Pub Date : 2025-02-04DOI: 10.1186/s13075-024-03441-3
Filip Van den Bosch, Atul Deodhar, Denis Poddubnyy, Walter P. Maksymowych, Désirée van der Heijde, Tae-Hwan Kim, Mitsumasa Kishimoto, Xenofon Baraliakos, Xianwei Bu, Ivan Lagunes-Galindo, In-Ho Song, Peter Wung, Koji Kato, Anna Shmagel
In SELECT-AXIS 2, upadacitinib improved the signs and symptoms of active non-radiographic axial spondyloarthritis (nr-axSpA) through 52 weeks versus placebo and was well tolerated. Here, we evaluated the efficacy and safety of upadacitinib through 2 years. The study enrolled eligible adult patients with a clinical diagnosis of nr-axSpA who met the 2009 Assessment of SpondyloArthritis international Society (ASAS) classification criteria and had objective signs of active inflammation on magnetic resonance imaging (MRI) of sacroiliac joints and/or high-sensitivity C-reactive protein. Patients were randomized 1:1 to receive double-blinded treatment with upadacitinib 15 mg once daily (QD) or placebo for 52 weeks, after which all patients received open-label treatment with upadacitinib 15 mg QD. Efficacy results over 104 weeks were reported as observed (AO) and either AO with non-responder imputation (AO-NRI; binary endpoints) or AO with mixed-effect model for repeated measures (continuous endpoints). Treatment-emergent adverse events (TEAEs) were summarized through week 104. Of 313 patients randomized and treated, 224 (continuous upadacitinib n = 117; placebo/upadacitinib n = 107) completed 104 weeks of treatment. In patients who received continuous upadacitinib, sustained improvement was observed through 2 years of treatment across efficacy endpoints including disease activity, pain, function, enthesitis, quality of life, and MRI measures of inflammation. At week 104, 57.1%, 59.0%, and 31.4% of patients achieved ASAS40 response, and low disease activity and inactive disease (as defined by Axial Spondyloarthritis Disease Activity Score), respectively (AO-NRI); week 104 outcomes were generally similar in patients who initially received placebo and were switched to upadacitinib at week 52. In total, 286 patients were exposed to ≥ 1 dose of upadacitinib, comprising 378.3 patient-years (PY) of exposure. Upadacitinib was generally well tolerated, with exposure-adjusted event rates (EAERs) for TEAEs, serious adverse events (AEs), and AEs leading to study drug discontinuation of 207.5, 8.7, and 5.3 events/100 PY, respectively. EAERs of TEAEs of special interest were broadly consistent with those reported through week 52. Treatment with upadacitinib demonstrated consistent improvement and maintenance of treatment effect across efficacy endpoints through 2 years; no new safety signals were identified with additional exposure. NCT04169373.
{"title":"Upadacitinib in active non-radiographic axial spondyloarthritis: 2-year data from the phase 3 SELECT-AXIS 2 study","authors":"Filip Van den Bosch, Atul Deodhar, Denis Poddubnyy, Walter P. Maksymowych, Désirée van der Heijde, Tae-Hwan Kim, Mitsumasa Kishimoto, Xenofon Baraliakos, Xianwei Bu, Ivan Lagunes-Galindo, In-Ho Song, Peter Wung, Koji Kato, Anna Shmagel","doi":"10.1186/s13075-024-03441-3","DOIUrl":"https://doi.org/10.1186/s13075-024-03441-3","url":null,"abstract":"In SELECT-AXIS 2, upadacitinib improved the signs and symptoms of active non-radiographic axial spondyloarthritis (nr-axSpA) through 52 weeks versus placebo and was well tolerated. Here, we evaluated the efficacy and safety of upadacitinib through 2 years. The study enrolled eligible adult patients with a clinical diagnosis of nr-axSpA who met the 2009 Assessment of SpondyloArthritis international Society (ASAS) classification criteria and had objective signs of active inflammation on magnetic resonance imaging (MRI) of sacroiliac joints and/or high-sensitivity C-reactive protein. Patients were randomized 1:1 to receive double-blinded treatment with upadacitinib 15 mg once daily (QD) or placebo for 52 weeks, after which all patients received open-label treatment with upadacitinib 15 mg QD. Efficacy results over 104 weeks were reported as observed (AO) and either AO with non-responder imputation (AO-NRI; binary endpoints) or AO with mixed-effect model for repeated measures (continuous endpoints). Treatment-emergent adverse events (TEAEs) were summarized through week 104. Of 313 patients randomized and treated, 224 (continuous upadacitinib n = 117; placebo/upadacitinib n = 107) completed 104 weeks of treatment. In patients who received continuous upadacitinib, sustained improvement was observed through 2 years of treatment across efficacy endpoints including disease activity, pain, function, enthesitis, quality of life, and MRI measures of inflammation. At week 104, 57.1%, 59.0%, and 31.4% of patients achieved ASAS40 response, and low disease activity and inactive disease (as defined by Axial Spondyloarthritis Disease Activity Score), respectively (AO-NRI); week 104 outcomes were generally similar in patients who initially received placebo and were switched to upadacitinib at week 52. In total, 286 patients were exposed to ≥ 1 dose of upadacitinib, comprising 378.3 patient-years (PY) of exposure. Upadacitinib was generally well tolerated, with exposure-adjusted event rates (EAERs) for TEAEs, serious adverse events (AEs), and AEs leading to study drug discontinuation of 207.5, 8.7, and 5.3 events/100 PY, respectively. EAERs of TEAEs of special interest were broadly consistent with those reported through week 52. Treatment with upadacitinib demonstrated consistent improvement and maintenance of treatment effect across efficacy endpoints through 2 years; no new safety signals were identified with additional exposure. NCT04169373.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"1 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143083493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-03DOI: 10.1186/s13075-025-03487-x
Chengzhong Zhang, Yan Lu
Further investigation is required to determine the etiology of systemic lupus erythematosus (SLE). The aim of this study is to assess the presence of miR-223 within neutrophils in SLE and investigate its impact on the expansion of Th17 cells. Experiments were performed in MRL/lpr mice, which were divided into control and miR-223 knockdown (miR-223-) group. We assessed miR-223 expression within neutrophils and Th17 expansion in MRL/lpr mice and patients with SLE using RT-PCR, luciferase reporter assay, Elisa, flow cytometry analysis. Signaling pathway, RT-PCR and western blot were conducted to elucidate the mechanism by which miR-223 within neutrophils expands Th17. We initially identified miR-223 as a pivotal factor in the pathogenesis of SLE in both MRL/lpr mice and SLE patients. Subsequently, knockdown of miR-223 led to a significant reduction in Th17 expansion in MRL/lpr mice. Moreover, inhibition of miR-223 effectively attenuated the recruitment and activation of neutrophils in SLE. Furthermore, we found rb6-8c5 treatment alleviated lupus symptoms of MRL/lpr mice and reduce the level of Th17. Finally, we elucidated that neutrophils potentiate the induction of Th17 through the activation of thePI3K-AKT pathway mediated by miR-223 during SLE-associated Th17 expansion. MiR-223 within neutrophil axis contributes to Th17 expansion by PI3K-AKT pathway in SLE, and miR-223 could be a therapeutic target of SLE.
