{"title":"Commentary on: “Nationwide temporal trends in adverse pregnancy outcomes and treatments in systemic lupus erythematosus pregnancy over two decades in Sweden”","authors":"Maria I. Zervou, George N. Goulielmos","doi":"10.1002/art.70155","DOIUrl":"https://doi.org/10.1002/art.70155","url":null,"abstract":"Click on the article title to read more.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"183 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147506779","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}
Jose U Scher, Iain B McInnes, Enrique R Soriano, Joseph F Merola, Paul Bird, Vinod Chandran, Edaire Cheng, Elena Reynoso, Warner Chen, Maoji Li, Lianne S Gensler, Philip J Mease, Christopher T Ritchlin
Assess guselkumab+golimumab combination versus guselkumab monotherapy in participants with active PsA and inadequate response to tumor necrosis factor inhibitors (TNFi-IR).
{"title":"Combination Therapy in Participants With Active Psoriatic Arthritis Using Subcutaneous Guselkumab and Golimumab: Week 24 Results From the Phase 2a, Multicenter, Randomized, Double-Blind, Proof-of-Concept AFFINITY Study","authors":"Jose U Scher, Iain B McInnes, Enrique R Soriano, Joseph F Merola, Paul Bird, Vinod Chandran, Edaire Cheng, Elena Reynoso, Warner Chen, Maoji Li, Lianne S Gensler, Philip J Mease, Christopher T Ritchlin","doi":"10.1002/art.70152","DOIUrl":"https://doi.org/10.1002/art.70152","url":null,"abstract":"Assess guselkumab+golimumab combination versus guselkumab monotherapy in participants with active PsA and inadequate response to tumor necrosis factor inhibitors (TNFi-IR).","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"49 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147506777","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}
Jeffrey B. Driban, Lisa B. Rokoff, Bing Lu, Timothy E. McAlindon, Charles B. Eaton, Mary B. Roberts, Diana Mathes, Colleen Lestician, Zhijin Carrie Xu, Zhihua Tina Fan, Shawn P. O'Leary, Ida K. Haugen, Jérémie Sellam, Alice Courties, Abby F. Fleisch
To examine whether concentrations of specific per- and polyfluoroalkyl substances (PFAS) and a mixture of PFAS relate to incident knee osteoarthritis (KOA) and knee pain progression.
{"title":"Per- and polyfluoroalkyl substances and knee osteoarthritis: data from the Osteoarthritis Initiative","authors":"Jeffrey B. Driban, Lisa B. Rokoff, Bing Lu, Timothy E. McAlindon, Charles B. Eaton, Mary B. Roberts, Diana Mathes, Colleen Lestician, Zhijin Carrie Xu, Zhihua Tina Fan, Shawn P. O'Leary, Ida K. Haugen, Jérémie Sellam, Alice Courties, Abby F. Fleisch","doi":"10.1002/art.70154","DOIUrl":"https://doi.org/10.1002/art.70154","url":null,"abstract":"To examine whether concentrations of specific per- and polyfluoroalkyl substances (PFAS) and a mixture of PFAS relate to incident knee osteoarthritis (KOA) and knee pain progression.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"44 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147506778","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}
OBJECTIVETo investigate the genetic architecture of low-frequency and rare variants of serum urate (SU) in East Asian populations, aiming to clarify its role as a heritable and modifiable risk factor for gout and cardiometabolic diseases.METHODSWe conducted the largest two-stage, whole-genomes sequencing-based, genome-wide scan for SU levels in East Asians, analyzing 9.1 million variants across 7,339 Han Chinese participants from the Healthy Zhejiang One Million People (HOPE) cohort.RESULTSWe verified associations at common and low-frequency loci and identified a novel, replicable male-specific locus at MAN1A2, along with a candidate low-frequency male-specific locus at CPE. Furthermore, using STAARpipeline framework, we probed rare missense and putative loss-of-function variant aggregates in genes such as SLC22A12, SLC2A9, and G6PC2, which were validated in our replication dataset or the UK Biobank. Moreover, we identified and replicated novel associations with rare promoter variants near HDC and SLC22A12, highlighting their potential role in the context of non-coding regulation. Additionally, deep learning-based fine-mapping revealed transcription factors such as HNF1A, RUNX1 and SRF as potential up-regulators of SU-associated genes.CONCLUSIONBy resolving East Asian-specific allelic architecture and revealing ancestral diversity in SU genetics, this study advanced translational opportunities for precision urate-lowering therapies and prioritizes novel candidates for future research.
