International Journal of Rheumatic Diseases最新文献

{"title":"Infections in Idiopathic Inflammatory Myopathies: Do Asians Need a Different Dose of Immunosuppression?","authors":"Jasmine Parihar, Takahisa Gono, Ho So, Latika Gupta, the APLAR myositis SIG","doi":"10.1111/1756-185X.70084","DOIUrl":"10.1111/1756-185X.70084","url":null,"abstract":"<p>Day et al. highlight the intricate challenges in managing rare rheumatic diseases like idiopathic inflammatory myopathies (IIMs), particularly when aggressive immunosuppression is complicated by opportunistic infections [<span>1</span>]. This rare disease-rare complication scenario is further complicated by the hypothesis that infections may trigger autoimmunity, creating a paradoxical management dilemma. Opportunistic infections, which often present atypically in myositis patients and may mimic active IIM, pose a significant clinical challenge [<span>2</span>]. Furthermore, infections are the leading cause of death in myositis patients, suggesting that clinicians need to manage the prevention and early detection of infection. Moreover, immunosuppressive drugs (ISDs) may lead to other iatrogenic immunodeficiency-associated lymphoproliferative disorders (OIIA-LPDs), particularly in patients treated with methotrexate [<span>3</span>]. The absence of well-defined guidelines for these complex scenarios underscores the urgent need for comprehensive research to inform evidence-based management strategies in these challenging cases.</p><p>In patients with IIM and other autoimmune diseases, infection risk is influenced by a complex interplay of disease characteristics and treatment. A dysregulated immune response, disease severity, and the use of immunosuppressive medications significantly increase infection risk in conditions such as systemic lupus erythematosus (SLE) with an infection rate of 29.2%–43.9% [<span>4</span>]. Opportunistic infections in myositis patients also present a significant clinical challenge, with a reported 33%–54% overall infection rate and 6%–12% classified as opportunistic, particularly within the first year of high-dose corticosteroid treatment [<span>5-7</span>]. Dermatomyositis patients, especially those with anti–MDA5-antibody positivity, face heightened infection risks independent of immunosuppressive therapy [<span>7-9</span>]. Other factors, such as methylprednisolone pulse therapy, combination therapy, disease onset after age 50 years, a lymphocyte count below 1200/mm<sup>3</sup>, high serum KL-6 levels, and the presence of interstitial lung disease (ILD), also contribute to higher infection risk [<span>10, 11</span>]. This issue is particularly acute in developing regions like Asia, where environmental factors and healthcare disparities, including inadequate vaccination protocols for immunosuppressed patients, exacerbate outcomes. The prevalence and impact of these infections underscore the urgent need for improved prevention strategies and management guidelines, especially in resource-limited settings.</p><p>Significant regional disparities in infection prevalence among myositis patients demand tailored management strategies. Asia reports higher mycobacterial infection rates (5.86%) compared to Europe (2.36%) and Latin America (2.47%) in IIM patients [<span>12</span>]. These patients show increased susceptibility t","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143038849","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":"Kawasaki Disease Can Come Calling as Aphon(e)ia: Laryngeal Weakness as the Presentation of Myositis in Kawasaki Disease","authors":"Gayathri Coimbatore Vaitheeswaran, Anirban Basu, Prabal Barman, Ridhima Aggarwal, Rakesh Kumar Pilania","doi":"10.1111/1756-185X.70091","DOIUrl":"10.1111/1756-185X.70091","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143038850","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: A Novel CCN6 Compound Heterozygous Mutation in Progressive Pseudorheumatoid Dysplasia","authors":"Yu-ying Yang, Wen-jia Chen, Chengde Yang, Jian-min Liu, Yu-tong