{"title":"MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus","authors":"Chengzhong Zhang, Yan Lu","doi":"10.1186/s13075-025-03487-x","DOIUrl":"https://doi.org/10.1186/s13075-025-03487-x","url":null,"abstract":"Further investigation is required to determine the etiology of systemic lupus erythematosus (SLE). The aim of this study is to assess the presence of miR-223 within neutrophils in SLE and investigate its impact on the expansion of Th17 cells. Experiments were performed in MRL/lpr mice, which were divided into control and miR-223 knockdown (miR-223-) group. We assessed miR-223 expression within neutrophils and Th17 expansion in MRL/lpr mice and patients with SLE using RT-PCR, luciferase reporter assay, Elisa, flow cytometry analysis. Signaling pathway, RT-PCR and western blot were conducted to elucidate the mechanism by which miR-223 within neutrophils expands Th17. We initially identified miR-223 as a pivotal factor in the pathogenesis of SLE in both MRL/lpr mice and SLE patients. Subsequently, knockdown of miR-223 led to a significant reduction in Th17 expansion in MRL/lpr mice. Moreover, inhibition of miR-223 effectively attenuated the recruitment and activation of neutrophils in SLE. Furthermore, we found rb6-8c5 treatment alleviated lupus symptoms of MRL/lpr mice and reduce the level of Th17. Finally, we elucidated that neutrophils potentiate the induction of Th17 through the activation of thePI3K-AKT pathway mediated by miR-223 during SLE-associated Th17 expansion. MiR-223 within neutrophil axis contributes to Th17 expansion by PI3K-AKT pathway in SLE, and miR-223 could be a therapeutic target of SLE.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"34 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Controlling disease activity and improving physical function would be more difficult in patients with late-onset rheumatoid arthritis (LORA) who have chronic lung disease (CLD) at baseline. Our aim was to evaluate 5-year outcomes of following a treat-to-target (T2T) strategy targeting low disease activity (LDA) in LORA with CLD. Data from 197 methotrexate (MTX)-naïve LORA patients (mean age 74.4 years) from a prospective, monocentric registry were analyzed. Patients were treated with MTX if they had one or more poor prognostic features. If they had interstitial lung disease (ILD), tacrolimus could be administered instead of MTX at the discretion of the attending physician. If patients exhibited no response according to the European League Against Rheumatism criteria at week 12 or had not achieved LDA by week 24, biological disease-modifying antirheumatic drugs (bDMARDs) were started targeting LDA. The primary outcomes were the 5-year simplified disease activity index (SDAI) remission and Health Assessment Questionnaire Disability Index (HAQ-DI) ≤ 0.5 by non-responder imputation analysis. Secondary outcomes were serious adverse events (SAEs). Of the 197 LORA patients, 47 had CLD at baseline. The proportion of patients using MTX at baseline was significantly lower in those with than without CLD. Tacrolimus was initiated in 25.5% of the CLD group. The proportion of patients on bDMARDs was higher in those with CLD at year 5. Achievement of SDAI remission at year 5 was 29.8% in patients with CLD and 44.0% in those without CLD (p = 0.555). Achievement of HAQ-DI ≤ 0.5 at year 5 was 36.2% and 45.3% in patients with and without CLD, respectively (p = 0.939). Non-adherence to T2T due to comorbidities or adverse events was observed in 34.0% and 18.7% of the patients with and without CLD, respectively (p = 0.027). Infections requiring hospitalization, deterioration of extra-articular manifestations and fractures were more frequently reported as SAEs in patients with CLD, and multivariable analysis showed that patients with CLD had a higher risk of developing these SAEs (adjusted hazard ratio:2.53, 95% CI 1.60–4.00, p < 0.001). For LORA patients with CLD, the T2T strategy is effective, but comorbidities and SAEs make the implementation of the T2T more difficult.