{"title":"Identification of Novel Non-coding Genetic Variants of Serum Urate Using Whole Genome Sequencing in 7,339 Chinese.","authors":"Qilong Tan,Hanyi Zhou,Junlin Jia,Jiameng Cui,Liyang Sun,Weifang Zheng,Huakang Tu,Xiaohang Xu,Mengying Wang,Dan Zhou,Wenyuan Li,Xifeng Wu","doi":"10.1002/art.70150","DOIUrl":"https://doi.org/10.1002/art.70150","url":null,"abstract":"OBJECTIVETo investigate the genetic architecture of low-frequency and rare variants of serum urate (SU) in East Asian populations, aiming to clarify its role as a heritable and modifiable risk factor for gout and cardiometabolic diseases.METHODSWe conducted the largest two-stage, whole-genomes sequencing-based, genome-wide scan for SU levels in East Asians, analyzing 9.1 million variants across 7,339 Han Chinese participants from the Healthy Zhejiang One Million People (HOPE) cohort.RESULTSWe verified associations at common and low-frequency loci and identified a novel, replicable male-specific locus at MAN1A2, along with a candidate low-frequency male-specific locus at CPE. Furthermore, using STAARpipeline framework, we probed rare missense and putative loss-of-function variant aggregates in genes such as SLC22A12, SLC2A9, and G6PC2, which were validated in our replication dataset or the UK Biobank. Moreover, we identified and replicated novel associations with rare promoter variants near HDC and SLC22A12, highlighting their potential role in the context of non-coding regulation. Additionally, deep learning-based fine-mapping revealed transcription factors such as HNF1A, RUNX1 and SRF as potential up-regulators of SU-associated genes.CONCLUSIONBy resolving East Asian-specific allelic architecture and revealing ancestral diversity in SU genetics, this study advanced translational opportunities for precision urate-lowering therapies and prioritizes novel candidates for future research.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"15 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147502158","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}
Manar Elsayed,Zoe Hsu,Finlay A McAlister,William D Leslie,Lisa M Lix,Sasha Bernatsky,Suzanne N Morin,Michelle M Graham,Aurore Fifi-Mah,Shahin Jamal,Janet Roberts,Carrie Ye
BACKGROUNDImmune checkpoint inhibitors (ICIs) for cancer can lead to immune-related adverse events, including ICI-associated inflammatory arthritis (ICI-IA). There are no validated International Classification of Diseases (ICD) code-based case definitions for ICI-IA.METHODSWe conducted a validation study using the Canadian Research Group of Rheumatology in Immuno-Oncology (CanRIO) database. Rheumatologist-confirmed ICI-IA was the reference standard, defined as new onset of at least one swollen joint on exam or synovitis on imaging following ICI exposure, without another cause or pre-existing IA. We compared ICD-9 (714.x and 696.0) and ICD-10 (M05.x, M06.x, and M07.x) IA diagnostic codes, against the reference standard. Seven core case definitions of different combinations of ICD codes from the physician claims database (PCD) and the discharge abstract database (DAD) were tested. Results were stratified by sex. Sensitivity testing with additional criteria were also evaluated.RESULTSWe included 228 patients in the final analysis: 100 with ICI-IA and 128 without ICI-IA. Sensitivity of the tested case definitions ranged from 1.0% to 88.0%, while specificity ranged from 86.7% to 100.0%. The case definition with ≥1 PCD IA code achieved the best balance of sensitivity (88.0%, 95% confidence interval [CI]: 81.6%, 94.4%) and specificity (86.7%, 95% CI: 80.8%, 92.6%). Case definition performances were similar between sexes. Additional criteria minimally improved specificity, but sacrificed sensitivity.CONCLUSIONICD code-based case definitions of ICI-IA can accurately detect ICI-IA and can be used to support ICI-IA surveillance and research with administrative health data.