Su","doi":"10.1111/1756-185X.70003","DOIUrl":"10.1111/1756-185X.70003","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023376","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 Series: The Challenge of Using Immune Checkpoint Inhibitors in Anti-Transcriptional Intermediary Factor 1\u0000 \u0000 \u0000 γ\u0000 \u0000 $$ gamma $$\u0000 Antibody-Positive Dermatomyositis","authors":"Liang Chen, Sabrina Fallavollita, Lama Sakr, Hangjun Wang, Marc Pusztaszeri, Khashayar Esfahani, Michael N. Pollak, Marie Hudson, Valérie Leclair","doi":"10.1111/1756-185X.70087","DOIUrl":"10.1111/1756-185X.70087","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023374","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":"Sjögren's Syndrome Is Associated With an Increased Risk of Vitiligo","authors":"Jing-Xing Li,&nbsp;Po-Chang Wu,&nbsp;Yu-Han Huang,&nbsp;Shu-Bai Hsu,&nbsp;Po-Yuan Wu","doi":"10.1111/1756-185X.70088","DOIUrl":"10.1111/1756-185X.70088","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Limited studies reported the correlation between Sjögren's syndrome (SS) and vitiligo. This study explores the association between SS and the risk of developing vitiligo and assesses comorbidity profiles and medication impacts.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a retrospective, population-based analysis using data from Taiwan's National Health Insurance Research Database, spanning 2008 to 2019. The primary outcome was the incidence of vitiligo, which was analyzed using Cox proportional hazards models, with additional subgroup and sensitivity analyses conducted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study incorporated 223 582 individuals with SS and 9 775 363 controls. A total of 208 942 pairs of the SS and controls were analyzed following propensity score matching. Non-matched and matched cohort analyses have consistent results. In matched analysis, individuals with SS had a 1.90-fold increased risk of developing vitiligo compared to those without SS after adjustment (95% confidence interval [Cl], 1.67–2.15; <i>p</i> &lt; 0.001). Age-related risk was evident, particularly in those aged 40–59 years and 60–79 years. Males had a lower risk of vitiligo than females. Comorbidities such as hyperlipidemia, chronic liver disease, hyperthyroidism, and spondylarthritis further increase the risk. During the first year following diagnosis, individuals with SS exhibited a significantly elevated risk of developing vitiligo compared to those without SS (aHR, 2.15; 95% Cl, 1.54–3.00; <i>p</i> &lt; 0.001). Over a decade of follow-up, the SS cohort showed a markedly higher cumulative risk of vitiligo than the non-SS cohort (log-rank <i>p</i> &lt; 0.001). Subgroup analysis revealed that systemic corticosteroid administration significantly mitigated the risk of developing vitiligo in SS patients (aHR, 0.67; 95% CI, 0.53–0.86; <i>p</i> &lt; 0.001) compared to patients who did not receive systemic corticosteroids.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>SS is significantly associated with an increased risk of developing vitiligo. Further research is warranted to elucidate the underlying mechanisms.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023353","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 of Sleep Duration and Daytime Napping With Risk of Hyperuricemia: A Systematic Review and Meta-Analysis","authors":"Xinwen Zhang,&nbsp;Guangcheng Wei,&nbsp;Xieyu Zhang,&nbsp;Junyi Guo,&nbsp;Jiahe Zhao,&nbsp;Xiaoxu Li,&nbsp;Xin Zhao,&nbsp;Jinjie Shi,&nbsp;Yue Yang,&nbsp;Su Fan,&nbsp;Hongli Wang,&nbsp;Kai Zhi,&nbsp;Ke Zhu,&nbsp;Jieyang Du,&nbsp;Wei Cao","doi":"10.1111/1756-185X.70050","DOIUrl":"10.1111/1756-185X.70050","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hyperuricemia (HUA), marked by elevated serum urate levels, is increasingly prevalent worldwide. The relationship between lifestyle factors such as sleep duration, daytime napping, and HUA risk remains unclear. Although some studies suggest that sleep variables, including short or long sleep durations and napping, may influence serum uric acid levels, results are inconsistent.