely distributed across Europe for its medicinal properties.&lt;/p&gt;&lt;p&gt;Over the next few centuries, various alkaloids were extracted and used primarily as an anti-malarial, quite extensively in World War II in the form of chloroquine, which was synthesized in the 1930s [&lt;span&gt;1&lt;/span&gt;]. It was at this time that recognition was made of its clinical utility for inflammatory arthritis and lupus; however, concerns about toxicity led to the development of HCQ in 1950 as a less toxic alternative.&lt;/p&gt;&lt;p&gt;Despite its broad use, the mechanism of action of HCQ is still not well understood, although there are several key mechanisms by which it is thought to exert its therapeutic actions [&lt;span&gt;2&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;HCQ is a weak base and is known to accumulate in acidic lysosomes where it causes an increase in pH that impairs key processes including autophagy and antigen processing. Inhibition of Toll-like receptor (TLR) signaling (particularly TLR7 and 9) through various mechanisms has also been postulated as a mechanism for its anti-inflammatory effect with downstream effects related to inhibition of various pro-inflammatory cytokines.&lt;/p&gt;&lt;p&gt;Rheumatologists are most familiar with HCQ use in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).&lt;/p&gt;&lt;p&gt;In the recent EULAR recommendations in 2023 for the management of SLE [&lt;span&gt;3&lt;/span&gt;], HCQ is recommended for all patients unless contraindicated.&lt;/p&gt;&lt;p&gt;These recommendations are supported by evidence of benefit across broad outcomes including patient survival, organ damage, flare rates, musculoskeletal manifestations, and cancer risk [&lt;span&gt;4&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Recently, the ubiquitous use of HCQ in SLE has been questioned, with a review by Caravaca-Fontan et al. highlighting the paucity of evidence for HCQ in lupus nephritis (LN) [&lt;span&gt;5&lt;/span&gt;], in particular, for remission induction, flare reduction, and kidney function recovery. This review also cited limitations of current evidence, including small study populations with predominantly observational and retrospective data that were prone to bias.&lt;/p&gt;&lt;p&gt;The same authors argued a need for further research on HCQ use for LN, in light of modern induction and maintenance protocols [&lt;span&gt;6&lt;/span&gt;]. Previous studies did not consider factors such as ","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919768","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":"Age- and Gender-Specific Dynamics of Hyperuricemia: A Longitudinal Community Study on Metabolic Trajectories and Comorbidity Stratification","authors":"Xianghui Wen,&nbsp;Yanli Zhang,&nbsp;Jieruo Gu,&nbsp;Yina Wang","doi":"10.1111/1756-185X.70254","DOIUrl":"https://doi.org/10.1111/1756-185X.70254","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This longitudinal study investigated age- and gender-specific disparities in hyperuricemia and their metabolic associations in a community-based cohort, addressing gaps in long-term uric acid trajectory data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A prospective cohort of 465 adults (123 males, 342 females) was stratified by serum uric acid (SUA &gt; 420 μmol/L) and followed annually for 3 years. Standardized assessments included anthropometric, biochemical, and clinical evaluations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Males had a 3.8-fold higher hyperuricemia prevalence than females (39.84% vs. 10.53%, <i>p</i> &lt; 0.001), with age-specific peaks in males (20–29 and &gt; 60 years) and females (&gt; 60 years). Hyperuricemic individuals exhibited elevated BMI (24.75 ± 3.38 vs. 22.43 ± 3.01 kg/m², <i>p</i> &lt; 0.001), systolic blood pressure (SBP: 124.62 ± 16.42 vs. 118.25 ± 14.99 mmHg, <i>p</i> = 0.001), fasting glucose (FBG: 5.48 ± 0.79 vs. 5.25 ± 0.80 mmol/L, <i>p</i> = 0.013), and renal dysfunction markers (serum creatinine: 74.10 ± 16.57 vs. 59.24 ± 14.68 μmol/L, <i>p</i> &lt; 0.001). Age-stratified comorbidity patterns showed dyslipidemia predominance in younger groups (58.82%) versus cardiorenal complications hypertension (31.03%), elevated FBG (41.38%) and renal impairment (75.86%) in older adults. Multivariate analysis identified age, sex, BMI, and lipid profiles as SUA determinants (<i>β</i> = −0.248 to 0.472, <i>p</i> &lt; 0.05), with eGFR inversely associated (<i>β</i> = −0.273, <i>p</i> &lt; 0.05). Longitudinal data revealed alanine aminotransferase (ALT) as a novel predictor (<i>β</i> = 0.125, <i>p</i> = 0.038), while baseline hyperuricemia did not predict long-term SUA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Hyperuricemia demonstrates significant age- and gender-related