ACR open rheumatology最新文献

{"title":"Development and Validation of Algorithms for Systemic Sclerosis Identification in Electronic Health Record Data.","authors":"Gulsen Ozen, Michael O'Rorke, Paul Romitti, Robyn Domsic","doi":"10.1002/acr2.90091","DOIUrl":"10.1002/acr2.90091","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to develop and validate International Classification of Diseases (ICD) code-based algorithms for identifying systemic sclerosis (SSc) cases within electronic health record (EHR) data and to evaluate algorithm performance.</p><p><strong>Methods: </strong>We identified patients with at least one ICD, Ninth Revision (ICD-9)/ICD-10 code for SSc in a large multicenter EHR dataset (TriNetX Research Network). A random sample of patients underwent detailed medical record review to confirm SSc diagnosis (gold standard). All ICD-9/10 codes assigned during inpatient or outpatient encounters and corresponding dates were extracted. SSc case status derived from seven prespecified algorithms was compared with the gold standard by calculating sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and receiver operating characteristic analyses.</p><p><strong>Results: </strong>Medical records from 549 of 1,098 patients with at least one SSc ICD-9/10 code were reviewed; 399 (72.7%) were confirmed SSc cases. The algorithm requiring at least two outpatient ICD-9/10 SSc codes at least 30 days apart with exclusion of scleroderma mimics within 24 months demonstrated the best overall performance (sensitivity 96%, specificity 71%, PPV 90%, NPV 87%, and area under the curve 0.91). Algorithms based on at least one inpatient ICD-9/10 code showed high specificity (91%) and PPV (93%) but poor sensitivity (45%) and NPV (38%). Adding inpatient codes to the outpatient code-based algorithms did not improve performance.</p><p><strong>Conclusion: </strong>An algorithm requiring at least two outpatient SSc ICD-9/10 codes ≥30 days apart without scleroderma mimics within 24 months reliably identifies SSc cases. This readily implementable approach outperforms previously published more complex algorithms and supports valid clinical and epidemiologic research in large datasets.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90091"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13249518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148213734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Images: Thrombocytopenia, anasarca, fever, reticulin fibrosis, and organomegaly syndrome presenting as bilateral adrenal hemorrhage.","authors":"Masaki Itagane, Mitsuyo Kinjo","doi":"10.1002/acr2.90098","DOIUrl":"10.1002/acr2.90098","url":null,"abstract":"","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90098"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13287834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Anifrolumab Treatment Normalizes Hematologic Parameters and Several Serologic Markers in Patients With Systemic Lupus Erythematosus.","authors":"Edward M Vital, Zahir Amoura, Kenneth C Kalunian, Ian N Bruce, Yoshiya Tanaka, Susan Manzi, Ihor Hupka, Jacob Knagenhjelm, Hussein Al-Mossawi, Catharina Lindholm","doi":"10.1002/acr2.90065","DOIUrl":"10.1002/acr2.90065","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the long-term effects of anifrolumab on hematologic and serologic parameters over four years.</p><p><strong>Methods: </strong>This analysis included 536 patients with moderate-to-severe systemic lupus erythematosus (SLE) who received intravenous anifrolumab 300 mg (n = 358) or placebo (n = 178) in the 52-week, phase 3 TULIP-1/2 trials (NCT02446912 and NCT02446899) and continued the same treatment in the 3-year, long-term extension (LTE, NCT02794285), or would have done if not discontinued early; 369 patients entered the LTE. Changes from baseline to week 208 in lymphocytes, hemoglobin, platelets, neutrophils, complement C3, C4, anti-double-stranded DNA (dsDNA), and Igs were analyzed descriptively. British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) response at week 52 was analyzed by treatment and lymphocyte, hemoglobin, and platelet normalization in responders versus nonresponders, regardless of treatment.