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A systematic review and meta-analysis was performed according to the PRISMA guidelines. Databases such as PubMed, Embase, Web of Science, and Cochrane Library were searched until February 2024. The data were extracted, and the quality of the study was assessed independently by two reviewers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ten studies involving a total of 231 978 participants were included. Short sleep duration was related to higher risk of HUA (odds ratio (OR) 1.10, 95% confidence interval (CI): 1.03–1.18), while long sleep duration had no significant effect (OR 0.98, 95% CI: 0.89–1.07). The risk of HUA and daytime napping was statistically significant(OR 1.34, 95% CI: 1.12–1.61).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Short sleep duration and prolonged daytime napping are associated with an increased risk of HUA. These findings suggest that sleep patterns should be considered in lifestyle interventions for HUA prevention. Further research is required to establish causal relationships.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023375","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":"Colchicine in Cardiovascular Disease: Mechanisms of Action and Therapeutic Potential","authors":"Shiuan-Tzuen Su,&nbsp;Yung-Heng Lee,&nbsp;James C.-C. Wei","doi":"10.1111/1756-185X.70081","DOIUrl":"10.1111/1756-185X.70081","url":null,"abstract":"&lt;p&gt;Colchicine, a well-known anti-inflammatory agent, has recently garnered interest in the field of cardiovascular medicine. We provide an overview of the history of colchicine and its known biological effects. The discussion encompasses colchicine's applications in rheumatology and immunology, as well as other fields, highlighting its research value in cardiovascular diseases.&lt;/p&gt;&lt;p&gt;Modern diets high in fat and salt contribute to the accumulation of high cholesterol levels, leading to arterial wall damage and lipid deposition. Excess cholesterol injures the endothelium, resulting in the accumulation of lipids and activation of the NLRP3 inflammasome, which increases levels of pro-inflammatory mediators, such as IL-1β and IL-18 [&lt;span&gt;1&lt;/span&gt;]. Chronic inflammation promotes atherosclerosis, rendering plaques unstable and prone to rupture, thereby causing thrombosis and myocardial infarction [&lt;span&gt;1, 2&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Colchicine is an inexpensive and effective anti-inflammatory medication. It inhibits the release of IL-1β, IL-6, and TNFα by suppressing the NLRP3 inflammasome and also inhibits microtubule growth and activity [&lt;span&gt;1, 2&lt;/span&gt;]. In terms of immune modulation, colchicine increases prostaglandin E2 levels [&lt;span&gt;1&lt;/span&gt;], inhibits neutrophil adhesion, aggregation, and migration [&lt;span&gt;1-3&lt;/span&gt;], suppresses the release of inflammatory cytokines (leukotriene B4, thromboxane A2, and cyclooxygenase 2), and reduces platelet function and endothelial activation [&lt;span&gt;2, 3&lt;/span&gt;], thereby decreasing thrombosis [&lt;span&gt;1&lt;/span&gt;]. Colchicine is absorbed in the gastrointestinal tract, metabolized by hepatic cytochrome P450 3A4, and ultimately excreted via bile [&lt;span&gt;2&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Therefore, colchicine exerts its anti-inflammatory effects through relevant immune modulation pathways, making it effective in treating gout, Behcet's disease, familial Mediterranean fever [&lt;span&gt;1&lt;/span&gt;], pericarditis [&lt;span&gt;1, 2&lt;/span&gt;], reducing ischemic and hemorrhagic stroke in patients with diabetes [&lt;span&gt;4&lt;/span&gt;], serving as additional therapy for hypopharyngeal cancer [&lt;span&gt;5&lt;/span&gt;], preventing recurrent keloids [&lt;span&gt;6&lt;/span&gt;], and being effective for osteoarthritis, recurrent aphthous stomatitis, and chronic urticaria [&lt;span&gt;7&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Table 1 highlights the potential clinical applications of cholchicine in various inflammatory disease.