{"title":"Long-term outcome of a treat-to-target strategy in late-onset rheumatoid arthritis with chronic lung disease: 5-year results of a prospective observational study","authors":"Manami Nomura, Takahiko Sugihara, Hiroyuki Baba, Tadashi Hosoya, Mari Kamiya, Tatsuro Ishizaki, Takumi Matsumoto, Kanae Kubo, Fumio Hirano, Masayo Kojima, Nobuyuki Miyasaka, Shinsuke Yasuda, Masayoshi Harigai","doi":"10.1186/s13075-025-03491-1","DOIUrl":"https://doi.org/10.1186/s13075-025-03491-1","url":null,"abstract":"Controlling disease activity and improving physical function would be more difficult in patients with late-onset rheumatoid arthritis (LORA) who have chronic lung disease (CLD) at baseline. Our aim was to evaluate 5-year outcomes of following a treat-to-target (T2T) strategy targeting low disease activity (LDA) in LORA with CLD. Data from 197 methotrexate (MTX)-naïve LORA patients (mean age 74.4 years) from a prospective, monocentric registry were analyzed. Patients were treated with MTX if they had one or more poor prognostic features. If they had interstitial lung disease (ILD), tacrolimus could be administered instead of MTX at the discretion of the attending physician. If patients exhibited no response according to the European League Against Rheumatism criteria at week 12 or had not achieved LDA by week 24, biological disease-modifying antirheumatic drugs (bDMARDs) were started targeting LDA. The primary outcomes were the 5-year simplified disease activity index (SDAI) remission and Health Assessment Questionnaire Disability Index (HAQ-DI) ≤ 0.5 by non-responder imputation analysis. Secondary outcomes were serious adverse events (SAEs). Of the 197 LORA patients, 47 had CLD at baseline. The proportion of patients using MTX at baseline was significantly lower in those with than without CLD. Tacrolimus was initiated in 25.5% of the CLD group. The proportion of patients on bDMARDs was higher in those with CLD at year 5. Achievement of SDAI remission at year 5 was 29.8% in patients with CLD and 44.0% in those without CLD (p = 0.555). Achievement of HAQ-DI ≤ 0.5 at year 5 was 36.2% and 45.3% in patients with and without CLD, respectively (p = 0.939). Non-adherence to T2T due to comorbidities or adverse events was observed in 34.0% and 18.7% of the patients with and without CLD, respectively (p = 0.027). Infections requiring hospitalization, deterioration of extra-articular manifestations and fractures were more frequently reported as SAEs in patients with CLD, and multivariable analysis showed that patients with CLD had a higher risk of developing these SAEs (adjusted hazard ratio:2.53, 95% CI 1.60–4.00, p < 0.001). For LORA patients with CLD, the T2T strategy is effective, but comorbidities and SAEs make the implementation of the T2T more difficult.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"38 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1186/s13075-025-03484-0
Rieke Alten, Claire Behar, Pierre Merckaert, Ebenezer Afari, Virginie Vannier-Moreau, Anael Ohayon, Sean E. Connolly, Aurélie Najm, Pierre-Antoine Juge, Gengyuan Liu, Angshu Rai, Yedid Elbez, Karissa Lozenski
The incorporation of machine learning is becoming more prevalent in the clinical setting. By predicting clinical outcomes, machine learning can provide clinicians with a valuable tool for refining precision medicine approaches and improving treatment outcomes. This was a post hoc analysis of pooled patient-level data from the global, real-world ACTION and ASCORE trials in patients with rheumatoid arthritis (RA) initiating abatacept. Patient demographic and disease characteristics were input across 10 machine learning models used to predict 12-month treatment retention. Retention was defined as treatment for > 365 days or ≤ 365 days in patients who achieved remission or major clinical response (based on European Alliance of Associations for Rheumatology response criteria). The pooled dataset was split into a training/validation cohort for model development and a test cohort for an unbiased evaluation of performance. SHapley Additive exPlanation (SHAP) values determined the level of importance and directionality for key patient features predicting abatacept retention. The pooled ACTION and ASCORE dataset included 5320 patients with RA (mean [standard deviation] age 57.7 [12.7] years; 79% female). The 12-month abatacept retention rate was 61% (n = 3236) with a discontinuation rate of 39% (n = 2037). In the training set (n = 4218), the gradient-boosting classifier model demonstrated the best performance (testing accuracy: 62%). This model had an area under the receiver operating characteristic curve (95% confidence interval) of 0.620 (0.586, 0.653) and F1 score of 0.659 (0.625, 0.689) in the test set of patients (n = 1055). Using this model, the five most important variables predicting 12-month abatacept retention were low body mass index (BMI), low American College of Rheumatology functional status class, anti-citrullinated protein antibody (ACPA) positivity, low Patient Global Assessment, and younger age. The gradient-boosting classifier model identified key patient features predictive of abatacept retention from this large, real-world study population. The SHAP values conveyed the directionality and importance of BMI, functional status, ACPA serostatus, Patient Global Assessment, and age for abatacept retention. Findings are consistent with previous observations and help validate the machine learning approach for predictive modelling in RA treatment, and may help inform clinical decision making. NCT02109666 (ACTION), NCT02090556 (ASCORE).