</p><p><strong>Results: </strong>Numerically greater improvements from baseline in lymphocyte, hemoglobin, platelet, and neutrophil levels were observed with anifrolumab over placebo. Comparing anifrolumab versus placebo, lymphocyte and hemoglobin normalization rates were higher and platelet normalization was comparable. BICLA response was associated with lymphocyte, hemoglobin, and platelet normalization over four years, regardless of treatment. Conversely, BICLA responses were higher with anifrolumab versus placebo, irrespective of baseline lymphocyte, hemoglobin, and platelet levels. Improvements in anti-dsDNA, C3, C4, and Igs from baseline were greater with anifrolumab versus placebo.</p><p><strong>Conclusion: </strong>The normalization of hematologic parameters and sustained improvements in serologic markers support the long-term efficacy of anifrolumab in patients with moderate-to-severe SLE. Clinical response to anifrolumab was associated with improvements in biomarkers, suggesting restoration of overall immune health.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90065"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13267668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148254887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Positive and Negative Cardiovascular Effects of JAK Inhibitors in Inflammation.","authors":"Aliki Zavoriti, Pierre Miossec","doi":"10.1002/acr2.90074","DOIUrl":"10.1002/acr2.90074","url":null,"abstract":"<p><p>Chronic inflammation, characteristic of many autoimmune diseases, such as rheumatoid arthritis (RA), or myeloproliferative neoplasms (MPNs), is an independent driver of accelerated cardiovascular (CV) risk, primarily through proinflammatory cytokines that induce atherosclerosis and endothelial dysfunction. Although biologic therapies (tumor necrosis factor [TNF], interleukin [IL]-6, or IL-1 inhibitors) improve both clinical manifestations and CV outcomes, JAK inhibitors (JAKi) present a paradox. JAKi provide potent systemic inflammation control, sometimes superior to biologic therapies, this effect does not translate into a proportional CV risk reduction in all patients. Instead, JAKi have been linked to increased adverse CV events in high-risk patient populations with RA, resulting in a Food and Drug Administration safety warning. Conversely, JAKi show therapeutic benefit in patients with MPNs. In MPNs, JAKi specifically target the JAK2 mutation, reducing blood cell proliferation and the associated prothrombotic state. This review compares the distinct biologic mechanisms underlying this JAKi CV paradox, contrasting the JAK2 mutation-driven pathology in MPNs with the widespread cytokine-driven alterations in inflammatory diseases. In the latter, the observed CV risk might stem from failure of JAKi to fully inhibit prothrombotic pathways induced by cytokines (TNF and IL-17) and the potential dose-related vascular toxicity. Understanding these binary effects will provide new insights into the divergent CV impact of JAKi.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90074"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Italian Olfactory Identification Test in Systemic Lupus Erythematosus: Association of Olfactory Impairment With Chronic Damage and Anti-β₂-Glycoprotein I Antibodies.","authors":"Marta Di Berardino, Pasquale Nigro, Lorenza Bruno, Giacomo Cafaro, Anna Colangelo, Roberto Dal Pozzolo, Francesco Tromby, Roberto Gerli, Lucilla Parnetti, Elena Bartoloni, Nicola Tambasco, Carlo Perricone","doi":"10.1002/acr2.90088","DOIUrl":"10.1002/acr2.90088","url":null,"abstract":"<p><strong>Objective: </strong>Olfactory dysfunction is a relatively frequent manifestation in systemic lupus erythematosus (SLE). The Italian Olfactory Identification Test (IOIT) may represent a suitable tool for detecting olfactory impairment in patients with SLE, due to its reliability and easiness of administration. This study aimed to evaluate the prevalence of smell impairment in patients with SLE and its correlation with clinical and serologic features.</p><p><strong>Methods: </strong>Consecutive patients with SLE and healthy controls were enrolled. Clinical history, disease indices, and main laboratory parameters were collected. Olfactory function was assessed using the IOIT, testing 33 cards with different microencapsulated odorants.