2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T713,To evaluate the association between immune-mediated inflammatory diseases (IMIDs) and uveitis DESIGN: Retrospective cohort and case-control study using electronic health record data. Patients diagnosed with uveitis and/or one of 12 IMIDs: rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), sarcoidosis, scleroderma, inflammatory bowel disease (IBD), multiple sclerosis (MS), ankylosing spondylitis, psoriasis, juvenile idiopathic arthritis (JIA), and giant cell arteritis (GCA), anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis, and other systemic vasculitis. Controls were patients without prior uveitis diagnosis or any IMIDs. We calculated the risk of developing uveitis in patients with each IMID, the odds of prior IMID diagnoses among patients with uveitis, and the risk of developing an IMID following a uveitis diagnosis. Relative risk (RR) and odds ratio (OR) estimates with 95% confidence intervals (CIs) for associations between IMIDs and uveitis. Patients with all 12 IMIDs had a significantly increased risk of developing uveitis. Highest risks were observed in ankylosing spondylitis (RR=7.71, 95% CI: 5.84-10.19), JIA (RR=5.13, 95% CI: 3.51-7.49), and systemic vasculitis (RR=4.61, 95% CI: 3.73 to 5.69). Increased risk was also found in sarcoidosis (RR=3.67, 95% CI: 3.02 to 4.47), GCA (RR=3.24, 95% CI: 2.58-4.07), and ANCA vasculitis (RR=3.18, 95% CI: 1.84-5.48). In addition, in patients with uveitis, both the odds of a prior IMID diagnosis and the risk of a future IMID diagnosis were significantly increased for all 12 IMIDs. IMIDs are strongly associated with uveitis, with significant bidirectional risk. Patients with uveitis should be monitored for potential IMID development, and those with IMIDs should undergo ophthalmologic evaluation when appropriate.31:T8ea, Imaging has become a cornerstone in the clinical management of giant cell arteritis (GCA), with its role extending beyond diagnosis to include disease monitoring, risk stratification of relapse, and therapeutic decision-making. While imaging modalities have been well-established for diagnostic purposes, growing evidence supports their utility in tracking disease activity and stratifying the risk of relapse. In this narrative review, we discuss the available evidence on the prognostic and therapeutic implications of imaging-guided stratification in GCA, and highlight areas that require further research. Ultrasound assessment of intima-media thickness shows measurable improvement following treatment. While this response is relatively rapid in the cranial arteries, it occurs slowly or very slowly in extracranial vessels. Moreover, ultrasound signs and quantitative indices may be useful for distinguishing remission from relapse. Similarly, arterial inflammation assessed by 18 F-fluorodeoxyglucose positron emission tomography ( 18 F-FDG PET) also improves with treatment. However, persistent large vessel vascular uptake is often observed in patients deemed to be in clinical remission. The clinical relevance of such subclinical imaging abnormalities remains unclear, underscoring the need for further research before imaging can be routinely employed for disease monitoring. Imaging may also provide valuable prognostic information. Evidence remains conflicting as to whether patients with large-vessel involvement detected by imaging may relapse more frequently, require glucocorticoid-sparing agents more often, and have an increased risk of cardiovascular events compared to those with isolated cranial GCA. However, quantifying vascular inflammation by ultrasound at diagnosis could support risk stratification and inform individualized treatment decisions. Moreover, elevated arterial uptake on 18 F-FDG PET at baseline has been associated with a higher likelihood of late vascular complications, such as aneurysm formation. 32:T6d0,This study investigated the role of IL-17 in Giant Cell Arteritis (GCA), which has remained uncertain despite previous research suggesting a contribution of Th17 cells to the disease. Temporal artery biopsies (TABs) were cultured ex vivo in MATRIGEL® with IL-17, secukinumab, or control IgG, and subsequently analyzed using bulk RNA-sequencing and RT-qPCR. Positive-TABs with GCA features were compared to negative-TABs or used to obtain in vitro cultures of myofibroblasts (MFs). Confocal microscopy analyzed IL-17 receptor expression. MFs and peripheral blood mononuclear cells co-cultures were used to study T-cell polarization. Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably IL6. RT-qPCR analysis confirmed that secukinumab decreased mRNA encoding IL-6, CCL20, and GM-CSF in positive-TABs, while IL-17 upregulated them in negative-TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL-17 receptor chains were expressed on MFs, and their expression was enhanced by IFN-γ. RT-qPCR and Luminex® analyses confirmed IL-17-driven upregulation of IL-6, CCL20, CCL2, GM-CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN-γ to the culture increased the expression level of IL-17 receptor chains, resulting in a synergistic effect. Additionally, IL-17 pre-treated MFs promoted Th17 polarization. IL-17 exacerbates vascular inflammation in GCA by activating MFs and synergizing with IFN-γ to increase production of pro-inflammatory cytokines (IL-6, GM-CSF), chemokines (CCL20, CCL2), and angiogenic factors (VEGF, indicating that IL-17 is a key contributor to disease pathogenesis.33:Tc6b, Objectives This study investigated the role of IL‐17 in Giant Cell Arteritis (GCA), which has remained uncertain despite previous research suggesting a contribution of Th17 cells to the disease. Methods Temporal artery biopsies (TABs) were cultured ex vivo in MATRIGEL® with IL‐17, secukinumab, or control IgG, and subsequently analyzed using bulk RNA‐sequencing and RT‐qPCR. Positive‐TABs with GCA features were compared to negative‐TABs or used to obtain in vitro cultures of myofibroblasts (MFs). Confocal microscopy analyzed IL‐17 receptor expression. MFs and peripheral blood mononuclear cells co‐cultures were used to study T‐cell polarization. Results Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably IL6 . RT‐qPCR analysis confirmed that secukinumab decreased mRNA encoding IL‐6, CCL20, and GM‐CSF in positive‐TABs, while IL‐17 upregulated them in negative‐TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL‐17 receptor chains were expressed on MFs, and their expression was enhanced by IFN‐γ. RT‐qPCR and Luminex® analyses confirmed IL‐17‐driven upregulation of IL‐6, CCL20, CCL2, GM‐CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN‐γ to the culture increased the expression level of IL‐17 receptor chains, resulting in a synergistic effect. Additionally, IL‐17 pre‐treated MFs promoted Th17 polarization. Conclusions IL‐17 exacerbates vascular inflammation in GCA by activating MFs and synergizing with IFN‐γ to increase production of pro‐inflammatory cytokines (IL‐6, GM‐CSF), chemokines (CCL20, CCL2), and angiogenic factors (VEGF, indicating that IL‐17 is a key contributor to disease pathogenesis.

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34:Tafe, Objective The objectives of this study were to evaluate the correlation and agreement between ultrasonography and computed tomography (CT) in measuring ascending aorta diameter in patients with giant cell arteritis (GCA) and to investigate the development of new ascending aortic aneurysms in patients with newly diagnosed GCA. Methods To achieve the primary objective, we performed a cross‐sectional study that included patients with GCA who were evaluated with both ultrasonography and CT of the ascending aorta within six months of each other. For the second objective, patients with baseline aortic imaging at GCA diagnosis were observed prospectively with new aortic imaging at the end of the follow‐up. A cutoff of ≥40 mm defined an aneurysm in both the ascending and the descending aorta. Results The cross‐sectional study included 140 patients with a total of 169 comparable CT and ultrasonography scans and a mean disease duration of 47.8 months (95% confidence interval [CI] 42.1–53.5). A strong positive correlation, as measured by Spearman's rho ( r = 0.801, P < 0.001), and a strong agreement, as indicated by an intraclass correlation coefficient of 0.849 ( P < 0.001), were found between ultrasonography and CT. In the prospective follow‐up study, 40 patients were included. Seven (17.5%) patients developed aneurysms in the ascending aorta in a mean follow‐up time of 54 months (95% CI 43.7–64.6); all of the patients experienced large vessel (LV) involvement (two patients with LV‐GCA and five patients with mixed‐GCA). Conclusion A strong correlation and agreement were observed between ultrasonography and CT measurements in assessing the diameter of the ascending aorta in patients with GCA. Ultrasonography may be a valuable tool for longitudinal monitoring and screening for aneurysm development. About 18% of patients developed aortic aneurysms over a mean follow‐up of 4.5 years, underscoring the critical need for regular aortic screening in this population. 