Pub Date : 2025-09-17DOI: 10.1016/S2665-9913(25)00282-6
Talha Burki
{"title":"Enabling and supporting public and patient involvement in arthritis research.","authors":"Talha Burki","doi":"10.1016/S2665-9913(25)00282-6","DOIUrl":"https://doi.org/10.1016/S2665-9913(25)00282-6","url":null,"abstract":"","PeriodicalId":48540,"journal":{"name":"Lancet Rheumatology","volume":" ","pages":""},"PeriodicalIF":16.4,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-16DOI: 10.1016/S2665-9913(25)00105-5
<div><h3>Background</h3><div>Fractures related to osteoporosis and low bone mineral density lead to substantial morbidity, mortality, and cost to individuals and health systems. Here we present the most up-to-date global, regional, and national estimates of the contribution of low bone mineral density to the burden of fractures from falls and additional categories of injuries from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021.</div></div><div><h3>Methods</h3><div>The burden of low bone mineral density was estimated from 1990 to 2020 in terms of years lived with disability (YLDs), disability-adjusted life years (DALYs), and deaths, for individuals aged 40 years and older, using data from population-based studies from 48 countries or territories (169 unique sources). Mean standardised femoral neck bone mineral density values were estimated by GBD location, age, and sex by meta-regression. Based on a separate meta-analysis of population-based studies from nine countries (12 unique sources), we also estimated the pooled relative risk of fractures per unit decrease in bone mineral density (g/cm<sup>2</sup>). The population-attributable fraction for low bone mineral density was calculated by comparing the observed distributions of standardised femoral neck bone mineral density to an age-specific and sex-specific counterfactual distribution, defined as the 99th percentile of five rounds of the National Health and Nutrition Examination Survey in the USA, by 5-year age group and sex. Hospital and emergency department data were used to derive the incidence of fractures for six categories of injury (road injuries, other transport injuries, falls, non-venomous animal contact, exposure to mechanical forces, and physical interpersonal violence) using ICD codes. Deaths due to fractures were estimated as the proportion of in-hospital deaths due to the specified injury causes for which a fracture (nature of injury code) was more severe than the cause of injury code. YLDs and DALYs attributable to low bone mineral density by cause of injury were also determined according to previous GBD methods.</div></div><div><h3>Findings</h3><div>In 2020, 8·32 million (95% UI 5·58–10·84) YLDs, 17·2 million (14·1–20·2) DALYs, and 477 000 (411 000–536 000) deaths were attributable to low bone mineral density globally in individuals aged 40 years and older. Between 1990 and 2020, global YLDs, DALYs, and deaths attributable to low bone mineral density increased by 91·8% (88·5–95·1), 89·8% (81·5–99·0), and 127·1% (108·5–144·5), respectively. Over this period, the age-standardised global rates of YLDs, DALYs, and deaths attributable to low bone mineral density showed modest decreases. In 2020, falls accounted for 76·2% (95% UI 74·2–78·3) of YLDs, 65·2% (62·9–67·6) of DALYs, and 71·0% (67·4–72·8) of deaths attributable to low bone mineral density, and road injuries largely accounted for the remaining amount: 12·4% (11·1–13·6) of YLDs, 24·6% (22·5–27·1) of