</p><p><strong>Results: </strong>The cohort included 100 subjects: 50 patients with SLE (mean age ± SD: 51.3 ± 14.2; disease duration ± SD: 20.9 ± 13.2; female-to-male ratio: 5:1) and 50 age- and sex-matched healthy controls. Hyposmia was observed in 30% of patients with SLE and 4% of healthy subjects. IOIT scores correlated significantly with cumulative organ damage measured by Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (P = 0.017, r = 0.336). Hyposmia was associated with anti-β₂-glycoprotein I (anti-β₂GPI) antibodies (P = 0.029) and antidepressant therapy (P = 0.019). Cumulative damage was demonstrated to be an independent risk factor for hyposmia (odds ratio = 1.42, 95% confidence interval 1.02-1.98; P = 0.038).</p><p><strong>Conclusion: </strong>The IOIT appears to be a suitable tool for evaluating olfactory dysfunction in SLE. The significant association between hyposmia and cumulative damage suggests that olfactory impairment may represent a clinical marker of long-term organ damage. The association between hyposmia and the use of antidepressant therapy confirms the close relationship between the sense of smell and mood regulation. Furthermore, the association with anti-β₂GPI reinforces the link between olfactory dysfunction and chronic damage in SLE.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90088"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13283763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148297770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Colchicine Inhibits Chemokine Production in Monosodium Urate-Stimulated Innate Immune Cells.","authors":"Laura M Merlo Pich, Titus Schlüter, Andrei Sarlea, Mihai G Netea, Calin Popa, Leo A B Joosten","doi":"10.1002/acr2.90052","DOIUrl":"10.1002/acr2.90052","url":null,"abstract":"<p><strong>Objective: </strong>Colchicine is a well-established, widely available drug used to treat inflammatory diseases driven by the innate immune system, most notably gout. Although much research has focused on neutrophils, the first responders in a gout flare, monocytes and lymphocytes, also play critical roles in sustaining the inflammatory response. However, the impact of colchicine on these cell types remains poorly understood. The objective of this study was to assess the in vitro effects of colchicine on primary peripheral blood mononuclear cells (PBMCs) stimulated with monosodium urate (MSU) crystals.</p><p><strong>Methods: </strong>PBMCs or monocytes from healthy volunteers were isolated and cultured with a one-hour preincubation of colchicine, followed by a 24-hour stimulation with MSU crystals and lipopolysaccharide. Supernatants were collected for cytokine quantification and chemotaxis assay, whereas cells were processed for RNA isolation, metabolic analysis, reactive oxygen species (ROS) activity, and phagocytosis.</p><p><strong>Results: </strong>Colchicine reduced the secretion of several chemokines, notably MCP-1, whereas no inhibitory effect on the release of proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor (TNF) was observed. Colchicine also reduced MCP-1 and TNF, but not IL-1β and IL-6, production in monocytes. Both MCP-1 messenger RNA expression and intracellular protein concentrations were inhibited by colchicine, suggesting an effect at transcriptional level. Lower chemokine production is responsible for reduced chemoattraction of monocytes. Moreover, colchicine attenuated ROS production and phagocytic activity in monocytes, alongside suppressing glycolytic metabolism and oxidative phosphorylation.</p><p><strong>Conclusion: </strong>Colchicine's anti-inflammatory mechanisms in monocytes and PBMCs consist mainly of reduction of chemokine production and chemoattraction accompanied by changes in cellular metabolism and attenuated ROS production.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 6","pages":"e90052"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13287321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148304309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative Muscle Magnetic Resonance Imaging Demonstrates Resolution of Muscle Edema in Refractory Dermatomyositis: A Post Hoc Analysis of a Proof-of-Concept Clinical Trial of Tofacitinib.","authors":"Mona Dabiri, Anshula Nallapati, Marwin Groener, Patrick Debs, Jemima Albayda, Eleni Tiniakou, Lisa Christopher-Stine, Laura Fayad, Julie J Paik","doi":"10.1002/acr2.90041","DOIUrl":"10.1002/acr2.90041","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate changes in muscle edema using short-tau inversion recovery (STIR) imaging and quantitative diffusion-weighted imaging (DWI) with apparent diffusion coefficient (ADC) mapping in patients with refractory dermatomyositis (DM) treated with tofacitinib.