Arthritis & Rheumatology最新文献

{"title":"Initial treatment strategies and outcomes across haemodynamic thresholds and risk stratification in incident systemic sclerosis-associated pulmonary arterial hypertension: a EUSTAR analysis.","authors":"Hilde Jenssen Bjørkekjær, Cosimo Bruni, Kaspar Broch, Cathrine Brunborg, Patricia E Carreira, Paolo Airò, Carmen Pilar Simeón-Aznar, Marie-Elise Truchetet, Alessandro Giollo, Alexandra Balbir-Gurman, Mickael Martin, Christopher P Denton, Armando Gabrielli, Francesco Del Galdo, Madelon C Vonk, Håvard Fretheim, Helle Bitter, Øyvind Midtvedt, Arne K Andreassen, Sverre Høie, Yoshiya Tanaka, Gabriela Riemekasten, Ulf Müller-Ladner, Marco Matucci-Cerinic, Ivan Castellví, Elise Siegert, Eric Hachulla, Øyvind Molberg, Oliver Distler, Anna-Maria Hoffmann-Vold","doi":"10.1002/art.70372","DOIUrl":"https://doi.org/10.1002/art.70372","url":null,"abstract":"<p><strong>Objective: </strong>Real-world initial treatment strategies in SSc-PAH remain incompletely described. We aimed to characterise these strategies across haemodynamic thresholds and risk strata and evaluate outcome associations.</p><p><strong>Methods: </strong>We analysed treatment-naïve SSc-PAH patients in EUSTAR (2000-2021) fulfilling the 2022 haemodynamic definition. Initial therapy comprised treatment initiated within 4 months of RHC. As-treated (AT) analyses were primary and intention-to-treat (ITT) analyses supportive. Outcomes were all-cause mortality and 36-month PAH progression.</p><p><strong>Results: </strong>Among 301 patients, 198 (66%) initiated therapy and 170 maintained therapy for ≥3 months. Therapy was initiated in 31% with milder haemodynamic impairment (mPAP 21-24 mmHg and/or PVR 2-3 WU) versus 79% fulfilling the previous haemodynamic definition; combination therapy increased from 14% to 67% across low- to high-risk strata. Over a median 3.9 years, 125 (42%) died and 85/227 (37%) progressed. Adjusted ITT analyses showed no association with either outcome, whereas adjusted AT analyses showed lower mortality risk with sustained monotherapy and combination therapy (HR 0.50, 95% CI 0.27-0.92 and HR 0.40, 95% CI 0.18-0.88, respectively) and lower PAH progression risk with sustained initial therapy (HR 0.37, 95% CI 0.18-0.76). In the milder haemodynamic subgroup, the mortality estimate was directionally consistent but imprecise.</p><p><strong>Conclusion: </strong>Initial treatment strategies reflected haemodynamic severity and baseline risk, while variation suggested potential implementation gaps. Sustained initial therapy was associated with lower risks of mortality and PAH progression. Contrasting ITT and AT estimates highlight challenges in observational treatment-outcome comparisons. Findings in the milder haemodynamic subgroup support dedicated prospective studies.</p>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178158","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":"Higher risk of Long COVID among patients with autoimmune rheumatic diseases and immunomodulatory therapy: a retrospective cohort analysis of national US data.","authors":"Namrata Singh, A Jerrod Anzalone, Holland Stevenson, Londyn Robinson, Lesley E Jackson, Sandra E Safo, Zachary Butzin-Dozier, Kaleb Michaud, Maria I Danila, Jasvinder A Singh, Rena C Patel","doi":"10.1002/art.70361","DOIUrl":"https://doi.org/10.1002/art.70361","url":null,"abstract":"<p><strong>Background: </strong>Little is known about the prevalence of and factors associated with Long COVID in patients with autoimmune rheumatic diseases (AIRDs).</p><p><strong>Methods: </strong>We conducted a retrospective cohort study using data from the National Clinical Cohort Collaborative (N3C). We included adults with a first documented SARS-CoV-2 infection between September 2021 and December 2023, with follow-up through December 2024. Long COVID was defined as ICD-10-CM code U09.9 or a Long COVID clinic visit occurring 28 to 365 days after first infection. We compared patients with AIRD with matched non-AIRD controls using 1:1 nearest-neighbor propensity score matching on age with exact matching on sex, race/ethnicity, SARS-CoV-2 variant-dominant period, and data-contributing organization. We estimated hazard ratios using multivariable Cox regression models. Among people with AIRD, we assessed risk by AIRD type and medication exposure before acute COVID-19.