{"title":"Predicting abatacept retention using machine learning","authors":"Rieke Alten, Claire Behar, Pierre Merckaert, Ebenezer Afari, Virginie Vannier-Moreau, Anael Ohayon, Sean E. Connolly, Aurélie Najm, Pierre-Antoine Juge, Gengyuan Liu, Angshu Rai, Yedid Elbez, Karissa Lozenski","doi":"10.1186/s13075-025-03484-0","DOIUrl":"https://doi.org/10.1186/s13075-025-03484-0","url":null,"abstract":"The incorporation of machine learning is becoming more prevalent in the clinical setting. By predicting clinical outcomes, machine learning can provide clinicians with a valuable tool for refining precision medicine approaches and improving treatment outcomes. This was a post hoc analysis of pooled patient-level data from the global, real-world ACTION and ASCORE trials in patients with rheumatoid arthritis (RA) initiating abatacept. Patient demographic and disease characteristics were input across 10 machine learning models used to predict 12-month treatment retention. Retention was defined as treatment for > 365 days or ≤ 365 days in patients who achieved remission or major clinical response (based on European Alliance of Associations for Rheumatology response criteria). The pooled dataset was split into a training/validation cohort for model development and a test cohort for an unbiased evaluation of performance. SHapley Additive exPlanation (SHAP) values determined the level of importance and directionality for key patient features predicting abatacept retention. The pooled ACTION and ASCORE dataset included 5320 patients with RA (mean [standard deviation] age 57.7 [12.7] years; 79% female). The 12-month abatacept retention rate was 61% (n = 3236) with a discontinuation rate of 39% (n = 2037). In the training set (n = 4218), the gradient-boosting classifier model demonstrated the best performance (testing accuracy: 62%). This model had an area under the receiver operating characteristic curve (95% confidence interval) of 0.620 (0.586, 0.653) and F1 score of 0.659 (0.625, 0.689) in the test set of patients (n = 1055). Using this model, the five most important variables predicting 12-month abatacept retention were low body mass index (BMI), low American College of Rheumatology functional status class, anti-citrullinated protein antibody (ACPA) positivity, low Patient Global Assessment, and younger age. The gradient-boosting classifier model identified key patient features predictive of abatacept retention from this large, real-world study population. The SHAP values conveyed the directionality and importance of BMI, functional status, ACPA serostatus, Patient Global Assessment, and age for abatacept retention. Findings are consistent with previous observations and help validate the machine learning approach for predictive modelling in RA treatment, and may help inform clinical decision making. NCT02109666 (ACTION), NCT02090556 (ASCORE).","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"15 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-31DOI: 10.1186/s13075-025-03488-w
Adrian Ciurea, Seraphina Kissling, Andrea Götschi, Lykke Midtbøll Ørnbjerg, Simon Horskjær Rasmussen, Bálint Tamási, Burkhard Möller, Michael J. Nissen, Bente Glintborg, Anne Gitte Loft, Almut Scherer, René Bräm, Karel Pavelka, Jakub Závada, Joao Madruga Dias, Paula Valente, Bjorn Gudbjornsson, Olafur Palsson, Vappu Rantalaiho, Ritva Peltomaa, Catalin Codreanu, Corina Mogosan, Florenzo Iannone, Marco Sebastiani, Gareth T. Jones, Gary J. Macfarlane, Isabel Castrejon, Ziga Rotar, Brigitte Michelsen, Johan K. Wallman, Irene van der Horst-Bruinsma, Oliver Distler, Mikkel Østergaard, Merete Lund Hetland, Raphael Micheroli, Caroline Ospelt
Efficacy of tumour necrosis factor inhibitors (TNFi) for peripheral arthritis in patients with psoriatic arthritis (PsA) has been established in randomized clinical trials that have used improvement in summated joint counts as an outcome. Whether joints at different anatomical locations might respond differentially to TNFi remains unknown. The aim of the study was to investigate potential variations in the responsiveness to a first tumour necrosis factor inhibitor (TNFi) among joints at distinct locations in patients with psoriatic arthritis (PsA) treated in routine clinical care. Bionaive PsA patients from nine European countries were included in this observational cohort study if ≥ 1 joint was swollen at the initiation of a first TNFi as monotherapy or added to methotrexate. Only the 28-joint count was available without imaging data confirming the presence of synovitis. The primary outcome was time to first resolution of joint swelling at each joint level. Hazard ratios (HR) for resolution comparing different joint locations were estimated using interval-censored mixed-effects Cox proportional hazards models, including a random effect for country and patient, adjusted for age and sex. A total of 1729 patients with 8397 swollen joints at the start of TNFi were included. Considering the upper extremity, a higher rate of resolution of joint swelling (HR, 95% CI) was observed for the shoulder (1.65, 1.16–2.35) and elbow (1.90, 1.38–2.61), while a lower rate was found for the wrist (0.72, 0.62–0.83) compared to the joints of digit 3. Within fingers, and using the same reference, joint swelling resolved fastest in digit 4 (1.77, 1.49–2.11) and digit 5 (1.88, 1.53–2.31). A lower rate of resolution of joint swelling was found for the knee in comparison to the elbow, the corresponding joint on the upper limb (0.56, 0.40–0.78). The time to resolution of joint swelling upon treatment with TNFi in patients with PsA seems to depend on the localisation of the affected joints.
