Annals of the Rheumatic Diseases最新文献

{"title":"Annals of the Rheumatic Diseases Collection on juvenile idiopathic arthritis (JIA) 2019-2024.","authors":"Lianne Kearsley-Fleet, Samantha L Smith, Athimalaipet V Ramanan, Kimme L Hyrich","doi":"10.1016/j.ard.2024.11.004","DOIUrl":"10.1016/j.ard.2024.11.004","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"375-381"},"PeriodicalIF":20.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405507","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":"An interpretable machine learning approach for detecting psoriatic arthritis in a UK primary care psoriasis cohort using electronic health records from the Clinical Practice Research Datalink.","authors":"Alexander Rudge, Neil McHugh, William Tillett, Theresa Smith","doi":"10.1016/j.ard.2025.01.051","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.051","url":null,"abstract":"<p><strong>Objectives: </strong>Develop an interpretable machine learning model to detect patients with newly diagnosed psoriatic arthritis (PsA) in a cohort of psoriasis patients and identify important clinical indicators of PsA in primary care.</p><p><strong>Methods: </strong>We developed models using UK primary care electronic health records from the Clinical Practice Research Datalink (CPRD). The study population consisted of a cohort of (PsA free) patients with incident psoriasis who were followed prospectively. We used Bayesian networks (BNs) to identify patients who developed PsA using primary care variables measured prior to diagnosis and compared the results to a random forest (RF). Variables included patient demographics, musculoskeletal symptoms, blood tests, and prescriptions. The importance of each variable used in the models was evaluated using permutation variable importance. Model discrimination was measured using the area under the receiver operating characteristic curve (AUC) and the area under the precision-recall curve (PRAUC).</p><p><strong>Results: </strong>We identified a cohort of 122,330 patients with an incident psoriasis diagnosis between 1998 and 2019 in the CPRD, of whom 2460 patients went on to develop PsA. Our best BN achieved an AUC of 0.823, and PRAUC of 0.221, compared to the AUC of 0.851 and PRAUC of 0.261 of the RF. Psoriasis duration, nonsteroidal anti-inflammatory drug prescriptions, nonspecific arthritis, nonspecific arthralgia, and C-reactive protein blood tests were all important variables in our models.</p><p><strong>Conclusions: </strong>We were able to identify psoriasis patients at higher risk, and important indicators, of PsA in UK primary care. Further work is required to evaluate our model's usefulness in assisting PsA screening.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536395","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":"Risk of developing psoriatic arthritis in patients with psoriasis initiating treatment with different classes of biologics.","authors":"Paolo Gisondi, Francesco Bellinato, Carlotta Galeone, Federica Turati, Luca Idolazzi, Alen Zabotti, Dennis McGonagle, Giampiero Girolomoni","doi":"10.1016/j.ard.2025.01.006","DOIUrl":"10.1016/j.ard.2025.01.006","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the risk of psoriatic arthritis (PsA) in plaque psoriasis (PsO) patients receiving different classes of biologics.</p><p><strong>Methods: </strong>A retrospective observational study involving consecutive bionaïve PsO patients starting biologic treatment was performed. We compared the occurrence of PsA by the class of the biologic (tumour necrosis factor [TNF], interleukin [IL]-17, or IL-23 inhibitors) using inverse probability of treatment weighting (IPTW) in the setting of multiple treatments to balance pretreatment covariates across cohorts and thus adjust for potential confounders. An IPTW Cox regression model was used to estimate hazard ratios (HRs) of PsA for IL-17 and IL-23 inhibitors versus TNF inhibitors.</p><p><strong>Results: </strong>In total, 622 patients, 430 (62.4%) males, mean ± SD age 46.9 ± 12.9 years, were included. They have been treated with TNF (n = 317, 50.9%), IL-17 (n = 164, 26.4%) or IL-23 inhibitors (n = 141, 22.7%) and followed for 2510 person-years (a mean of 4.1 ± 2.1 years per person). TNF, IL-17, and IL-23 inhibitor cohorts had a total of 1569, 486, and 455 person-years of follow-up. A total of 60 (10%) out of 622 patients on biologic therapy developed incident PsA during the observation period: 45 (14.2%) in the TNF, 9 (5.5%) in the IL-17, and 6 (4.3%) in the IL-23 inhibitor cohorts. After IPTW, the 3 treatment cohorts were well-balanced, and the HRs of PsA were 0.63 (95% CI, 0.38-1.05) for IL-17 and 0.57 (95% CI, 0.34-0.96) for IL-23 compared with the TNF treatment group.