</p><p><strong>Results: </strong>In the matched cohort of 187,106 patients, Long COVID occurred in 2.8% of AIRD patients and 1.5% among non-AIRD patients. In multivariable analyses, AIRD was associated with an increased risk of Long COVID compared with non-AIRD patients (aHR 1.56, 95% CI 1.45-1.67). Among patients with AIRD, higher acute COVID-19 severity, pulmonary disease, obesity, and exposure to rituximab or glucocorticoids were associated with an increased risk of Long COVID. Sjögren's syndrome was associated with a higher risk of Long COVID.</p><p><strong>Conclusion: </strong>The higher risk of developing Long COVID among AIRD patients compared with those without AIRD underscores the need to identify potential risk factors for Long COVID in this population to minimize its long-term effects.</p>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178160","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":"EXPRESSION OF CONCERN: Induction of Scleroderma Fibrosis in Skin-humanized Mice by Administration of Anti-platelet-derived Growth Factor Receptor Agonistic Autoantibodies.","authors":"","doi":"10.1002/art.70365","DOIUrl":"https://doi.org/10.1002/art.70365","url":null,"abstract":"<p><strong>Expression of concern: </strong>M. M. Luchetti, G. Moroncini, M. Jose Escamez, S. Svegliati Baroni, T. Spadoni, A. Grieco, C. Paolini, A. Funaro, E. V. Avvedimento, F. Larcher, M. Del Rio, and A. Gabrielli, \"Induction of Scleroderma Fibrosis in Skin-humanized Mice by Administration of Anti-platelet-derived Growth Factor Receptor Agonistic Autoantibodies,\" Arthritis & Rheumatology 68, no. 9 (2016): 2263-2273, https://doi.org/10.1002/art.39728. This Expression of Concern is for the above article, published online on 25 April 2016 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, S. Louis Bridges, Jr.; the American College of Rheumatology; and Wiley Periodicals LLC. Concerns were raised by a third party on PubPeer [1] regarding a high level of similarity between the beta-actin bands in Figures 1C and 2B. Additional investigation by the publisher also found that there was evidence of splicing in the PDGFR-alpha band in Figure 3B. The authors responded to an inquiry by the publisher and shared original data. However, original data were not available for the bands originally published in Figure 3B, and the authors supplied data from replicate experiments performed during the same period of the original experiments. A review of these data found that not all of the data could be verified. Therefore, this Expression of Concern has been agreed to in order to inform and alert readers as to the results of this investigation. The authors have been informed of the Expression of Concern.</p><p><strong>Reference: </strong>1. Psychotria siamica. Comments on \"Induction of Scleroderma Fibrosis in Skin-Humanized Mice by Administration of Anti-Platelet-Derived Growth Factor Receptor Agonistic Autoantibodies,\" PubPeer, November 2025. https://pubpeer.com/publications/33B47982F70FD05FFA5D7CE38D417A.</p>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149163316","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":"Angiolymphoid Hyperplasia With Eosinophilia Mimicking Temporal Arteritis","authors":"Jonas Menz, Konstanze Holl‐Ulrich, Lukas Brachaczek, Gabriela Riemekasten, Peter Lamprecht","doi":"10.1002/art.70370","DOIUrl":"https://doi.org/10.1002/art.70370","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"59 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130523","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":"Training Opportunities Within the National Institute of Arthritis and Musculoskeletal and Skin Diseases","authors":"Janelle Hauserman, Isaah