{"title":"Differences in the response to TNF inhibitors at distinct joint locations in patients with psoriatic arthritis: results from nine European registries","authors":"Adrian Ciurea, Seraphina Kissling, Andrea Götschi, Lykke Midtbøll Ørnbjerg, Simon Horskjær Rasmussen, Bálint Tamási, Burkhard Möller, Michael J. Nissen, Bente Glintborg, Anne Gitte Loft, Almut Scherer, René Bräm, Karel Pavelka, Jakub Závada, Joao Madruga Dias, Paula Valente, Bjorn Gudbjornsson, Olafur Palsson, Vappu Rantalaiho, Ritva Peltomaa, Catalin Codreanu, Corina Mogosan, Florenzo Iannone, Marco Sebastiani, Gareth T. Jones, Gary J. Macfarlane, Isabel Castrejon, Ziga Rotar, Brigitte Michelsen, Johan K. Wallman, Irene van der Horst-Bruinsma, Oliver Distler, Mikkel Østergaard, Merete Lund Hetland, Raphael Micheroli, Caroline Ospelt","doi":"10.1186/s13075-025-03488-w","DOIUrl":"https://doi.org/10.1186/s13075-025-03488-w","url":null,"abstract":"Efficacy of tumour necrosis factor inhibitors (TNFi) for peripheral arthritis in patients with psoriatic arthritis (PsA) has been established in randomized clinical trials that have used improvement in summated joint counts as an outcome. Whether joints at different anatomical locations might respond differentially to TNFi remains unknown. The aim of the study was to investigate potential variations in the responsiveness to a first tumour necrosis factor inhibitor (TNFi) among joints at distinct locations in patients with psoriatic arthritis (PsA) treated in routine clinical care. Bionaive PsA patients from nine European countries were included in this observational cohort study if ≥ 1 joint was swollen at the initiation of a first TNFi as monotherapy or added to methotrexate. Only the 28-joint count was available without imaging data confirming the presence of synovitis. The primary outcome was time to first resolution of joint swelling at each joint level. Hazard ratios (HR) for resolution comparing different joint locations were estimated using interval-censored mixed-effects Cox proportional hazards models, including a random effect for country and patient, adjusted for age and sex. A total of 1729 patients with 8397 swollen joints at the start of TNFi were included. Considering the upper extremity, a higher rate of resolution of joint swelling (HR, 95% CI) was observed for the shoulder (1.65, 1.16–2.35) and elbow (1.90, 1.38–2.61), while a lower rate was found for the wrist (0.72, 0.62–0.83) compared to the joints of digit 3. Within fingers, and using the same reference, joint swelling resolved fastest in digit 4 (1.77, 1.49–2.11) and digit 5 (1.88, 1.53–2.31). A lower rate of resolution of joint swelling was found for the knee in comparison to the elbow, the corresponding joint on the upper limb (0.56, 0.40–0.78). The time to resolution of joint swelling upon treatment with TNFi in patients with PsA seems to depend on the localisation of the affected joints.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"37 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To evaluate the ability to discriminate giant cell arteritis (GCA) from Takayasu arteritis (TAK) according to the modified 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) GCA classification criteria. Patients enrolled in the Japanese nationwide retrospective registry were evaluated using the criteria with partial modification; wall thickening of descending thoracic-abdominal aorta were mainly diagnosed by contrast-enhanced computed tomography (CT) or magnetic resonance imaging instead of evaluating with positron emission tomography (PET)-CT. The discriminability of the criteria was evaluated using C-statistic (> 0.7: good ability). Newly diagnosed patients with GCA (n = 139) and TAK (n = 129) were assessed, and 23.3% of TAK were aged 50 years or older at onset. The sensitivity of the modified 2022 ACR/EULAR GCA classification criteria with a score ≥ 6 was 82.0%, 68.5%, and 32.1% in all GCA, GCA with large-vessel involvement, and GCA without cranial arteritis, respectively. The specificity of the modified criteria was 96.1% for the 129 TAK as controls. Five patients with late-onset TAK met the modified criteria, and four had cranial signs and symptoms, two had bilateral axillary artery involvement, and four had descending thoracic-abdominal aorta involvement. The discriminability of the criteria was good (C-statistic: 0.986, 95% confidence interval [CI]: 0.976–0.996) and remained good after excluding age (C-statistic: 0.927, 95% CI: 0.894–0.961). The discriminability of a set of large-vessel lesions (bilateral axillary artery and descending thoracic-abdominal aorta) and inflammatory markers was markedly decreased with poor C-statistic value (C-statistic: 0.598, 95% CI: 0.530–0.667). Discriminability was improved after adding polymyalgia rheumatica (PMR) (C-statistic: 0.757, 95% CI: 0.700–0.813) or age (C-statistic: 0.913, 95%CI: 0.874–0.951) to the set of large-vessel lesions. In GCA patients with a score ≤ 5, 52% had bilateral subclavian and/or axillary artery involvement. The modified 2022 ACR/EULAR GCA classification criteria well performed in classifying GCA and TAK without PET-CT in routine clinical practice. A set of items included in the modified GCA classification criteria had good discriminative ability for GCA and TAK, even when age was excluded. However, age restriction or PMR was required to distinguish GCA without cranial lesions from TAK.
{"title":"Performance of the modified 2022 ACR/EULAR giant cell arteritis classification criteria without age restriction for discriminating from Takayasu arteritis","authors":"Takahiko Sugihara, Masayoshi Harigai, Haruhito A. Uchida, Hajime Yoshifuji, Yasuhiro Maejima, Jun Ishizaki, Yoshiko Watanabe, Hiroaki Dobashi, Yoshinori Komagata, Naoto Tamura, Yoshikazu Nakaoka","doi":"10.1186/s13075-025-03486-y","DOIUrl":"https://doi.org/10.1186/s13075-025-03486-y","url":null,"abstract":"To evaluate the ability to discriminate giant cell arteritis (GCA) from Takayasu arteritis (TAK) according to the modified 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) GCA classification criteria. Patients enrolled in the Japanese nationwide retrospective registry were evaluated using the criteria with partial modification; wall thickening of descending thoracic-abdominal aorta were mainly diagnosed by contrast-enhanced computed tomography (CT) or magnetic resonance imaging instead of evaluating with positron emission tomography (PET)-CT. The discriminability of the criteria was evaluated using C-statistic (> 0.7: good ability). Newly diagnosed patients with GCA (n = 139) and TAK (n = 129) were assessed, and 23.3% of TAK were aged 50 years or older at onset. The sensitivity of the modified 2022 ACR/EULAR GCA classification criteria with a score ≥ 6 was 82.0%, 68.5%, and 32.1% in all GCA, GCA with large-vessel involvement, and GCA without cranial arteritis, respectively. The specificity of the modified criteria was 96.1% for the 129 TAK as controls. Five patients with late-onset TAK met the modified criteria, and four had cranial signs and symptoms, two had bilateral axillary artery involvement, and four had descending thoracic-abdominal aorta involvement. The discriminability of the criteria was good (C-statistic: 0.986, 95% confidence interval [CI]: 0.976–0.996) and remained good after excluding age (C-statistic: 0.927, 95% CI: 0.894–0.961). The discriminability of a set of large-vessel lesions (bilateral axillary artery and descending thoracic-abdominal aorta) and inflammatory markers was markedly decreased with poor C-statistic value (C-statistic: 0.598, 95% CI: 0.530–0.667). Discriminability was improved after adding polymyalgia rheumatica (PMR) (C-statistic: 0.757, 95% CI: 0.700–0.813) or age (C-statistic: 0.913, 95%CI: 0.874–0.951) to the set of large-vessel lesions. In GCA patients with a score ≤ 5, 52% had bilateral subclavian and/or axillary artery involvement. The modified 2022 ACR/EULAR GCA classification criteria well performed in classifying GCA and TAK without PET-CT in routine clinical practice. A set of items included in the modified GCA classification criteria had good discriminative ability for GCA and TAK, even when age was excluded. However, age restriction or PMR was required to distinguish GCA without cranial lesions from TAK.