</p><p><strong>Conclusions: </strong>The risk of developing PsA appeared slightly different in patients receiving diverse classes of biologics.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"435-441"},"PeriodicalIF":20.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370265","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":"Characterisation of the antinociceptive effect of baricitinib in the collagen antibody-induced arthritis mouse model.","authors":"Nils Simon, Resti Rudjito, Lydia Moll, Katalin Sandor, Juan Antonio Vazquez-Mora, Zerina Kurtović, Alexandra Kuliszkiewicz, Carlos E Morado Urbina, Sven David Arvidsson, Eduardo Mendoza-Sánchez, Giovanni E López-Delgado, Qing Luo, Qiaolin Deng, Arisai Martínez Martínez, Jens Gammeltoft Gerwien, Paul Karila, Venkatesh Krishnan, Juan Miguel Jiménez-Andrade, Camilla I Svensson","doi":"10.1016/j.ard.2025.01.005","DOIUrl":"10.1016/j.ard.2025.01.005","url":null,"abstract":"<p><strong>Objectives: </strong>Many rheumatoid arthritis (RA) patients continue to experience persistent pain even after successful management of joint inflammation. Clinical data indicate that RA patients treated with the JAK inhibitor baricitinib consistently achieve pain relief that cannot be entirely attributed to its anti-inflammatory effects. In this study, we investigated the antinociceptive properties of baricitinib using the collagen antibody-induced arthritis (CAIA) model in which mechanical hypersensitivity persists long after resolution of joint inflammation.</p><p><strong>Methods: </strong>The effects of baricitinib, etanercept (tumour necrosis factor inhibitor), and LP-922761 (adaptor protein-2 (AP2) associated kinase 1 (AAK1) inhibitor) on pain-like behaviour in CAIA mice were examined. Tissue samples from the late, low-grade inflammatory phase were examined for the effect of the treatments. Additionally, in vitro experiments using dorsal root ganglion (DRG) cells were conducted to assess baricitinib's influence on neuronal excitability and cell morphology.</p><p><strong>Results: </strong>Baricitinib reduced CAIA-induced joint inflammation, but its antinociceptive effects were most pronounced during the late phase when etanercept was ineffective. Administering baricitinib both early and late significantly decreased CAIA-induced bone loss, synovial innervation, and baseline STAT3 phosphorylation in ankle joints and DRGs. Unlike etanercept, baricitinib effectively reduced pain-like behaviour and synovial hyperinnervation when administered exclusively in the late phase. Additionally, baricitinib modulated glial cell morphology and neuronal excitability in vitro. Notably, it inhibited AAK1 signalling in DRGs, with AAK1 kinase activity blockade providing an antinociceptive effect in the CAIA model.</p><p><strong>Conclusions: </strong>Our data suggests that baricitinib has antinociceptive effects by targeting not only immune cells but also neurons and glia cells via inhibition of 2 signalling pathways linked to chronic pain.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"421-434"},"PeriodicalIF":20.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381636","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":"Interleukin-18 and interleukin-1β blockade to control inflammation in PAMI syndrome before and after HSCT.","authors":"Benjamin Fournier, Laurye-Anne Eveillard, Agathe Escudier, Guilaine Boursier, Anne Welfringer, Bénédicte Neven, Brigitte Bader-Meunier","doi":"10.1016/j.ard.2024.12.002","DOIUrl":"10.1016/j.ard.2024.12.002","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"e1-e3"},"PeriodicalIF":20.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405510","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":"Integrative analysis reveals the multilateral inflammatory mechanisms of CD14 monocytes in gout.","authors":"Ahmed Alaswad, Georgiana Cabău, Tania O Crişan, Liang Zhou, Martijn Zoodsma, Javier Botey-Bataller, Wenchao Li, Cristina Pamfil, Mihai G Netea, Tony Merriman, Cheng-Jian Xu, Yang Li, Leo A B Joosten","doi":"10.1016/j.ard.2025.01.046","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.046","url":null,"abstract":"<p><strong>Objectives: </strong>Gout, prevalent inflammatory arthritis caused by urate crystal deposition, involves immune cell activation, yet the precise role of CD14 monocytes in initiating the inflammatory response is poorly understood. This study aimed to characterise the molecular and cellular landscape of CD14 monocytes in gout using single-cell transcriptomic analysis.