Vincent","doi":"10.1002/art.70347","DOIUrl":"https://doi.org/10.1002/art.70347","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"40 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130525","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":"Tph and Tfh cells as biomarkers and targets in rheumatic diseases","authors":"Abigail E. Schiff, Deepak A. Rao","doi":"10.1002/art.70362","DOIUrl":"https://doi.org/10.1002/art.70362","url":null,"abstract":"The role of B cell‐helper T cells, including T follicular helper cells (Tfh), T peripheral helper cells (Tph), and others, in autoimmune rheumatic diseases is reviewed, focusing on clinical applications. A case is presented where the presence of B helper T cells could help decide the next medication to use in a patient with rheumatoid arthritis refractory to TNF inhibitors. The review covers topics including the biology of B cell and T cell interactions, the origin and function of B cell‐helper T cells, disease associations, B cell‐helper T cells as a marker of disease phenotype and treatment response, and therapeutic approaches. B cell‐helper T cells are a subset of CD4+ T cells that are specialized to aid in B cell development and affinity maturation. B cell‐helper T cells, including Tfh and Tph cells, are positively correlated with increased disease activity and lymphoid aggregate‐associated phenotypes in multiple autoantibody‐associated immune conditions. Higher numbers of circulating Tfh and Tph cells are also associated with greater likelihood of response to certain biologics in rheumatoid arthritis. In the future, Tfh and Tph cell levels may be used as both biomarkers of disease activity and targets to treat multiple autoantibody‐associated rheumatic diseases, leading to a new era of personalized medicine.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"12 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130522","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":"Outcomes of Tapering Biologic and Targeted Synthetic DMARDs in Rheumatoid Arthritis: A Multicenter Randomized Non‐Inferiority Trial","authors":"Dong‐Jin Park,Sung‐Eun Choi,Ji‐Hyoun Kang,Jung‐Yoon Choe,Hye‐Soon Lee,So‐Young Bang,Yun‐Hong Cheon,Sang‐Il Lee,Mingyo Kim,Yoon‐Kyoung Sung,Soo‐Kyung Cho,Jae Hyun Jung,Sung Hae Chang,Sung Won Lee,Yeon‐Ah Lee,Seung‐Geun Lee,Hyun‐Sook Kim,Seung‐Ki Kwok,Seung‐Cheol Shim,Shin‐Seok Lee","doi":"10.1002/art.70363","DOIUrl":"https://doi.org/10.1002/art.70363","url":null,"abstract":"Objective Evidence supporting tapering of biologic or targeted synthetic disease‐modifying antirheumatic drugs (b/tsDMARDs) in rheumatoid arthritis (RA) patients with sustained low disease activity (LDA) remains limited. We evaluated the efficacy and safety of a structured b/tsDMARD tapering strategy in patients with RA who had achieved sustained LDA. Methods In this 24‐week, multicenter, randomized, open‐label, non‐inferiority trial, patients with RA receiving stable‐dose b/tsDMARDs and maintaining DAS28‐ESR‐defined LDA for at least 6 months were randomized to either stepwise dose tapering or dose continuation. The primary endpoint was maintenance of DAS28‐ESR LDA at week 24. The non‐inferiority margin was prespecified as ‐10%. Secondary endpoints included disease activity measures, remission rates, patient‐reported outcomes, quality of life, and adverse events. Results A total of 348 patients were randomized to the continuation group (n=177) or tapering group (n=171). In the per‐protocol population, LDA was maintained in 89.6% and 88.2% of patients, respectively, with a risk difference of ‐1.43% (95% CI ‐8.09 to 5.23), meeting the prespecified criterion for non‐inferiority. Similar findings were observed in the full analysis set. Most patients experiencing disease worsening regained low disease activity after protocol‐guided treatment re‐escalation during follow‐up without permanent treatment discontinuation. Most secondary outcomes were comparable between groups, although some disease activity measures favored continuation, including DAS28‐CRP at week 12 and DAS28‐ESR and SDAI at week 24. Adverse events were uncommon in both groups. Conclusion In RA patients with sustained LDA, structured b/tsDMARD tapering was non‐inferior to treatment continuation for maintaining disease control over 24 weeks.