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"50 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-30DOI: 10.1186/s13075-025-03478-y
Konstantinos Triantafyllias, Mohammed Alhaddad, Andreas Schwarting, Veronika Balaklytska, Xenofon Baraliakos
Optical spectral transmission (OST) is a modern diagnostic method capable of quantifying inflammation in the finger and wrist joints of arthritis patients by assessing the blood-specific absorption of light transmitted through a tissue. The diagnostic performance of this modality has not been adequately examined and data regarding OST associations with magnetic resonance imaging (MRI) are limited. Aim of this study was therefore to investigate the performance of OST in assessing joint inflammation as compared to MRI in patients with inflammatory arthritis (IA). Data from patients who underwent MRI and OST for suspected IA were analyzed. For comparison, a historical healthy control (HC) group with OST was also accounted. MRI findings were quantified using the Rheumatoid Arthritis MRI Score (RAMRIS). Diagnostic accuracy of OST was evaluated using Receiver Operating Characteristics (ROC), while correlation analyses were conducted to explore relationships between OST and MRI, as well as disease activity markers. Overall, 71 patients with known rheumatic diseases (n = 1,542 wrist and finger joints) and 114 HC (n = 2,508 joints) subjects were included. 51 patients showed inflammatory signs on MRI (MRI+). These also showed significantly higher OST scores (16.41 ± 5.53) than subjects without MRI inflammation (MRI-) (11.52 ± 5.03) or HC (10.78 ± 4.19) (all; p < 0.001). OST showed significant correlations with RAMRIS-synovitis and tenosynovitis scores in the MRI + group (rho = 0.541, p < 0.001; rho = 0.341, p = 0.01, respectively). Significant correlations were observed between OST and clinical parameters for disease activity. Using MRI as a reference, the best diagnostic value of OST was observed at the wrist level in the MRI + group, by an AUC of 0.833 (95%CI 0.700-0.966). OST showed an excellent performance compared to MRI and correlated significantly with RAMRIS scores and clinical parameters in IA patients, also differentiating IA from HC.
{"title":"Diagnostic performance of optical spectral transmission compared to magnetic resonance imaging in patients with inflammatory arthritis","authors":"Konstantinos Triantafyllias, Mohammed Alhaddad, Andreas Schwarting, Veronika Balaklytska, Xenofon Baraliakos","doi":"10.1186/s13075-025-03478-y","DOIUrl":"https://doi.org/10.1186/s13075-025-03478-y","url":null,"abstract":"Optical spectral transmission (OST) is a modern diagnostic method capable of quantifying inflammation in the finger and wrist joints of arthritis patients by assessing the blood-specific absorption of light transmitted through a tissue. The diagnostic performance of this modality has not been adequately examined and data regarding OST associations with magnetic resonance imaging (MRI) are limited. Aim of this study was therefore to investigate the performance of OST in assessing joint inflammation as compared to MRI in patients with inflammatory arthritis (IA). Data from patients who underwent MRI and OST for suspected IA were analyzed. For comparison, a historical healthy control (HC) group with OST was also accounted. MRI findings were quantified using the Rheumatoid Arthritis MRI Score (RAMRIS). Diagnostic accuracy of OST was evaluated using Receiver Operating Characteristics (ROC), while correlation analyses were conducted to explore relationships between OST and MRI, as well as disease activity markers. Overall, 71 patients with known rheumatic diseases (n = 1,542 wrist and finger joints) and 114 HC (n = 2,508 joints) subjects were included. 51 patients showed inflammatory signs on MRI (MRI+). These also showed significantly higher OST scores (16.41 ± 5.53) than subjects without MRI inflammation (MRI-) (11.52 ± 5.03) or HC (10.78 ± 4.19) (all; p < 0.001). OST showed significant correlations with RAMRIS-synovitis and tenosynovitis scores in the MRI + group (rho = 0.541, p < 0.001; rho = 0.341, p = 0.01, respectively). Significant correlations were observed between OST and clinical parameters for disease activity. Using MRI as a reference, the best diagnostic value of OST was observed at the wrist level in the MRI + group, by an AUC of 0.833 (95%CI 0.700-0.966). OST showed an excellent performance compared to MRI and correlated significantly with RAMRIS scores and clinical parameters in IA patients, also differentiating IA from HC.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"30 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes. Fresh RA patients’ whole blood was transfused into NOD-SCID mice. Metabolism-regulatory tissues were examined after sacrifice. To verify the findings, tissues of the rats with long-lasting adjuvant-induced arthritis (AIA) were analyzed. Some rats were injected with human plasma and GPIHBP1, and their blood TG was monitored. Various cells were stimulated by cytokines or rheumatic subjects’ serum. Some pre-adipocytes were cultured by human serum or in the presence of HUVEC cells and GPIHBP1. TG decrease occurred in blood and white adipose tissues (WAT) of the RA blood-transfused NOD-SCID mice and chronic AIA rats. Fatty acids (FA) oxidation in muscles was accelerated a bit, while TG catabolism status in their livers was varied. TNF-α, IL-1β, IL-6 and RA/AIA serum promoted expression of TG utilization-related enzymes and FA uptake transporters in pre-adipocytes, but barely affected LPL. Mild IL-6 stimulus promoted GPIHBP1 release of HUVEC cells. GPIHBP1 was increased in RA serum. This change can decrease blood TG in rats, which was overshadowed by an injection of excessive GPIHBP1. RA serum slightly inhibited LPL secretion in pre-adipocytes. Both HUVEC cells co-culture and GPIHBP1 supplement reduced LPL distribution on pre-adipocytes, and eliminated LPL activity difference between normal and RA serum-treated cells. No TG uptake difference was observed in these circumstances. RA-associated inflammation induces GPIHBP1 secretion of endothelial cells, which facilitates blood TG hydrolysis and uptake to compensate the loss in WAT.