{"title":"The global, regional, and national burden attributable to low bone mineral density, 1990–2020: an analysis of a modifiable risk factor from the Global Burden of Disease Study 2021","authors":"","doi":"10.1016/S2665-9913(25)00105-5","DOIUrl":"10.1016/S2665-9913(25)00105-5","url":null,"abstract":"<div><h3>Background</h3><div>Fractures related to osteoporosis and low bone mineral density lead to substantial morbidity, mortality, and cost to individuals and health systems. Here we present the most up-to-date global, regional, and national estimates of the contribution of low bone mineral density to the burden of fractures from falls and additional categories of injuries from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021.</div></div><div><h3>Methods</h3><div>The burden of low bone mineral density was estimated from 1990 to 2020 in terms of years lived with disability (YLDs), disability-adjusted life years (DALYs), and deaths, for individuals aged 40 years and older, using data from population-based studies from 48 countries or territories (169 unique sources). Mean standardised femoral neck bone mineral density values were estimated by GBD location, age, and sex by meta-regression. Based on a separate meta-analysis of population-based studies from nine countries (12 unique sources), we also estimated the pooled relative risk of fractures per unit decrease in bone mineral density (g/cm<sup>2</sup>). The population-attributable fraction for low bone mineral density was calculated by comparing the observed distributions of standardised femoral neck bone mineral density to an age-specific and sex-specific counterfactual distribution, defined as the 99th percentile of five rounds of the National Health and Nutrition Examination Survey in the USA, by 5-year age group and sex. Hospital and emergency department data were used to derive the incidence of fractures for six categories of injury (road injuries, other transport injuries, falls, non-venomous animal contact, exposure to mechanical forces, and physical interpersonal violence) using ICD codes. Deaths due to fractures were estimated as the proportion of in-hospital deaths due to the specified injury causes for which a fracture (nature of injury code) was more severe than the cause of injury code. YLDs and DALYs attributable to low bone mineral density by cause of injury were also determined according to previous GBD methods.</div></div><div><h3>Findings</h3><div>In 2020, 8·32 million (95% UI 5·58–10·84) YLDs, 17·2 million (14·1–20·2) DALYs, and 477 000 (411 000–536 000) deaths were attributable to low bone mineral density globally in individuals aged 40 years and older. Between 1990 and 2020, global YLDs, DALYs, and deaths attributable to low bone mineral density increased by 91·8% (88·5–95·1), 89·8% (81·5–99·0), and 127·1% (108·5–144·5), respectively. Over this period, the age-standardised global rates of YLDs, DALYs, and deaths attributable to low bone mineral density showed modest decreases. In 2020, falls accounted for 76·2% (95% UI 74·2–78·3) of YLDs, 65·2% (62·9–67·6) of DALYs, and 71·0% (67·4–72·8) of deaths attributable to low bone mineral density, and road injuries largely accounted for the remaining amount: 12·4% (11·1–13·6) of YLDs, 24·6% (22·5–27·1) of ","PeriodicalId":48540,"journal":{"name":"Lancet Rheumatology","volume":"7 12","pages":"Pages e873-e894"},"PeriodicalIF":16.4,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-04DOI: 10.1016/S2665-9913(25)00165-1
Edoardo Cipolletta PhD , Georgina Nakafero PhD , Davide Rozza PhD , Satveer K Mahil PhD , Prof Catherine H Smith PhD , Prof Richard D Riley PhD , Prof Abhishek Abhishek PhD
<div><h3>Background</h3><div>Allopurinol, the most prescribed urate-lowering drug, is a known cause of severe cutaneous adverse reactions. We aimed to develop and validate a model to assess the risk of allopurinol-induced severe cutaneous adverse reactions in adults newly prescribed allopurinol.