{"title":"Validation of International Classification of Diseases (ICD) code-based case definitions of immune checkpoint inhibitor associated inflammatory arthritis from administrative health data.","authors":"Manar Elsayed,Zoe Hsu,Finlay A McAlister,William D Leslie,Lisa M Lix,Sasha Bernatsky,Suzanne N Morin,Michelle M Graham,Aurore Fifi-Mah,Shahin Jamal,Janet Roberts,Carrie Ye","doi":"10.1002/art.70149","DOIUrl":"https://doi.org/10.1002/art.70149","url":null,"abstract":"BACKGROUNDImmune checkpoint inhibitors (ICIs) for cancer can lead to immune-related adverse events, including ICI-associated inflammatory arthritis (ICI-IA). There are no validated International Classification of Diseases (ICD) code-based case definitions for ICI-IA.METHODSWe conducted a validation study using the Canadian Research Group of Rheumatology in Immuno-Oncology (CanRIO) database. Rheumatologist-confirmed ICI-IA was the reference standard, defined as new onset of at least one swollen joint on exam or synovitis on imaging following ICI exposure, without another cause or pre-existing IA. We compared ICD-9 (714.x and 696.0) and ICD-10 (M05.x, M06.x, and M07.x) IA diagnostic codes, against the reference standard. Seven core case definitions of different combinations of ICD codes from the physician claims database (PCD) and the discharge abstract database (DAD) were tested. Results were stratified by sex. Sensitivity testing with additional criteria were also evaluated.RESULTSWe included 228 patients in the final analysis: 100 with ICI-IA and 128 without ICI-IA. Sensitivity of the tested case definitions ranged from 1.0% to 88.0%, while specificity ranged from 86.7% to 100.0%. The case definition with ≥1 PCD IA code achieved the best balance of sensitivity (88.0%, 95% confidence interval [CI]: 81.6%, 94.4%) and specificity (86.7%, 95% CI: 80.8%, 92.6%). Case definition performances were similar between sexes. Additional criteria minimally improved specificity, but sacrificed sensitivity.CONCLUSIONICD code-based case definitions of ICI-IA can accurately detect ICI-IA and can be used to support ICI-IA surveillance and research with administrative health data.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"1 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147495019","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}
OBJECTIVEBaricitinib is a JAK1 inhibitor that showed efficacy in patients with systemic lupus erythematosus (SLE) in a phase 2 study, but failed to meet the primary endpoint in phase 3 trials. To understand this discrepancy and identify SLE patients responsive to baricitinib, we carried out baseline and longitudinal transcriptomic analysis in patients enrolled in the phase 2 trial.METHODSWhole blood samples from 272 SLE patients were analyzed. Clinical response was assessed using SLE Responder Index-4 (SRI-4) after 24 weeks of placebo or baricitinib (2 or 4 mg daily). Gene expression profiling was carried out using Gene Set Variation Analysis (GSVA) of 32 immune-related gene modules.RESULTSEight distinct molecular endotypes (A-H) were identified from baseline GSVA scores, with progressively increasing immune disturbances. Baseline demographics were similar across endotypes, with modest but significant differences in anti-dsDNA and complement levels, but no SLEDAI differences. Significant clinical responses to baricitinib were confined to endotypes D and G (p=0.004 and 0.048 vs placebo, with effect sizes of 41.54% and 31.89% respectively). Importantly, patient clustering based on clinical features failed to identify treatment-responsive subsets. Endotype G demonstrated the most pronounced treatment-related transcriptional modulation, with dose-dependent suppression of interferon, JAK1/JAK2/TYK2 signaling, immunoproteasome and inflammatory pathways evident as early as week 2 and sustained through week 24. Transcriptional changes in response to baricitinib were largely confined to clinical responders in endotype G. Feature importance analysis identified the interferon and Treg signatures as major predictors of response.CONCLUSIONTranscriptomic analysis identified SLE patient subsets responsive to baricitinib.