{"title":"GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues","authors":"Meng-Ke Song, Meng-Fan Gu, Ling Liu, Lian-Jun He, Peng Ye, Kui Yang, Dan-Dan Wang, Opeyemi Joshua Olatunji, Qin Yin, Jian Zuo","doi":"10.1186/s13075-025-03483-1","DOIUrl":"https://doi.org/10.1186/s13075-025-03483-1","url":null,"abstract":"Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes. Fresh RA patients’ whole blood was transfused into NOD-SCID mice. Metabolism-regulatory tissues were examined after sacrifice. To verify the findings, tissues of the rats with long-lasting adjuvant-induced arthritis (AIA) were analyzed. Some rats were injected with human plasma and GPIHBP1, and their blood TG was monitored. Various cells were stimulated by cytokines or rheumatic subjects’ serum. Some pre-adipocytes were cultured by human serum or in the presence of HUVEC cells and GPIHBP1. TG decrease occurred in blood and white adipose tissues (WAT) of the RA blood-transfused NOD-SCID mice and chronic AIA rats. Fatty acids (FA) oxidation in muscles was accelerated a bit, while TG catabolism status in their livers was varied. TNF-α, IL-1β, IL-6 and RA/AIA serum promoted expression of TG utilization-related enzymes and FA uptake transporters in pre-adipocytes, but barely affected LPL. Mild IL-6 stimulus promoted GPIHBP1 release of HUVEC cells. GPIHBP1 was increased in RA serum. This change can decrease blood TG in rats, which was overshadowed by an injection of excessive GPIHBP1. RA serum slightly inhibited LPL secretion in pre-adipocytes. Both HUVEC cells co-culture and GPIHBP1 supplement reduced LPL distribution on pre-adipocytes, and eliminated LPL activity difference between normal and RA serum-treated cells. No TG uptake difference was observed in these circumstances. RA-associated inflammation induces GPIHBP1 secretion of endothelial cells, which facilitates blood TG hydrolysis and uptake to compensate the loss in WAT.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"8 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-24DOI: 10.1186/s13075-025-03480-4
Margo Tuerlings, Evelyn Houtman, Elisa J.H. Muusers, Janneke Simon, Maurice W. de Haan, Ilja Boone, Yolande F.M. Ramos, Rachid Mahdad, Ingrid Meulenbelt
To explore IL11 co-expression profiles in our previously reported RNA-sequencing dataset of OA articular cartilage, in interaction with IL6, and to investigate the effects of hrIL11 administration as potential therapeutic strategy for OA articular cartilage using our biomimetic aged human osteochondral explant model of OA. We used RNA-sequencing datasets of macroscopically preserved and lesioned OA articular cartilage (N = 35 patients). Spearman correlations were calculated between IL11 and IL6 expression levels and genes expressed in cartilage (N = 20048 genes). Osteochondral explants were isolated from macroscopically preserved and lesioned areas of the joint and were kept in culture for two weeks, with or without exposure to 200ng/ml hrIL11. We found no overlap in correlating genes between IL11 and IL6, indicating their distinct roles in articular cartilage. Moreover, we identified more genes being correlated to IL11 in the lesioned compared to preserved articular cartilage (N = 203 and 106 genes, respectively). Upon treatment of ex vivo OA articular cartilage with hrIL11, we overall observed unbeneficial effects on chondrocyte phenotype, as illustrated by upregulation of MMP13, EPAS1, RUNX2, and POSTN. We did not observe significant differences in Mankin scores upon addition of hrIL11. The current study showed that treatment of OA articular cartilage with hrIL11 is unlikely to be beneficial despite previous indications of hrIL11 as potential druggable target. These findings underscore the importance of functionally investigating OA risk genes. Better understanding of IL11 signaling and the underlying pathways is necessary towards the development of OA treatment strategy.