</p><p><strong>Methods: </strong>This post hoc imaging analysis included patients from a 12-week, open-label trial of tofacitinib 11 mg daily in refractory DM. Bilateral thigh magnetic resonance imaging was obtained at baseline and week 12 using standardized STIR, T1-weighted, and DWI sequences. Muscle edema (ME) and fascial edema were assessed qualitatively on STIR imaging. ADC values were measured in muscles demonstrating baseline STIR hyperintensity using three nonoverlapping regions of interest per muscle. Clinical outcomes included Manual Muscle Testing of eight muscle groups (MMT-8).</p><p><strong>Results: </strong>Ten patients completed the study. Baseline ME was present in 32 of 320 thigh muscles (10%) across four patients. Quantitative ADC analysis, performed in the 32 edematous muscles, demonstrated significant decreases in tissue diffusivity in 11 muscles (34.5%), including the rectus femoris, vastus lateralis, vastus medialis, sartorius, gracilis, and adductors. Absolute ADC reductions ranged from -0.18 to -0.37 × 10^-3 mm²/s. Two patients with baseline proximal weakness showed parallel improvement in MMT-8 scores and ADC values, whereas two patients with normal strength showed subclinical ADC improvement.</p><p><strong>Conclusion: </strong>Tofacitinib resulted in marked clinical and radiologic improvement in refractory DM. Quantitative ADC mapping detected resolution of muscle inflammation, including subclinical improvement not evident on strength or enzyme testing. ADC metrics may serve as objective imaging biomarkers of treatment response in DM.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 5","pages":"e90041"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Serum Proadrenomedullin Levels in Rheumatoid Arthritis Versus Spondyloarthritis: Insights From a Biobank Cohort.","authors":"Nefeli Stavroula Papastathopoulou, Elisa Assirelli, Simona Neri, Susanna Naldi, Jacopo Ciaffi, Luana Mancarella, Veronica Brusi, Lucia Lisi, Federica Pignatti, Piero Ruscitti, Francesco Ursini","doi":"10.1002/acr2.90061","DOIUrl":"10.1002/acr2.90061","url":null,"abstract":"<p><strong>Objective: </strong>Proadrenomedullin (pro-ADM) is a peptide implicated in immunomodulation, with higher levels observed in inflammatory conditions, cardiovascular impairment, and sepsis. Although extensively studied in acute disorders, its potential as a biomarker in inflammatory arthritis remains underexplored. This study aims to examine serum pro-ADM levels across different types of inflammatory arthritis and to investigate correlations with disease characteristics.</p><p><strong>Methods: </strong>We included 163 patients with inflammatory arthritis who were prospectively enrolled in our institutional Biobank. Among them, 99 patients had rheumatoid arthritis (RA), 36 patients had psoriatic arthritis (PsA), 22 patients had axial spondyloarthritis (axSpA), and 6 patients had undifferentiated spondyloarthritis (uSpA). Serum pro-ADM levels were measured using enzyme-linked immunosorbent assay, with cross-sectional assessment at baseline in all patients and longitudinal follow-up in a subset of 31 patients with RA.</p><p><strong>Results: </strong>At baseline, patients with RA exhibited significantly higher serum pro-ADM levels (median 51.7 pg/mL) in comparison to PsA, axSpA, and uSpA (median values between 33.9 and 35.6 pg/mL; all P < 0.001). Pro-ADM showed good discriminative ability in distinguishing RA from SpA but had no correlation with markers of inflammation, disease duration, or disease activity indices. In patients with RA with follow-up data, pro-ADM levels exhibited a significant decrease from 52.5 to 30.1 pg/mL after six months (P = 0.023). However, changes in pro-ADM did not correlate with changes in the Disease Activity Score in 28 joints using the C-reactive protein level.</p><p><strong>Conclusion: </strong>Serum pro-ADM levels are markedly elevated in RA relative to SpA, although they do not correlate with inflammatory burden or disease activity. In RA, pro-ADM levels decrease following treatment initiation or modification; nonetheless, they lack predictive value for treatment response. These findings suggest that pro-ADM reflects disease-specific pathophysiologic differences rather than representing a dynamic biomarker.