</div></div><div><h3>Methods</h3><div>In this retrospective new-user cohort study, we developed and validated a prognostic model using primary care, hospitalisation, and mortality data extracted from the UK Clinical Practice Research Datalink (CPRD) primary care database, for the period Jan 1, 2001, to March 29, 2021. Data from CPRD Aurum was used for model development and data from and CPRD GOLD was used for model validation. Adults (aged ≥18 years) residing in England who were newly prescribed allopurinol were followed up for 100 days to assess whether a severe cutaneous adverse reaction was recorded in hospitalisation or mortality records. Risk predictors included in the model were age, sex, ethnicity, chronic kidney disease stage, initial allopurinol dose, ischaemic heart disease, and heart failure. The primary outcome was to predict the 100-day risk of allopurinol-induced severe cutaneous adverse reactions in people newly prescribed allopurinol. We developed the model using multivariable Cox regression and pseudo-values, followed by penalisation and external validation. We assessed calibration, discrimination, and clinical utility in the risk range of 0·0001 to 0·003. People with lived experience of allopurinol use or gout were not involved in developing this research question, but will be involved in the dissemination of results.</div></div><div><h3>Findings</h3><div>225 761 patients newly prescribed allopurinol were registered in the CPRD Aurum database (development cohort) and 173 812 were included in the study. 44 630 (25·7%) of 173 812 patients were female, 129 182 (74·3%) were male, 154 323 (88·8%) were White, and the mean age was 63·9 years (SD 15·0). Of the patients newly prescribed allopurinol with data in the CPRD GOLD database (validation cohort), 55 395 patients were screened and 41 610 were included in the study. 10 829 (26·0%) of 41 610 patients were female, 30 781 (74·0%) were male, 37 242 (89·5%) were White and the mean age was 64·4 years (SD 14·9). 63 (0·04%) severe cutaneous adverse events occurred in 173 812 patients in the development cohort and 16 (0·04%) occurred in 41 610 patients in the validation cohort. Age (adjusted hazard ratio 1·03 [95% CI 1·01–1·06]), chronic kidney disease stages 3, 4, and 5 (2·24 [1·20–4·17] for stage 3; 6·65 [2·90–15·23] for stage 4; 18·85 [6·32–56·19] for stage 5), initial allopurinol dose of 300 mg or higher (5·99 [3·56–0·08]), South Asian ethnicity (5·35 [2·37–12·07]), and other Asian ethnicity (5·63 [1·34–23·61]) were associated with the 100-day risk of allopurinol-induced severe cutaneous adverse reactions. In the development dataset, after optimism-adjustment, the model's explained variation (Roy
{"title":"Development and validation of a prognostic model for predicting the risk of allopurinol-induced severe cutaneous adverse reactions: a retrospective new-user cohort study using linked primary care, hospitalisation, and mortality data","authors":"Edoardo Cipolletta PhD , Georgina Nakafero PhD , Davide Rozza PhD , Satveer K Mahil PhD , Prof Catherine H Smith PhD , Prof Richard D Riley PhD , Prof Abhishek Abhishek PhD","doi":"10.1016/S2665-9913(25)00165-1","DOIUrl":"10.1016/S2665-9913(25)00165-1","url":null,"abstract":"<div><h3>Background</h3><div>Allopurinol, the most prescribed urate-lowering drug, is a known cause of severe cutaneous adverse reactions. We aimed to develop and validate a model to assess the risk of allopurinol-induced severe cutaneous adverse reactions in adults newly prescribed allopurinol.</div></div><div><h3>Methods</h3><div>In this retrospective new-user cohort study, we developed and validated a prognostic model using primary care, hospitalisation, and mortality data extracted from the UK Clinical Practice Research Datalink (CPRD) primary care database, for the period Jan 1, 2001, to March 29, 2021. Data from CPRD Aurum was used for model development and data from and CPRD GOLD was used for model validation. Adults (aged ≥18 years) residing in England who were newly prescribed allopurinol were followed up for 100 days to assess whether a severe cutaneous adverse reaction was recorded in hospitalisation or mortality records. Risk predictors included in the model were age, sex, ethnicity, chronic kidney disease stage, initial allopurinol dose, ischaemic heart disease, and heart failure. The primary outcome was to predict the 100-day risk of allopurinol-induced severe cutaneous adverse reactions in people newly prescribed allopurinol. We developed the model using multivariable Cox regression and pseudo-values, followed by penalisation and external validation. We assessed calibration, discrimination, and clinical utility in the risk range of 0·0001 to 0·003. People with lived experience of allopurinol use or gout were not involved in developing this research question, but will be involved in the dissemination of results.