&lt;/p&gt;&lt;p&gt;In acute gout attacks without tophi, colchicine should be taken daily at a dose of 0.6–1.2 mg for at least 3 months until serum uric acid is &lt; 5–6 mg/dL. If tophi are present, the treatment duration should be extended to 6 months [&lt;span&gt;8&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Colchicine has garnered significant attention in recent years for its therapeutic potential in acute pericarditis, coronary artery disease (CAD) [&lt;span&gt;9&lt;/span&gt;], atrial fibrillation, and post-pericardiotomy syndrome [&lt;span&gt;3&lt;/span&gt;]. Studies have shown that among 941 patients with acute gouty inflammation, the risk of major adverse cardiovascular ","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023379","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":"Monosodium Urate Crystal Deposition and Its Association With Major Cardiovascular Events","authors":"Shiuan-Tzuen Su,&nbsp;Yung-Heng Lee,&nbsp;Wuu-Tsun Perng,&nbsp;James C.-C. Wei","doi":"10.1111/1756-185X.70080","DOIUrl":"10.1111/1756-185X.70080","url":null,"abstract":"&lt;p&gt;Monosodium urate (MSU) crystal deposition is a pathological hallmark of gout, not only causing joint inflammation but also potentially exerting adverse effects on the cardiovascular system. Increasing evidence indicates a significant correlation between MSU crystal deposition and major adverse cardiovascular events (MACE), including myocardial infarction, stroke, and cardiovascular death. Understanding this correlation is crucial for the comprehensive management of patients with gout.&lt;/p&gt;&lt;p&gt;Purines in food are building blocks of DNA and RNA, and most mammals can utilize uricase enzyme to break down purines. However, humans lack a functional uricase enzyme, and factors such as a purine-rich diet, alcohol intake, use of diuretics, and obesity in men lead to hyperuricemia [&lt;span&gt;1&lt;/span&gt;]. MSU crystals rapidly deposit in the first metatarsophalangeal (MTP) joint. Once recognized and phagocytosed by synovial fluid macrophages, MSU crystals trigger the activation of the NLRP3 inflammasome and IL-1β [&lt;span&gt;2&lt;/span&gt;]. IL-1β is the primary mediator of the acute inflammatory response in gout [&lt;span&gt;3&lt;/span&gt;], acting on IL-1 receptors to promote the release of other inflammatory cytokines (TNF-α, IL-6, and IL-8) [&lt;span&gt;3, 4&lt;/span&gt;]. IL-6 stimulates the liver to secrete CRP [&lt;span&gt;3-5&lt;/span&gt;], thereby inducing a robust local inflammatory response. Other conditions, such as low temperature, cartilage dehydration, local edema, or avascularity in extremities, facilitate urate deposition in the pinna and distal interphalangeal joints of the fingers and toes [&lt;span&gt;1&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The inflammatory and immune responses elicited by MSU crystals are key mechanisms in the pathogenesis of gout. A thorough understanding of these mechanisms aids not only in the diagnosis and treatment of gout, but also provides significant insights into related chronic inflammatory diseases.&lt;/p&gt;&lt;p&gt;Under ultrasound or DECT diagnosis, hyperuricemia leads to the deposition of MSU inflammatory crystals within and around joints, then triggering gout [&lt;span&gt;6&lt;/span&gt;]. Gout has a higher prevalence in men and postmenopausal women [&lt;span&gt;1, 7&lt;/span&gt;], with an estimated prevalence of 3.2% in the UK, 3.9% in the USA [&lt;span&gt;6&lt;/span&gt;], and 3.8% in Taiwan [&lt;span&gt;8&lt;/span&gt;]. Even if MSU deposits are found in the heart, they do not necessarily cause gout [&lt;span&gt;1, 3-5&lt;/span&gt;]. Gout is associated with cardiovascular diseases and is categorized into acute gout arthritis, chronic gouty arthritis, and tophi [&lt;span&gt;9, 10&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The deposition of MSU crystals is a key pathological mechanism of gout, leading to acute and chronic inflammatory responses [&lt;span&gt;10&lt;/span&gt;], joint and soft tissue damage, and renal impairment. Understanding the mechanisms of MSU crystal deposition and associated pathological phenomena is crucial for the diagnosis, treatment, and prevention of gout.