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"1 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149089218","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":"Mesenchymal Stromal Cells Fuel Immunometabolic Reprogramming of Type 2 Conventional Dendritic Cells to Alleviate Systemic Sclerosis","authors":"Zhikang Wang, Sha Liu, Xinping Liu, Yang Ou, Yue Zhang, Huamei Li, Mian Liu, Zhonghui Hu, Dandan Wang, Lingyun Sun","doi":"10.1002/art.70359","DOIUrl":"https://doi.org/10.1002/art.70359","url":null,"abstract":"Objective To investigate the clinical efficacy and underlying mechanisms of mesenchymal stromal cell (MSC) therapy in systemic sclerosis (SSc). Methods We prospectively evaluated the efficacy of MSC therapy in SSc patients. To elucidate the therapeutic mechanisms, we integrated paired multi‐omics data: proteomics (n=7), metabolomics (n=7), and both bulk (n=6) and single‐cell (n=2) RNA‐seq. Baseline disease‐associated signatures were mainly defined by publicly available datasets of peripheral blood mononuclear cells (PBMCs, 21 SSc vs. 6 healthy donors). Results MSC therapy significantly ameliorated skin fibrosis (median mRSS decrease 7.0 [IQR, 3.8–9.3], <jats:italic>P</jats:italic> &lt; 0.05) and stabilized lung function after 6 months. In parallel with these clinical improvements, plasma proteomic analysis demonstrated that MSC therapy suppressed Hedgehog‐mediated fibrotic pathways ( <jats:italic>P</jats:italic> <jats:sub>adj</jats:sub> &lt; 0.05). Transcriptomic profiling revealed that pathogenic type 2 conventional dendritic cells (cDC2s) exhibit intrinsic oxidative phosphorylation (OXPHOS) defects ( <jats:italic>P</jats:italic> <jats:sub>adj</jats:sub> &lt; 0.05) in SSc. MSC therapy effectively repaired these defects and concurrently suppressed cDC2‐related inflammatory pathways in PBMCs and plasma ( <jats:italic>P</jats:italic> <jats:sub>adj</jats:sub> &lt; 0.05). Consistent with these findings, single‐cell RNA‐seq revealed OXPHOS recovery in cDC2s alongside an increased proportion of homeostatic subsets. Conclusions Our study underscores the MSC‐mediated immunometabolic reprogramming to restore immune homeostasis by targeting upstream OXPHOS defects of cDC2s in SSc. <jats:boxed-text content-type=\"graphic\" position=\"anchor\"> <jats:graphic xmlns:xlink=\"http://www.w3.org/1999/xlink\" mimetype=\"image/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic/art70359-toc-0001-m.png\"> <jats:alt-text>image</jats:alt-text> </jats:graphic> </jats:boxed-text>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"8 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087411","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":"Oral glucocorticoid dose patterns and organ damage in systemic lupus erythematosus – a nationwide cohort study","authors":"Annica Dominicus, Álvaro Gomez, Ngoc V. Nguyen, Karin Blomkvist Sporre, Francesca Faustini, Elisabet Svenungsson, Elizabeth V. Arkema","doi":"10.1002/art.70360","DOIUrl":"https://doi.org/10.1002/art.70360","url":null,"abstract":"Background Evaluating the relationship between glucocorticoid (GC) exposure and organ damage in systemic lupus erythematosus (SLE) is challenging since GC dose varies over time. It is unclear which exposure time window captures the full impact of GC usage. Methods We studied a nationwide cohort of individuals with newly diagnosed SLE 2006‐2022 with follow‐up until January 2024 through a linkage of Swedish national registers. Long‐term oral GC exposure was assessed from pharmacy dispensations to identify which dosing patterns had the strongest association with organ damage overall, and within the ocular, cardiovascular, peripheral vascular, gastrointestinal, diabetes, and malignancy domains. We used Weighted Cumulative Exposure models to estimate the weights of