</div></div><div><h3>Findings</h3><div>225 761 patients newly prescribed allopurinol were registered in the CPRD Aurum database (development cohort) and 173 812 were included in the study. 44 630 (25·7%) of 173 812 patients were female, 129 182 (74·3%) were male, 154 323 (88·8%) were White, and the mean age was 63·9 years (SD 15·0). Of the patients newly prescribed allopurinol with data in the CPRD GOLD database (validation cohort), 55 395 patients were screened and 41 610 were included in the study. 10 829 (26·0%) of 41 610 patients were female, 30 781 (74·0%) were male, 37 242 (89·5%) were White and the mean age was 64·4 years (SD 14·9). 63 (0·04%) severe cutaneous adverse events occurred in 173 812 patients in the development cohort and 16 (0·04%) occurred in 41 610 patients in the validation cohort. Age (adjusted hazard ratio 1·03 [95% CI 1·01–1·06]), chronic kidney disease stages 3, 4, and 5 (2·24 [1·20–4·17] for stage 3; 6·65 [2·90–15·23] for stage 4; 18·85 [6·32–56·19] for stage 5), initial allopurinol dose of 300 mg or higher (5·99 [3·56–0·08]), South Asian ethnicity (5·35 [2·37–12·07]), and other Asian ethnicity (5·63 [1·34–23·61]) were associated with the 100-day risk of allopurinol-induced severe cutaneous adverse reactions. In the development dataset, after optimism-adjustment, the model's explained variation (Roy","PeriodicalId":48540,"journal":{"name":"Lancet Rheumatology","volume":"7 12","pages":"Pages e840-e850"},"PeriodicalIF":16.4,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vacuoles, E1 enzyme, X-linked, autoinflammatory, and somatic (VEXAS) syndrome is a newly identified disorder caused by an acquired monogenic somatic UBA1 gene mutation, affecting nuclear and cytoplasmic ubiquitination. This mutation triggers immune dysregulation, leading to diverse clinical and pathological features resembling inflammatory rheumatic diseases. Blood abnormalities stem from myeloid precursor dysfunction, presenting as elevated concentrations of inflammatory markers and cytokines, leukopenia, and macrocytosis. These abnormalities can lead to inflammatory arthritis, vasculitis, polychondritis, thrombosis, and connective tissue disease-like syndromes. This Review explores the clinical and mechanistic links between VEXAS syndrome and rheumatic diseases, offering guidance on current best management strategies. Although rare, VEXAS syndrome has high morbidity and mortality, providing valuable insights into how genetic mutations drive immune system activation and rheumatic disease development.
{"title":"VEXAS syndrome and immune-mediated rheumatic diseases: overlaps in clinical features and mechanisms","authors":"Arvind Kaul PhD , Adam Al-Hakim MRCP , Prof Helen Lachmann FMedSci , Austin Kulasekararaj MD , Prof Sinisa Savic PhD","doi":"10.1016/S2665-9913(25)00197-3","DOIUrl":"10.1016/S2665-9913(25)00197-3","url":null,"abstract":"<div><div>Vacuoles, E1 enzyme, X-linked, autoinflammatory, and somatic (VEXAS) syndrome is a newly identified disorder caused by an acquired monogenic somatic <em>UBA1</em> gene mutation, affecting nuclear and cytoplasmic ubiquitination. This mutation triggers immune dysregulation, leading to diverse clinical and pathological features resembling inflammatory rheumatic diseases. Blood abnormalities stem from myeloid precursor dysfunction, presenting as elevated concentrations of inflammatory markers and cytokines, leukopenia, and macrocytosis. These abnormalities can lead to inflammatory arthritis, vasculitis, polychondritis, thrombosis, and connective tissue disease-like syndromes. This Review explores the clinical and mechanistic links between VEXAS syndrome and rheumatic diseases, offering guidance on current best management strategies. Although rare, VEXAS syndrome has high morbidity and mortality, providing valuable insights into how genetic mutations drive immune system activation and rheumatic disease development.</div></div>","PeriodicalId":48540,"journal":{"name":"Lancet Rheumatology","volume":"7 10","pages":"Pages e719-e733"},"PeriodicalIF":16.4,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-04DOI: 10.1016/S2665-9913(25)00153-5