35:T441,Giant cell arteritis (GCA) is a large-vessel vasculitis, potentially causing complications such as blindness and strokes. This study aims to gain insights into the pathogenesis of GCA by identifying specific DNA methylation signatures in the arterial tissue of patients with this vasculitis. DNA methylation profiling was analyzed in 79 temporal artery biopsy samples (69 patients with GCA and 10 controls) by performing an epigenome-wide association study (EWAS). Differential analysis was performed to identify differentially methylated positions (DMPs) and differentially methylated regions (DMRs). Lastly, we compared our findings with previous transcriptomics and epigenomics studies on GCA-affected arteries. EWAS identified 3,644 DMPs (P Our study identified GCA-specific DNA methylation signatures in arterial tissue, revealing disrupted inflammatory and vascular pathways and suggesting the involvement of exhausted T cells in this condition. These findings offer new insights into GCA pathogenesis and provide new potential targets for the treatment of this debilitating disease.36:Taaf, Objective Giant cell arteritis (GCA) is a large‐vessel vasculitis, potentially causing complications such as blindness and strokes. This study aims to gain insights into the pathogenesis of GCA by identifying specific DNA methylation signatures in the arterial tissue of patients with this vasculitis. Methods DNA methylation profiling was analyzed in 79 temporal artery biopsy samples (69 patients with GCA and 10 controls) by performing an epigenome‐wide association study (EWAS). Differential analysis was performed to identify differentially methylated positions (DMPs) and differentially methylated regions (DMRs). Lastly, we compared our findings with previous transcriptomics and epigenomics studies on GCA‐affected arteries. Results EWAS identified 3,644 DMPs ( P adj < 0.05, |Δβ| > 0.3), indicating a profound alteration within GCA‐affected arterial tissue. These DMPs were annotated to 1,517 potentially dysregulated genes. A total of 282 additional genes were identified by annotation of significant DMRs. Pathway enrichment analysis revealed a significant alteration of inflammatory mechanisms, such as interleukin‐2 and interleukin‐7, as well as pathways related to vascular remodeling. Omics study comparison revealed 37 genes consistently affected across datasets, many of them linked to immune signaling and T cell regulation. Notably, markers of exhausted T cells, including SLAMF6 and HAVCR2 , were present among them. Conclusion Our study identified GCA‐specific DNA methylation signatures in arterial tissue, revealing disrupted inflammatory and vascular pathways and suggesting the involvement of exhausted T cells in this condition. These findings offer new insights into GCA pathogenesis and provide new potential targets for the treatment of this debilitating disease. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Giant Cell Arteritis: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Giant Cell Arteritis (condition). Clinician-written summaries and actionable practice insights. 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Summaries and tags are based on the abstract and results sections of the survey paper, as provided. Clinical trial data from the SmPC (e.g., SELECT-GCA) is referenced only for context, not summarized as the primary study.","value_numeric":null}],"summaries":{"what_studied":"This cross-sectional retrospective survey (Adelphi Real-World GCA Disease Specific Programme, May–October 2024) assessed real-world glucocorticoid (GC) burden, treatment patterns, and rheumatologist attitudes toward advanced therapies in 846 patients with giant cell arteritis (GCA) managed by 196 rheumatologists across EU-5 countries and the US.","key_result":"Despite rheumatologists intending to stop GCs by 24 months, 80% of patients were still on GCs at 24–<36 months (mean 8.4 mg/day) and 75% at ≥48 months (mean 5.3 mg/day). Median cumulative GC dose over 12 months ranged from 2,196 mg (diagnosed >24 months ago) to 5,200 mg (diagnosed 12–24 months ago). Although ≥90% of rheumatologists agreed advanced therapies should be started early, only 48% reported prescribing one at any point post-diagnosis. Most common GC-related adverse events were weight gain, fatigue, and fluid retention.","limitations":"Retrospective survey design limits causal inference; rheumatologist-reported data on adverse events and dosing may be subject to recall bias; patient self-report was limited to 26% of cases, which may not be representative.","practice_takeaway":"Most GCA patients remain on prolonged GC therapy well beyond the intended 24-month target, creating significant adverse-event burden. Clinicians should consider initiating steroid-sparing advanced therapies (e.g., upadacitinib 15 mg once daily, now EU-approved for GCA) early in the disease course to close the gap between intent and practice."