{"title":"Exploring the therapeutic effect of human recombinant IL11 on lesioned OA human osteochondral explants","authors":"Margo Tuerlings, Evelyn Houtman, Elisa J.H. Muusers, Janneke Simon, Maurice W. de Haan, Ilja Boone, Yolande F.M. Ramos, Rachid Mahdad, Ingrid Meulenbelt","doi":"10.1186/s13075-025-03480-4","DOIUrl":"https://doi.org/10.1186/s13075-025-03480-4","url":null,"abstract":"To explore IL11 co-expression profiles in our previously reported RNA-sequencing dataset of OA articular cartilage, in interaction with IL6, and to investigate the effects of hrIL11 administration as potential therapeutic strategy for OA articular cartilage using our biomimetic aged human osteochondral explant model of OA. We used RNA-sequencing datasets of macroscopically preserved and lesioned OA articular cartilage (N = 35 patients). Spearman correlations were calculated between IL11 and IL6 expression levels and genes expressed in cartilage (N = 20048 genes). Osteochondral explants were isolated from macroscopically preserved and lesioned areas of the joint and were kept in culture for two weeks, with or without exposure to 200ng/ml hrIL11. We found no overlap in correlating genes between IL11 and IL6, indicating their distinct roles in articular cartilage. Moreover, we identified more genes being correlated to IL11 in the lesioned compared to preserved articular cartilage (N = 203 and 106 genes, respectively). Upon treatment of ex vivo OA articular cartilage with hrIL11, we overall observed unbeneficial effects on chondrocyte phenotype, as illustrated by upregulation of MMP13, EPAS1, RUNX2, and POSTN. We did not observe significant differences in Mankin scores upon addition of hrIL11. The current study showed that treatment of OA articular cartilage with hrIL11 is unlikely to be beneficial despite previous indications of hrIL11 as potential druggable target. These findings underscore the importance of functionally investigating OA risk genes. Better understanding of IL11 signaling and the underlying pathways is necessary towards the development of OA treatment strategy.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"63 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143027231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To investigate cancer incidence and the potential influence of immunosuppressive agents in Korean systemic lupus erythematosus (SLE) patients. We conducted a retrospective analysis utilizing data from the Korea Healthcare Bigdata Linked Platform, which integrated the National Central Cancer Registry and National Health Insurance Service databases covering the period 2008–2017. Incidence rates (IRs) per 10,000 person-years (PYs) for site-specific cancers of SLE patients were calculated using ICD-O-3 codes. Multivariable logistic regression analysis was utilized to assess the association between immunosuppressive agents and cancer development in SLE patients. A total of 10,013 predominantly female (91%) Korean SLE patients with a mean age of 36.9 ± 15.2 years were included. During a follow-up of 62,268.5 PYs, 368 patients developed cancer. The IRs per 10,000 PYs for total, solid, and hematologic cancers were 59.07, 54.09, and 5.78, respectively. The most prevalent cancers (measured in IRs per 10,000 PYs) were thyroid (17.01, 95% CI 13.78–20.25), breast (8.67, 95% CI 6.36–10.98), stomach (4.49, 95% CI 2.83–6.16), colorectal (4.17, 95% CI 2.57–5.78), and cervical (3.85, 95% CI 2.31–5.39). Approximately half (50.8%) of SLE patients with cancer were diagnosed at the localized Surveillance, Epidemiology, and End Results (SEER) stage. No statistically significant association was found between immunosuppressive agents and cancer development (Odds Ratio 1.03, 95% CI 0.80–1.34). Our study shows that Korean SLE patients using immunosuppressive agents are not significantly more likely to develop cancer. Further research with extended observation is warranted to corroborate these findings.
探讨免疫抑制剂在韩国系统性红斑狼疮（SLE）患者中的癌症发生率及潜在影响。我们利用韩国医疗保健大数据链接平台的数据进行了回顾性分析，该平台整合了2008-2017年期间的国家中央癌症登记处和国民健康保险服务数据库。使用ICD-O-3代码计算SLE患者部位特异性癌症的发病率（IRs）每10,000人年（PYs）。采用多变量logistic回归分析来评估免疫抑制剂与SLE患者癌症发展之间的关系。共纳入10013例韩国SLE患者，以女性为主（91%），平均年龄36.9±15.2岁。在62,268.5个月的随访期间，368名患者患上了癌症。总癌、实体癌和血液癌的每10000年ir分别为59.07、54.09和5.78。最常见的癌症（以每10,000 PYs的IRs测量）是甲状腺（17.01,95% CI 13.78-20.25），乳腺癌（8.67,95% CI 6.36-10.98），胃癌（4.49,95% CI 2.83-6.16），结肠直肠癌（4.17,95% CI 2.57-5.78）和宫颈癌（3.85,95% CI 2.31-5.39）。大约一半（50.8%）的SLE合并癌症患者在局部监测、流行病学和最终结果（SEER）阶段被诊断出来。免疫抑制剂与癌症发展之间无统计学意义的关联（优势比1.03,95% CI 0.80-1.34）。我们的研究表明，韩国SLE患者使用免疫抑制剂并没有显著增加患癌的可能性。有必要进行进一步的研究和广泛的观察来证实这些发现。
{"title":"Cancer incidence and the influence of immunosuppressive agents in Korean patients with systemic lupus erythematosus: a retrospective cohort study","authors":"Soo-Kyung Cho, Jung-Yong Han, Yena Jeon, Seung-Hun You, Sun-Young Jung, Eun Jin Jang, Yoon-Kyoung Sung","doi":"10.1186/s13075-025-03482-2","DOIUrl":"https://doi.org/10.1186/s13075-025-03482-2","url":null,"abstract":"To investigate cancer incidence and the potential influence of immunosuppressive agents in Korean systemic lupus erythematosus (SLE) patients. We conducted a retrospective analysis utilizing data from the Korea Healthcare Bigdata Linked Platform, which integrated the National Central Cancer Registry and National Health Insurance Service databases covering the period 2008–2017. Incidence rates (IRs) per 10,000 person-years (PYs) for site-specific cancers of SLE patients were calculated using ICD-O-3 codes. Multivariable logistic regression analysis was utilized to assess the association between immunosuppressive agents and cancer development in SLE patients. A total of 10,013 predominantly female (91%) Korean SLE patients with a mean age of 36.9 ± 15.2 years were included. During a follow-up of 62,268.5 PYs, 368 patients developed cancer. The IRs per 10,000 PYs for total, solid, and hematologic cancers were 59.07, 54.09, and 5.78, respectively. The most prevalent cancers (measured in IRs per 10,000 PYs) were thyroid (17.01, 95% CI 13.78–20.25), breast (8.67, 95% CI 6.36–10.98), stomach (4.49, 95% CI 2.83–6.16), colorectal (4.17, 95% CI 2.57–5.78), and cervical (3.85, 95% CI 2.31–5.39). Approximately half (50.8%) of SLE patients with cancer were diagnosed at the localized Surveillance, Epidemiology, and End Results (SEER) stage. No statistically significant association was found between immunosuppressive agents and cancer development (Odds Ratio 1.03, 95% CI 0.80–1.34). Our study shows that Korean SLE patients using immunosuppressive agents are not significantly more likely to develop cancer. Further research with extended observation is warranted to corroborate these findings.","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"33 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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