Venkatesh Krishnan PhD , Stuart Y Keller BSc , Christine Chew PhD , Jonathan T Sims PhD , Ching-Yun Chang PhD , Ernst R Dow PhD , Robert J Benschop PhD , Rona Wang MD , Prof Athimalaipet V Ramanan FMedSci
<div><h3>Background</h3><div>Baricitinib has previously been shown to improve clinical response in patients with juvenile idiopathic arthritis (JIA) in the JUVE-BASIS trial. In this post-hoc analysis we aimed to identify whether pharmacodynamic changes in serum biomarkers in response to baricitinib treatment could help reaffirm the clinical utility of baricitinib in patients with JIA.</div></div><div><h3>Methods</h3><div>JUVE-BASIS was a randomised, double-blind, placebo-controlled, withdrawal, efficacy, safety, phase 3 trial, done in 75 centres in 20 countries. Eligible patients were children and adolescents (aged 2 to <18 years), with polyarticular JIA (positive or negative for rheumatoid factor), extended oligoarticular JIA, enthesitis-related arthritis, or juvenile psoriatic arthritis, as per the International League of Associations for Rheumatology criteria and an inadequate response (≥12 weeks) or intolerance to one or more conventional synthetic or biological disease-modifying antirheumatic drugs (DMARDs). Here we report post-hoc analyses of serum samples from patients who received open-label baricitinib in the 12-week lead-in period of the JUVE-BASIS trial. Samples were assessed using an Olink Explore 3072 panel at baseline and week 12. Baricitinib-mediated pharmacodynamic changes in serum protein markers were measured as changes from baseline to week 12 derived from a mixed model with repeated measurement. Pearson correlations of the change in serum biomarkers and clinical disease activity (JADAS-27 scores) comparing baseline with week 12 were examined. Proportional changes in biomarkers were classified into three response subsets based on JIA-ACR response rates: JIA-ACR <30% (non-responders), JIA-ACR 30–70% (responders), and JIA-ACR 70–100% (super-responders). People with lived experience of JIA were not involved in the design or conduct of this study. The JUVE-BASIS trial was registered with <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span>, <span><span>NCT03773978</span><svg><path></path></svg></span>, and is completed.</div></div><div><h3>Findings</h3><div>Between Dec 17, 2018 and March 3, 2021, 220 patients were enrolled in JUVE-BASIS and received at least one dose of baricitinib in the open-label lead-in period. In this post-hoc analysis, 168 serum samples from 84 patients were analysed: 67 (80%) of 84 patients were female, 17 (20%) were male, 67 (80%) were White and the mean age was 14 years (SD 2). 10 (12%) of 84 were non-responders, 27 (32%) were responders, and 47 (56%) were super-responders based on clinical response. Several serum biomarkers showed significant changes following 12 weeks of baricitinib treatment for all patients with higher magnitude changes seen in responders and super-responders. Changes in biomarkers associated with macrophage activation (CCL7, CCL18, and IL-6) and regulation of matrix composition (matrix metalloproteinase-3) were positively correlated with clinical response.</div><
背景：Baricitinib先前在JUVE-BASIS试验中被证明可以改善幼年特发性关节炎（JIA）患者的临床反应。在这项事后分析中，我们旨在确定baricitinib治疗后血清生物标志物的药效学变化是否有助于重申baricitinib在JIA患者中的临床应用。方法：JUVE-BASIS是一项随机、双盲、安慰剂对照、停药、疗效、安全性的3期试验，在20个国家的75个中心进行。研究结果：在2018年12月17日至2021年3月3日期间，220名患者入组juv - basis，并在开放标签导入期间接受了至少一剂巴西替尼。在这项事后分析中，分析了84例患者的168份血清样本：84例患者中67例（80%）为女性，17例（20%）为男性，67例（80%）为白人，平均年龄为14岁（SD 2）。84例患者中10例（12%）为无反应者，27例（32%）为反应者，47例（56%）为基于临床反应的超反应者。baricitinib治疗12周后，所有患者的几种血清生物标志物均出现显著变化，反应者和超反应者的变化幅度较大。与巨噬细胞活化相关的生物标志物（CCL7、CCL18和IL-6）和基质组成调节（基质金属蛋白酶-3）的变化与临床反应呈正相关。解释：据我们所知，这是首次在baricitinib对JIA患者进行干预试验的背景下测量血清蛋白标志物的研究。与临床反应相关的生物标志物变化可能允许医生潜在地识别最有可能对巴西替尼治疗有反应的患者。融资：礼来公司（Eli Lilly and Company）获得Incyte许可。
