{"title":"Comment on: “Association of MUC5B Promoter Variant With Interstitial Lung Disease in Systemic Sclerosis”","authors":"Umut Bakay","doi":"10.1111/1756-185x.70474","DOIUrl":"10.1111/1756-185x.70474","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 11","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145512175","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}
Pin-Jiun Chen, Rou-Yi Chen, Su-Boon Yong, Chia-Jung Li
<p>Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in children, defined by persistent arthritis of unknown origin beginning before 16 years of age and classified into seven subtypes under the ILAR criteria [<span>1</span>]. Growth impairment is one of the most visible long-term complications, affecting both final height and developmental outcomes. The degree of impairment differs by subtype: children with systemic JIA are most vulnerable due to early onset, systemic inflammation, and prolonged disease activity. Enthesitis-related arthritis often allows near-normal growth, whereas polyarticular and extended oligoarticular subtypes show intermediate outcomes. Psoriatic and undifferentiated JIA follow more heterogeneous patterns, influenced more by inflammatory activity than the subtype itself [<span>2</span>].</p><p>Growth restriction in JIA is not merely a cosmetic concern. Short stature and impaired pubertal progression reflect disease burden, treatment toxicity, and systemic inflammation. These consequences extend into adulthood, influencing musculoskeletal development, function, and psychosocial well-being. Nationwide cohort data from Taiwan further demonstrated that JIA patients continue to face substantial disease burden and adverse outcomes in adulthood [<span>3</span>]. This reflects a broader paradigm of genetic and inflammatory interactions underlying long-term outcomes.</p><p>Growth impairment in JIA arises from complex interactions between chronic inflammation, treatment exposures, and nutritional status. Glucocorticoid exposure remains a central determinant. Cumulative dose and treatment duration correlate strongly with reduced height velocity and compromised adult stature [<span>4</span>]. Suppression of the GH–IGF-1 axis and direct skeletal toxicity explain much of this effect.</p><p>Inflammatory cytokines, particularly IL-6, disrupt growth through IGF-1 suppression and effects on growth plates. The persistence of systemic inflammation in uncontrolled JIA amplifies these mechanisms. Biologic therapies have improved outcomes by reducing inflammation and reducing steroid dependence. Anti-TNF therapy increases height velocity in severe cases [<span>5</span>], while IL-6 blockade with tocilizumab has been associated with catch-up growth and normalization of IGF-1, particularly when glucocorticoids are tapered [<span>6</span>].</p><p>Endocrine interventions with recombinant GH have demonstrated limited efficacy, and benefits are blunted by ongoing inflammation or persistent steroid exposure. Taken together, minimizing glucocorticoids, controlling systemic inflammation, and appropriately timing endocrine therapy are the mainstay strategies. Importantly, a multidisciplinary approach encompassing rheumatology, endocrinology, and nutrition appears essential to safeguard long-term growth trajectories.</p><p>Recent evidence has sharpened the epidemiological picture. A Taiwanese cohort demonstrated that early-ons
{"title":"Growth Impairment in Juvenile Idiopathic Arthritis: An Overlooked Therapeutic Target Introduction","authors":"Pin-Jiun Chen, Rou-Yi Chen, Su-Boon Yong, Chia-Jung Li","doi":"10.1111/1756-185x.70477","DOIUrl":"10.1111/1756-185x.70477","url":null,"abstract":"<p>Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic disease in children, defined by persistent arthritis of unknown origin beginning before 16 years of age and classified into seven subtypes under the ILAR criteria [<span>1</span>]. Growth impairment is one of the most visible long-term complications, affecting both final height and developmental outcomes. The degree of impairment differs by subtype: children with systemic JIA are most vulnerable due to early onset, systemic inflammation, and prolonged disease activity. Enthesitis-related arthritis often allows near-normal growth, whereas polyarticular and extended oligoarticular subtypes show intermediate outcomes. Psoriatic and undifferentiated JIA follow more heterogeneous patterns, influenced more by inflammatory activity than the subtype itself [<span>2</span>].</p><p>Growth restriction in JIA is not merely a cosmetic concern. Short stature and impaired pubertal progression reflect disease burden, treatment toxicity, and systemic inflammation. These consequences extend into adulthood, influencing musculoskeletal development, function, and psychosocial well-being. Nationwide cohort data from Taiwan further demonstrated that JIA patients continue to face substantial disease burden and adverse outcomes in adulthood [<span>3</span>]. This reflects a broader paradigm of genetic and inflammatory interactions underlying long-term outcomes.</p><p>Growth impairment in JIA arises from complex interactions between chronic inflammation, treatment exposures, and nutritional status. Glucocorticoid exposure remains a central determinant. Cumulative dose and treatment duration correlate strongly with reduced height velocity and compromised adult stature [<span>4</span>]. Suppression of the GH–IGF-1 axis and direct skeletal toxicity explain much of this effect.</p><p>Inflammatory cytokines, particularly IL-6, disrupt growth through IGF-1 suppression and effects on growth plates. The persistence of systemic inflammation in uncontrolled JIA amplifies these mechanisms. Biologic therapies have improved outcomes by reducing inflammation and reducing steroid dependence. Anti-TNF therapy increases height velocity in severe cases [<span>5</span>], while IL-6 blockade with tocilizumab has been associated with catch-up growth and normalization of IGF-1, particularly when glucocorticoids are tapered [<span>6</span>].</p><p>Endocrine interventions with recombinant GH have demonstrated limited efficacy, and benefits are blunted by ongoing inflammation or persistent steroid exposure. Taken together, minimizing glucocorticoids, controlling systemic inflammation, and appropriately timing endocrine therapy are the mainstay strategies. Importantly, a multidisciplinary approach encompassing rheumatology, endocrinology, and nutrition appears essential to safeguard long-term growth trajectories.</p><p>Recent evidence has sharpened the epidemiological picture. A Taiwanese cohort demonstrated that early-ons","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 11","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185x.70477","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145504449","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":"Letter to the Editor: “Identification of Causal Effects of Mitochondrial Dysfunction on the Risk of Multiple Autoimmune Disorders: Multi-Omics Mendelian Randomization and Colocalization Analyses”","authors":"Xiaohong Song","doi":"10.1111/1756-185x.70467","DOIUrl":"10.1111/1756-185x.70467","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 11","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145488636","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":"Sicca Complex in Different Autoimmune Diseases and Its Association With Anti-Centromere Antibody","authors":"Shih-Chi Chen, Lung-Fang Chen, Chien-Sheng Wu, Yu-Chuan Shen, Hui-Ching Hsu","doi":"10.1111/1756-185x.70465","DOIUrl":"10.1111/1756-185x.70465","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 11","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145488683","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}