disparities, with persistent metabolic abnormalities contributing to cardiorenal and hepatic risks. Younger populations face dyslipidemia and liver dysfunction, whereas older adults exhibit hypertension and renal impairment. Regular monitoring and age-specific interventions are critical for mitigating metabolic syndrome progression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919767","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 Retinopathy and Systemic Sclerosis: A Systematic Review and Meta-Analysis","authors":"Alireza Fatemi,&nbsp;Aylin Taghipour,&nbsp;Yasmin Yazdooei,&nbsp;Mahdis Fatemi,&nbsp;Akram Hashemi,&nbsp;Nafiseh Abdolahi","doi":"10.1111/1756-185X.70253","DOIUrl":"https://doi.org/10.1111/1756-185X.70253","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Objectives</h3>\u0000 \u0000 <p>Studies have indicated a potential link between retinopathy and systemic sclerosis (SSc), but the precise nature of this association remains unclear. This systematic review and meta-analysis aims to synthesize available evidence to evaluate the relationship between SSc and retinopathy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A systematic search was conducted across four major databases and gray literature to collect all relevant studies. The quality of the selected articles was assessed for risk of bias using standardized tools.</p>\u0000 \u0000 <p>A meta-analysis was performed using standardized mean difference (Std. Mean Difference) to estimate the association between retinopathy and SSc. Additional analyses for heterogeneity, sensitivity, subgroups, and publication bias were also conducted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Twelve studies (359 cases, 314 controls) were included in the systematic review. A meta-analysis of eight studies found a nonsignificant and negligible association (pooled Std. Mean Difference = 0.08; 95% CI = −0.31 to 0.48; <i>p</i> = 0.67) between SSc and retinopathy, with no publication bias (<i>p</i> = 0.5362). Differences in Std. Mean Difference were observed in subgroup analyses but did not sufficiently explain the heterogeneity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The findings suggest no strong association between retinopathy and SSc. While some subgroup analyses revealed potential variations, they did not fully clarify the observed heterogeneity. Further research with larger, well-designed studies is necessary to determine whether retinopathy could serve as a biomarker for SSc.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Systematic Review Registration Number (PROSPERO)</h3>\u0000 \u0000 <p>CRD42024529644 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=529644.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919834","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 Role of Abatacept on Inflammation and Fibrosis in Hypochlorous Acid-Induced Fibrosis Mice","authors":"Bingying Dai,&nbsp;Meng Meng,&nbsp;Weilin Chen,&nbsp;Junyu Zhou,&nbsp;Qiming Meng,&nbsp;Liqing Ding,&nbsp;Shasha Xie,&nbsp;Ding Bao,&nbsp;Xiaojing Li,&nbsp;Lijuan Zhao,&nbsp;Ting Huang,&nbsp;Chunliu Lv,&nbsp;Hui Luo,&nbsp;Sijia Liu,&nbsp;Honglin Zhu","doi":"10.1111/1756-185X.70250","DOIUrl":"https://doi.org/10.1111/1756-185X.70250","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To investigate the effect of abatacept in the hypochlorous acid (HCLO)-induced fibrosis model and to analyze changes in immune cell fractions within the abatacept-treated early diffuse systemic sclerosis (SSc) cohort.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Fibrosis was induced in BALB/c mice by subcutaneous injection of HCLO, and abatacept was injected intraperitoneally on alternate days starting on day 28. After 6 weeks, we assessed the pathological changes, inflammation, myofibroblast activation, and the percentage of ICOS in CD3+ T cells. Potential pathways affected by abatacept were also investigated. Finally, we analyzed immune infiltration and multiple scores in early diffuse SSc patients and in the skin and lung tissues of the HCLO model after abatacept administration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Abatacept significantly decreased the proportion of M2 macrophages in the abatacept-treated HCLO model and the inflammatory improver subset of SSc patients. Furthermore, abatacept reduced CD28 signaling, the inflammation-related pathway, and the ICOS expression on CD3+ T cells in HCLO mice. In the inflammatory subset of SSc patients and HCLO mice, microenvironmental and immune scores tended to decrease after abatacept treatment. Unexpectedly, abatacept had no effect on skin or lung collagen content in HCLO mice. The number of T cells and myofibroblasts was not reduced in the abatacept-treated HCLO group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Although abatacept did not improve skin and lung fibrosis in the HCLO mice, it reduced the immune response signature and the proportion of M2 macrophages. These findings suggest that further research is needed to assess the therapeutic value of abatacept in SSc patients and preclinical mouse models.