&lt;/p&gt;&lt;p&gt;Factors contributing to cardiovascular diseases include obesity, diabetes, hypertension, dyslipidemia, smoking, and g","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023383","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":"LncRNA-HHCP5 Regulates KLF5 in ceRNA and m6A Pathways to Inhibit the Progression of Osteoarthritis","authors":"Peng Jiang,&nbsp;Yuxuan Song,&nbsp;Pengfei Li,&nbsp;Yanhui Yang,&nbsp;Jiyang Zhang","doi":"10.1111/1756-185X.70035","DOIUrl":"10.1111/1756-185X.70035","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In the current study, IL-1β-induced C28/I2 cells were used to establish an in vitro model of OA. The expression of HCP5 in OA cartilage tissue and in the in vitro model of OA was detected by RT-qPCR. Cell viability and apoptosis were assessed by CCK-8 and Annexin V-PI double staining. Western blotting was employed to detect the protein expression of MMP-13 and aggrecan.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results showed that the findings suggested that HCP5 was downregulated in OA cartilage tissue and IL-1β-induced C28/I2 cells. HCP5 overexpression greatly enhanced IL-1β-induced proliferation of C28/I2 cells, as well as prevented cell apoptosis and degradation of extracellular matrix (ECM). Besides, we have shown that HCP5 is a ceRNA that regulates KLF5 by sponging miR-375. Furthermore, KLF5 is also regulated by m6A regulation induced by HCP5. Finally, overexpression of miR-375, the m6A modification inhibitor, as well as KLF5 inhibition reversed the impact of HCP5 on IL-1β-induced C28/I2 cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In summary, the present study demonstrated that the HCP5/KLF5 axis inhibited the progression of osteoarthritis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005442","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":"Analysis of related factors for systemic lupus erythematosus flare after SARS-Cov-2 infection: A retrospective cohort study","authors":"Qian Li,&nbsp;Jun-Kang Zhao,&nbsp;Jun-Yan Zhang,&nbsp;Rong Li,&nbsp;Li Zhao,&nbsp;Ya-Zhen Su,&nbsp;Yang Liu,&nbsp;Ke Xu,&nbsp;Li-Yun Zhang","doi":"10.1111/1756-185X.15407","DOIUrl":"10.1111/1756-185X.15407","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Since COVID-19 infections are more common in systemic lupus erythematosus (SLE) patients, most recent research has focused on the outcome of COVID-19, with fewer studies on disease activity in SLE. This research aims to evaluate flares in SLE with COVID-19 infection while investigating predictive factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A questionnaire survey was conducted to collect information on patients with previously diagnosed SLE from multi-center. SLE patients infected with COVID-19 after December 7, 2022, were selected. Detailed information covering demographic characteristics, SLE and COVID-19 clinical features, disease activity, and medication was collected through an electronic questionnaire. A multivariate logistic regression model was constructed to evaluate the predictive factors for SLE disease onset after COVID-19 infection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 240 patients were finally included in our analysis. Thirty (12.5%) of those enrolled reported an SLE flare. Multivariate analysis with logistic models confirmed that SLE in the active stage (OR 2.617, 95% CI 1.008–6.514, <i>p</i> = .041) and COVID-19 duration (OR 4.140, 95% CI 1.412–11.694, <i>p</i> = .008) were predictors for flare in SLE patients with Covid-19 infection. In contrast, immunosuppressants were associated with a low incidence of flare of SLE (OR 0.138, 95% CI 0.042–0.46, <i>p</i> = .005).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The active phase of SLE and the progression of COVID-19 were the main risk factors for disease exacerbation in SLE patients, while the use of immunosuppressive medications was associated with a lower risk of flare-ups. These findings provide valuable insights for managing SLE patients during the COVID-19 pandemic.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005357","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}