{"title":"Serum biomarkers associated with baricitinib response in patients with juvenile idiopathic arthritis: a post-hoc analysis of the phase 3 JUVE-BASIS trial","authors":"Venkatesh Krishnan PhD , Stuart Y Keller BSc , Christine Chew PhD , Jonathan T Sims PhD , Ching-Yun Chang PhD , Ernst R Dow PhD , Robert J Benschop PhD , Rona Wang MD , Prof Athimalaipet V Ramanan FMedSci","doi":"10.1016/S2665-9913(25)00153-5","DOIUrl":"10.1016/S2665-9913(25)00153-5","url":null,"abstract":"<div><h3>Background</h3><div>Baricitinib has previously been shown to improve clinical response in patients with juvenile idiopathic arthritis (JIA) in the JUVE-BASIS trial. In this post-hoc analysis we aimed to identify whether pharmacodynamic changes in serum biomarkers in response to baricitinib treatment could help reaffirm the clinical utility of baricitinib in patients with JIA.</div></div><div><h3>Methods</h3><div>JUVE-BASIS was a randomised, double-blind, placebo-controlled, withdrawal, efficacy, safety, phase 3 trial, done in 75 centres in 20 countries. Eligible patients were children and adolescents (aged 2 to <18 years), with polyarticular JIA (positive or negative for rheumatoid factor), extended oligoarticular JIA, enthesitis-related arthritis, or juvenile psoriatic arthritis, as per the International League of Associations for Rheumatology criteria and an inadequate response (≥12 weeks) or intolerance to one or more conventional synthetic or biological disease-modifying antirheumatic drugs (DMARDs). Here we report post-hoc analyses of serum samples from patients who received open-label baricitinib in the 12-week lead-in period of the JUVE-BASIS trial. Samples were assessed using an Olink Explore 3072 panel at baseline and week 12. Baricitinib-mediated pharmacodynamic changes in serum protein markers were measured as changes from baseline to week 12 derived from a mixed model with repeated measurement. Pearson correlations of the change in serum biomarkers and clinical disease activity (JADAS-27 scores) comparing baseline with week 12 were examined. Proportional changes in biomarkers were classified into three response subsets based on JIA-ACR response rates: JIA-ACR <30% (non-responders), JIA-ACR 30–70% (responders), and JIA-ACR 70–100% (super-responders). People with lived experience of JIA were not involved in the design or conduct of this study. The JUVE-BASIS trial was registered with <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span>, <span><span>NCT03773978</span><svg><path></path></svg></span>, and is completed.</div></div><div><h3>Findings</h3><div>Between Dec 17, 2018 and March 3, 2021, 220 patients were enrolled in JUVE-BASIS and received at least one dose of baricitinib in the open-label lead-in period. In this post-hoc analysis, 168 serum samples from 84 patients were analysed: 67 (80%) of 84 patients were female, 17 (20%) were male, 67 (80%) were White and the mean age was 14 years (SD 2). 10 (12%) of 84 were non-responders, 27 (32%) were responders, and 47 (56%) were super-responders based on clinical response. Several serum biomarkers showed significant changes following 12 weeks of baricitinib treatment for all patients with higher magnitude changes seen in responders and super-responders. Changes in biomarkers associated with macrophage activation (CCL7, CCL18, and IL-6) and regulation of matrix composition (matrix metalloproteinase-3) were positively correlated with clinical response.</div><","PeriodicalId":48540,"journal":{"name":"Lancet Rheumatology","volume":"7 11","pages":"Pages e799-e807"},"PeriodicalIF":16.4,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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