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70250","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143926095","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":"Investigating the Association Between Social Support and Quality of Life in People With Rheumatoid Arthritis: A Systematic Review of the Literature","authors":"Noreena Coyle,&nbsp;Stella Kuit,&nbsp;Simon Dunne","doi":"10.1111/1756-185X.70234","DOIUrl":"https://doi.org/10.1111/1756-185X.70234","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by symptoms such as pain, inflammation of joints, fatigue, and impaired functionality. Depression and anxiety are common in this population of patients. Research suggests that social support, whether received or perceived, can improve the Quality of Life (QoL) of people with RA. This systematic review examined the relationship between social support and QoL in individuals with RA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Five databases were searched with no restriction on dates. Studies were included if they used validated instruments or interventions and examined the association between QoL and social support in people with RA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Seventeen studies were included in the review, involving 2043 participants aged 18–88. Overall, the findings suggest that positive social support, whether received or perceived, enhances the QoL of individuals with RA, particularly with their mental health and also with some physical symptoms like pain. However, negative social support was found to have the opposite effect, potentially worsening the QoL for those with RA. Fatigue was also identified as indirectly mediating between social support and its impact on participants' quality of life.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The review underscores the significance of social support, especially from family and friends, in shaping the well-being of individuals with RA. The findings highlight the need for further research to better understand the specific types and sources of social support that are most beneficial for improving QoL, and for gold standard measurement instruments for QoL and social support in this population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70234","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914074","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":"Impact of Gut Microbiota and Probiotics on Rheumatoid Arthritis: A Potential Treatment Challenge","authors":"Thekkuttuparambil Ananthanarayanan Ajith,&nbsp;Bejoy Anita","doi":"10.1111/1756-185X.70266","DOIUrl":"https://doi.org/10.1111/1756-185X.70266","url":null,"abstract":"<div>\u0000 \u0000 <p>Over the past few decades, there has been a surge in global study on the relationship between gut microbiota and human health. Numerous human illnesses have been linked to dysbiosis. Gram-positive <i>firmicutes</i> and Gram-negative <i>bacteroidetes</i> are the two leading bacterial phyla that make up 90% of the gut microbiome. Many symbionts in the gut environment establish intricate relationships with host defense to stop both local and non-native dangerous bacteria from colonizing and invading. Dysbiosis alters the paracellular route and damages the epithelium, enabling them to penetrate the epithelium and come into contact with the immune cells. Impaired intestinal barrier function, immune regulation mediated by metabolites derived from the gut microbiota, posttranslational modification of host proteins such as increased citrullination, regulation of the gut microbiota's effect on immune cells, intestinal epithelial cell autophagy, interaction between the microbiome and human leukocyte antigen alleles, and interaction with microRNAs are some of the mechanisms involved in rheumatoid arthritis (RA). The gut microbiota, <i>Prevotella copri</i>, and <i>Collinsella</i> spp. were shown to be higher in the early/preclinical phases of RA, while <i>Bacteroidetes, Bifidobacteria, and Eubacterium rectale</i> were found to be lower. Probiotic-based early dietary intervention may reduce inflammation and slow the rate of joint deterioration, and such intervention can also aid in the restoration of gut microbiota equilibrium. This review article describes the gut microbial dysbiosis and role of probiotics in RA.</p>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914432","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}