}},{"doi":"10.1177/1759720x261477872","pmid":"42621212","title":"Glucocorticoid discontinuation and clinical phenotypes in patients with giant cell arteritis: A retrospective cohort study from a fast track clinic","journal_title":"Therapeutic Advances in Musculoskeletal Disease","journal_issn":"1759-720X","published_at":"2026-08-17T00:00:00.000Z","url":"https://doi.org/10.1177/1759720x261477872","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-26T06:20:05.983Z","updated_at":"2026-08-26T06:20:05.983Z","tags":[{"paper_doi":"10.1177/1759720x261477872","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"brand","value":"Rinvoq","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"generic","value":"prednisolone","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"generic","value":"tocilizumab","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"generic","value":"upadacitinib","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"modality","value":"Glucocorticoid","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"modality","value":"IL-6 Inhibitor","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"sample_size","value":"n=172","value_numeric":172},{"paper_doi":"10.1177/1759720x261477872","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"warning","value":"26% of patients had no positive imaging or TAB; GCA diagnosis in these cases was clinical only, which may introduce diagnostic heterogeneity.","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"warning","value":"The 4- and 5-year cumulative incidence estimates (both 69%) are based on very few patients at risk (n=8 and n=1, respectively) and should be interpreted with great caution.","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"warning","value":"The study was conducted at a single centre in Denmark; generalisability to other healthcare settings or ethnicities is uncertain.","value_numeric":null},{"paper_doi":"10.1177/1759720x261477872","tag_type":"warning","value":"Upadacitinib is mentioned in the introduction as newly approved for GCA but was not used in this cohort; its brand name 'Rinvoq' tag is inferred from the generic name and may not be explicitly stated in the paper.","value_numeric":null}],"summaries":{"what_studied":"A retrospective cohort study of 172 GCA patients diagnosed at a fast track clinic (FTC) between Sept 2018 and Dec 2021, followed until Dec 2023 (median 40.6 months), to estimate the probability of glucocorticoid (GC) discontinuation and assess whether symptom- or laboratory-based phenotypes predicted treatment outcomes.","key_result":"Cumulative incidence of GC discontinuation was 10% at 1 year, 43% at 2 years, 58% at 3 years, and 69% at 4–5 years. Patients with a prior GCA/PMR diagnosis (26% of cohort) had significantly lower odds of discontinuing GC (sHR 0.54, 95% CI 0.30–0.96). Four symptom-based and three lab-based phenotype clusters were identified, but neither predicted GC discontinuation or time to first relapse.","limitations":"Single-centre retrospective design with missing data for some variables; cluster analyses may be underpowered given cohort size; patient numbers at risk dropped sharply after 3 years, making 4–5 year estimates unreliable.","practice_takeaway":"Patients with a prior GCA or PMR diagnosis are at higher risk of prolonged GC dependency and should be counselled accordingly. Symptom patterns and baseline inflammatory markers alone are not useful for predicting who will successfully stop GC therapy."}},{"doi":"10.1016/j.ard.2026.06.009","pmid":"42481270","title":"2025 EULAR recommendations for the management of polymyalgia rheumatica and primary large vessel vasculitis","journal_title":"Annals of the Rheumatic Diseases","journal_issn":"0003-4967","published_at":"2026-07-21T00:00:00.000Z","url":"https://doi.org/10.1016/j.ard.2026.06.009","source_score":14,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-25T13:57:47.110Z","updated_at":"2026-07-25T13:57:47.110Z","tags":[{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"brand","value":"Rinvoq","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"condition","value":"Large Vessel Vasculitis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"condition","value":"Takayasu Arteritis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"generic","value":"methotrexate","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"generic","value":"prednisone","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"generic","value":"upadacitinib","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"modality","value":"Glucocorticoid","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"modality","value":"IL-6 Receptor Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"study_design","value":"Clinical Practice Guideline","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"warning","value":"Brand tag 'Rinvoq' added for upadacitinib; confirm formulary availability and licensed indications for GCA in the relevant jurisdiction, as this may be a newer indication.","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"warning","value":"Level of evidence assigned as '4' (expert consensus/guideline) since