{"title":"Subsets of Lupus Patients Identified by Gene Expression Profiles Exhibit Differential Clinical Responsiveness to Baricitinib.","authors":"Prathyusha Bachali,Amrie Grammer,Peter E Lipsky","doi":"10.1002/art.70130","DOIUrl":"https://doi.org/10.1002/art.70130","url":null,"abstract":"OBJECTIVEBaricitinib is a JAK1 inhibitor that showed efficacy in patients with systemic lupus erythematosus (SLE) in a phase 2 study, but failed to meet the primary endpoint in phase 3 trials. To understand this discrepancy and identify SLE patients responsive to baricitinib, we carried out baseline and longitudinal transcriptomic analysis in patients enrolled in the phase 2 trial.METHODSWhole blood samples from 272 SLE patients were analyzed. Clinical response was assessed using SLE Responder Index-4 (SRI-4) after 24 weeks of placebo or baricitinib (2 or 4 mg daily). Gene expression profiling was carried out using Gene Set Variation Analysis (GSVA) of 32 immune-related gene modules.RESULTSEight distinct molecular endotypes (A-H) were identified from baseline GSVA scores, with progressively increasing immune disturbances. Baseline demographics were similar across endotypes, with modest but significant differences in anti-dsDNA and complement levels, but no SLEDAI differences. Significant clinical responses to baricitinib were confined to endotypes D and G (p=0.004 and 0.048 vs placebo, with effect sizes of 41.54% and 31.89% respectively). Importantly, patient clustering based on clinical features failed to identify treatment-responsive subsets. Endotype G demonstrated the most pronounced treatment-related transcriptional modulation, with dose-dependent suppression of interferon, JAK1/JAK2/TYK2 signaling, immunoproteasome and inflammatory pathways evident as early as week 2 and sustained through week 24. Transcriptional changes in response to baricitinib were largely confined to clinical responders in endotype G. Feature importance analysis identified the interferon and Treg signatures as major predictors of response.CONCLUSIONTranscriptomic analysis identified SLE patient subsets responsive to baricitinib.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"16 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147495018","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}
{"title":"Reply to Comment on \"Interstitial Lung Disease in ANCA-Associated Vasculitis: A European Multicentre Study\".","authors":"Aglaia Chalkia,David Jayne","doi":"10.1002/art.70140","DOIUrl":"https://doi.org/10.1002/art.70140","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"3 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483738","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}
Pankti Mehta, Shangyi Gao, Virginia Carrizo Abarza, Fadi Kharouf, Daniel Pereira, Richard J. Cook, Dafna D. Gladman, Vinod Chandran, Denis Poddubnyy
To examine the association between radiographic structural damage and physical function (PF) in psoriatic arthritis (PsA).
探讨银屑病关节炎（PsA）影像学结构损伤与身体功能（PF）的关系。
{"title":"Functional Impact of Structural Damage in Psoriatic Arthritis: Insights from a Prospective Cohort Study","authors":"Pankti Mehta, Shangyi Gao, Virginia Carrizo Abarza, Fadi Kharouf, Daniel Pereira, Richard J. Cook, Dafna D. Gladman, Vinod Chandran, Denis Poddubnyy","doi":"10.1002/art.70145","DOIUrl":"https://doi.org/10.1002/art.70145","url":null,"abstract":"To examine the association between radiographic structural damage and physical function (PF) in psoriatic arthritis (PsA).","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"44 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147478773","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}
{"title":"Skeletal Fluorosis Presenting with Diffuse Periostitis and Polyarticular Synovitis","authors":"Mitali Sen","doi":"10.1002/art.70148","DOIUrl":"https://doi.org/10.1002/art.70148","url":null,"abstract":"Click on the article title to read more.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"7 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147478775","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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