</p><p><strong>Methods: </strong>Single-cell RNA sequencing was performed on peripheral blood mononuclear cells from 8 gout patients and 6 age- and sex-matched healthy controls. The findings were validated using publicly available datasets. Differential gene expression and pathway enrichment analyses were conducted to identify gout's key molecular regulators and cellular subclusters.</p><p><strong>Results: </strong>At the molecular level, we identified hypoxia-related pathways, including HIF1A, as key regulators of interleukin-1β production in CD14 monocytes in gout. We also observed significant downregulation of CLEC12A across all CD14 monocyte subclusters. At the cellular level, an S100A^high CD14 monocyte subcluster, characterized by high expression of S100A8/A9/A12 and linked to inflammatory and metabolic pathways, was found to drive NLRP3 and CLEC7A inflammasome activation, as well as prostaglandin secretion. In vitro stimulation with monosodium urate crystals revealed that the differentially expressed genes were enriched in S100A^high monocytes, highlighting the synergistic role of these pathways in driving gout inflammation. Additionally, gout genome-wide association study-prioritised genes underscored the role of fatty acid metabolism in inflammation, promoting prostaglandin secretion from S100A^high monocytes.</p><p><strong>Conclusions: </strong>These findings provide new insights into the role of CD14 monocytes in gout pathogenesis, particularly the contribution of hypoxia and fatty acid metabolism pathways, and suggest potential therapeutic targets for precision medicine in gout treatment.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536396","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":"Three years is the minimal effective duration of sustained clinical remission which prevents impaired kidney function and damage accrual in lupus nephritis.","authors":"Mariele Gatto, Giulia Frontini, Claudia Furlan, Marta Calatroni, Claudio Cruciani, Francesco Reggiani, Elisa Bellis, Luca Iaccarino, Renato Alberto Sinico, Gabriella Moroni, Andrea Doria","doi":"10.1016/j.ard.2025.02.004","DOIUrl":"https://doi.org/10.1016/j.ard.2025.02.004","url":null,"abstract":"<p><strong>Objectives: </strong>To assess the minimum effective duration of remission preventing damage accrual (Systemic Lupus International Collaborating Clinics damage index [SDI]) and impaired kidney function (IKF: estimated glomerular filtration rate of <60 mL/min/1.73 m² for at least 3 months) in active lupus nephritis (LN).</p><p><strong>Methods: </strong>Patients with biopsy-proven LN followed up at least twice yearly were enrolled; clinical variables were collected regularly. Sustained clinical remission (sCR) was defined as estimated glomerular filtration rate of >60 mL/min/1.73 m², proteinuria of <0.5 g/24 h and clinical systemic lupus erythematosus disease activity index of 0 for at least 1 year. Log-linear regression and a time-dependent Cox proportional hazard model were used to assess the minimum duration of sCR capable of preventing SDI increase and IKF development.</p><p><strong>Results: </strong>In total, 293 patients with LN were included (median follow-up: 15.7 [10.4-22.9] years) of whom 84.3% achieved sCR lasting 8.7 (5.4-13.1) years. At last observation, the increase in SDI was higher in patients who never achieved sCR (median: 2 [1-2.5] vs 1 [0-1.5]; P < .001). A minimum duration of 3 years of sCR prevented SDI increase (% change = -41.1%; P = .003). The analysis on IKF involved only patients with the longest follow-up; 224 patients had ≥10 years of observation. Among them, 50 (22.3%) developed IKF. A minimum duration of 3 years of sCR prevented IKF (hazard ratio = 0.10; P < .001). IKF-free survival rate at 10, 20, and 25 years was 87%, 68%, and 40% for patients who never achieved sCR and 99%, 96%, and 91% for patients with at least 3 years of sCR, respectively (P < .001).</p><p><strong>Conclusions: </strong>Three years is the minimum duration of sCR protecting against development of IKF and damage accrual in patients with LN.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536541","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":"Safety of colchicine on fertility, pregnancy, and lactation: a systematic review and meta-analysis informing the EULAR/PReS recommendations for familial Mediterranean fever.","authors":"Teresa Otón, Erdal Sağ, Loreto Carmona, Seza Ozen","doi":"10.1016/j.ard.2025.02.005","DOIUrl":"https://doi.org/10.1016/j.ard.2025.02.005","url":null,"abstract":"<p><strong>Objectives: </strong>To summarise the evidence of colchicine's effects on fertility, pregnancy, and lactation in the treatment of patients with familial Mediterranean fever (FMF).