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 5","pages":"e90061"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13129696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral Pain Processing Following TNFα Inhibitor Treatment in Rheumatoid Arthritis: A Randomized Double-Blind Placebo-Controlled fMRI Study.","authors":"Julie Klinke, Peter Fransson, Karin B Jensen, Reem Altawil, Eva Kosek, Jon Lampa","doi":"10.1002/acr2.90069","DOIUrl":"10.1002/acr2.90069","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the effects of tumor necrosis factor α (TNFα) blockade treatment, adalimumab (ADA), on cerebral pain processing in relevant brain regions in patients with rheumatoid arthritis (RA). Its secondary aim was to identify pretreatment markers in cerebral pain processing that might predict treatment response.</p><p><strong>Methods: </strong>A total of 25 patients with RA were randomly allocated treatment with 40 mg ADA (n = 14) or placebo (PBO) (n = 11) injected subcutaneously. During functional magnetic resonance imaging (fMRI), patients underwent individually calibrated pressure-pain stimulation on the most inflamed interphalangeal joint and on an unaffected control site before and after four weeks of treatment.</p><p><strong>Results: </strong>The ADA but not the PBO group showed significant changes in subjective, clinician-rated, and objective measures. Both groups exhibited significant activations in pain-relevant brain regions during the fMRI task. Cerebral activations did not change following treatment nor did they correlate pre- or post-treatment with changes in systemic inflammation (measured as the change in erythrocyte sedimentation rate [ΔESR]). Baseline cerebral activations did not correlate with treatment response in terms of ΔESR nor with pain or fatigue outcomes. However, in an exploratory analysis, five baseline activation clusters in the ADA group, and one in the PBO group, correlated positively with changes in swollen joint count (P < 0.001).</p><p><strong>Conclusions: </strong>Our study did not observe any associations between treatment with TNFα inhibitors and changes in cerebral pain processing, indicating that this treatment may not have a clear central effect.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 5","pages":"e90069"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147977713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Health-Related Behaviors Associated With Knee Pain Increase: A Longitudinal Community-Based Cohort Study That Examines Osteoarthritis.","authors":"Morgan L Wolff, Sarah H Nash, Cora E Lewis, Michael C Nevitt, David T Felson, Tuhina Neogi, James C Torner","doi":"10.1002/acr2.90043","DOIUrl":"10.1002/acr2.90043","url":null,"abstract":"<p><strong>Objectives: </strong>To understand the impact of lifestyle changes on osteoarthritis outcomes during the COVID-19 pandemic in a group of older Midwestern adults.</p><p><strong>Methods: </strong>We conducted a cross-sectional mailed survey in May of 2022 among participants of the Multicenter Osteoarthritis Study (MOST) in participants that completed their prior clinic visit. We assessed the perceived changes in health behaviors and barriers/facilitators to healthy eating and physical activity from before to during the COVID-19 pandemic. We used a generalized estimating equation to model knee-level pain increase from a previous survey, as a function of demographic variables and changes in behavioral factors.</p><p><strong>Results: </strong>We surveyed 502 MOST participants. There were significant differences in perceived health-related behaviors and barriers/facilitators to healthy eating and physical activity associated with knee-level pain increase during the COVID-19 pandemic. After multivariable-adjustment, increased knee-level pain was positively associated with previous frequent knee pain and use of weight control products.</p><p><strong>Conclusion: </strong>Changes in perceived health-related behaviors and barriers/facilitators to healthy eating and physical activity, along with previous osteoarthritis disease status, may impact knee pain in older adults. These results may be informative to promote health among older adults with and without osteoarthritis during future times of generalized stress.</p>","PeriodicalId":93845,"journal":{"name":"ACR open rheumatology","volume":"8 5","pages":"e90043"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}