the average daily dose at different time points and determine the relative importance of exposure on organ damage accrual, adjusted for confounders. Results Among 3749 patients with newly diagnosed SLE (82.1% female, median age 48.0 years), the increased risk of first organ damage overall associated with GC dosing was well‐captured by the past 2 years (adjusted HR=1.42 [95%CI 1.31‐1.53] for 5 mg/day), and fairly well captured by the past 1 year (adjusted HR=1.34 [95%CI 1.23‐1.42] for 5 mg/day). For cardiovascular damage, dose patterns over the past 3 years substantially contributed to the associated increased risk. Conclusions In evaluations of overall organ damage in SLE, GC exposure during at least the previous year should be considered to capture the associated increased risk. For cardiovascular damage, the time window for assessing GC exposure and disease activity should be extended to the last 3 years.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"10 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149086302","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":"The association between systemic inflammation as measured by calprotectin and autoantibody load in rheumatoid arthritis","authors":"Caroline Grönwall,Linda Mathsson Alm,Helga Westerlind,Isabel Gehring,Nasim Ghasemzadeh,Niels Steen Krogh,Siri Lillegraven,Espen Haavardsholm,Martina Johannesson,Tore K. Kvien,Johan Rönnelid,Tue Wenzel Kragstrup,Bente Glintborg,Merete Lund Hetland,Hilde Berner Hammer,The Danish Rheumatologic Biobank Study Group, Swedish Rheumatology Quality Register Biobank Study Group(SRQb),Johan Askling,Oliver Hendricks,Estrid Høgdall,Dorte Vendelbo Jensen,Heidi Lausten Munk,Jens Kristian Pedersen,Torkell Ellingsen,Anne Gitte Loft,Ellen‐Margrethe Hauge,Salome Kristensen,Lene Dreyer,Asta Linauskas,Søren Jacobsen,Carl Turesson,Solbritt Rantapää Dahlqvist,Lena Björkman,Alf Kastbom,Eva Baecklund","doi":"10.1002/art.70357","DOIUrl":"https://doi.org/10.1002/art.70357","url":null,"abstract":"Background Plasma calprotectin is a marker of neutrophil activity. Its relation to the clinical phenotype and autoantibodies in rheumatoid arthritis (RA) is only partly understood. We therefore aimed to investigate the association between calprotectin and clinical parameters, CRP, ESR, anti‐CCP2 and other anti‐modified protein autoantibodies (AMPAs) in patients with RA. Methods Rheumatoid factor (RF), anti‐cyclic citrullinated peptide 2 (CCP2) isotypes and plasma calprotectin were centrally measured in a cross‐sectional cohort of 4521 Scandinavian RA patients using fluoroenzyme immunoassays. IgG to 15 citrullinated (Cit) and four carbamylated or acetylated (Carb/Acet) peptides were measured by multiplex solid‐phase array. CRP and ESR values were obtained from clinical measurements at the time of blood sampling. Results Calprotectin levels correlated with ESR (ρ=0.53), CRP (ρ=0.47), VAS pain (ρ=0.24), SJC28 (ρ=0.39), and TJC28 (ρ=0.26; p&lt;0.0001 for all). Patients with both elevated CRP (&gt;10mg/L) and calprotectin (&gt;15 AU/ml) (14%, N=613) had significantly higher VAS pain, SJC28, and TJC28 than patients with only elevated CRP (p&lt;0.0001), in early and established disease. Patients with elevated calprotectin, independent of CRP levels, had significantly higher proportions of AMPA positivity including anti‐CCP2. When patients were divided into six groups based on increasing number of Cit/Carb/Acet‐reactivities and anti‐CCP2 IgG levels, elevated calprotectin was associated with increasing AMPA load, particularly in the presence of RF IgM. The differences between AMPA load groups remained after adjusting for sex, age, RF IgM, and disease duration. Conclusions Plasma calprotectin is positively associated with seropositivity and AMPA load by autoantibody levels and the breadth of the autoantibody response.","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"11 1","pages":""},"PeriodicalIF":13.3,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149089274","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}