</p><p><strong>Methods: </strong>Two reviewers and a methodologist conducted the systematic review. Together with an expert in FMF, they established the protocol and the PICOt questions. Medline via PubMed, Embase, and the Cochrane Library were searched from inception until August 23, 2023. All clinical trials, cohort studies, or case series focused on the safety of colchicine in FMF, concerning reproductive issues or breastfeeding, and involving at least 5 patients were eligible. The risk of bias in the studies was assessed using the Newcastle-Ottawa Scale. Meta-analysis was planned for at least 2 homogeneous studies with fixed-effect models using the Mantel-Haenszel method to obtain the pooled risk ratio (RR) and 95% CI.</p><p><strong>Results: </strong>Twenty-five studies were included overall of moderate to low quality. The RR of miscarriage or foetal loss with colchicine in FMF was 0.87 (95% CI, 0.67-1.12), showing a heterogeneity of 31%. The percentage of birth defects in the exposed group ranged from 0.6% to 4.0%, not very different, comparable to the rates of women with FMF without exposure to colchicine. Regarding fertility, there were no apparent differences between colchicine-exposed and nonexposed groups, neither among women nor men (sperm assessment). Only 1 study reported breastfeeding data, showing no growth differences among exposed and nonexposed babies.</p><p><strong>Conclusions: </strong>Colchicine appears to have a good risk-benefit profile regarding reproductive safety. Ideally, higher-quality studies should be performed, especially regarding male fertility.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536529","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":"Responsiveness of systemic lupus erythematosus subjects to iberdomide based on molecular endotypes.","authors":"Prathyusha Bachali, Andrea Daamen, Shimon Korish, Yanhua Hu, Peter Schafer, Amrie Grammer, Peter E Lipsky","doi":"10.1016/j.ard.2025.01.044","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.044","url":null,"abstract":"<p><strong>Objectives: </strong>Iberdomide is a cereblon E3-ligase modulator that promotes proteasomal degradation of the transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) and was shown to be efficacious among subjects with generalised systemic lupus erythematosus (SLE). This study sought to identify baseline gene expression profiles of SLE subjects responsive to iberdomide and analyse the impact of this agent on gene expression.</p><p><strong>Methods: </strong>Whole blood samples obtained from 276 female SLE subjects in the phase 2b iberdomide trial (NCT03161483) were assessed by RNA sequencing followed by gene set variation analysis (GSVA) using 32 informative gene modules. Unsupervised K-means clustering categorised subjects according to molecular endotypes at baseline. Each endotype was compared for treatment related gene expression changes.</p><p><strong>Results: </strong>K-means clustering of GSVA scores from whole blood yielded 5 patient subsets (endotypes A-E) with increases in molecular abnormalities indicative of enhanced immune activity. Significant clinical responses to iberdomide, determined using the SLE Responder Index 4, were confined to endotypes C and E. The most important treatment related gene modules in responders in endotype E were Treg cells, B cells, and interferon, whereas unfolded proteins, oxidative phosphorylation and anergic/activated T cells were associated with responsiveness in endotype C.</p><p><strong>Conclusions: </strong>Molecular profiles of SLE subjects identified pharmacodynamic effects of iberdomide that occurred in all endotypes as well as changes in specific gene modules altered in endotypes associated with a significant clinical response. Thus, gene expression-based molecular profiling may be useful to enrich clinical trials for treatment-responsive subjects and also monitor the pharmacodynamic impact of therapy.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143530935","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":"Teclistamab in relapsed systemic sclerosis after autologous haematopoietic stem cell transplantation.","authors":"Elise Siegert, Robert Biesen, Maria Dzamukova, Christian Furth, Meike Probst, Felix Doellinger, Thula Walter-Rittel, Anja Fleischmann, Artur Wilhelm, Anne Elisabeth Beenken, Edgar Wiebe, Ann-Christin Pecher, Jörg Henes, Stefan Florian, David Simon, Arnd Kleyer, Gerd-Rüdiger Burmester, Ulrich Keller, Jan Krönke, Gerhard Krönke, Tobias Alexander","doi":"10.1016/j.ard.2025.01.043","DOIUrl":"https://doi.org/10.1016/j.ard.2025.01.043","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498081","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}