this is a recommendations paper, not a primary clinical trial; individual underlying recommendations may carry different evidence grades not specified in the abstract.","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"warning","value":"No sample size is applicable — this is a task force consensus document, not a patient-level study.","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.009","tag_type":"warning","value":"The DOI and publication date (2026-07-21) are in the future relative to typical indexing cycles — verify final publication status before citing in clinical use.","value_numeric":null}],"summaries":{"what_studied":"Updated EULAR recommendations for managing polymyalgia rheumatica (PMR), giant cell arteritis (GCA), and Takayasu arteritis (TAK), developed by an international task force using systematic literature reviews of evidence published since the 2015 PMR and 2018 GCA/TAK guidelines.","key_result":"The task force produced 4 overarching principles, 12 recommendations, and 2 quality indicators with high levels of agreement. Key updates include: immediate GC start for suspected GCA (without waiting for confirmatory tests); GC initiation at 15–25 mg/day for PMR and 40–60 mg/day for GCA/TAK; IL-6 receptor inhibitors as adjunctive therapy for PMR and GCA; upadacitinib as an option for GCA; and mandatory GC-sparing agents for all TAK patients.","limitations":"As a consensus recommendations paper, the strength of individual recommendations depends on underlying trial evidence, which may be limited for some conditions (especially TAK). The systematic reviews cover only data published after prior guideline versions, so older evidence is inherited rather than re-evaluated.","practice_takeaway":"Refer all suspected GCA patients to a specialist within 24 hours and start glucocorticoids immediately — do not wait for biopsy or imaging results. For GCA or TAK, combine GC with a GC-sparing agent (IL-6 receptor inhibitor, upadacitinib, or methotrexate) in selected patients; all TAK patients should receive combination therapy."}},{"doi":"10.1038/s41584-026-01413-2","pmid":"42463536","title":"Secukinumab shows diverging efficacy in PMR and GCA","journal_title":"Nature Reviews Rheumatology","journal_issn":"1759-4790","published_at":"2026-07-16T00:00:00.000Z","url":"https://doi.org/10.1038/s41584-026-01413-2","source_score":6,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-18T13:39:48.448Z","updated_at":"2026-07-18T13:39:48.448Z","tags":[{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"modality","value":"IL-17A Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"study_design","value":"Research Highlight (Phase III Trial Summary)","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"Level of evidence is assigned based on the underlying referenced phase III trials, not the research highlight format itself.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"The brand name 'Cosentyx' is the known proprietary name for secukinumab but is not explicitly mentioned in the source text.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously based on the diverging efficacy signal across two phase III trials; full data review is needed to confirm clinical impact.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"This is a publisher preview/research highlight only — the full article is behind a paywall and no primary trial data or patient numbers are accessible from the provided text.","value_numeric":null}],"summaries":{"what_studied":"A research highlight summarizing two phase III trials evaluating secukinumab (an IL-17A inhibitor) in polymyalgia rheumatica (PMR) and giant cell arteritis (GCA), both conditions currently managed with glucocorticoids.","key_result":"Secukinumab showed diverging efficacy between PMR and GCA across the two trials; however, specific outcome data and numbers are not available in this publisher preview.","limitations":"This is a brief research highlight with no access to full trial data — specific efficacy figures, sample sizes, and safety profiles are not reported in the available text.","practice_takeaway":"IL-17A inhibition with secukinumab may offer a steroid-sparing option in PMR and/or GCA, but clinicians should await full trial data before changing practice, as efficacy appears to differ between the two conditions."}},{"doi":"10.1093/cid/ciag158","pmid":"42414860","title":"State-of-the-Art Review: Contemporary Ambulatory Approach to Adult Fever of Unknown Origin","journal_title":"Clinical Infectious Diseases","journal_issn":"1058-4838","published_at":"2026-07-08T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13341253/","source_score":53,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-12T13:19:43.785Z","updated_at":"2026-07-12T13:19:43.785Z","tags":[{"paper_doi":"10.1093/cid/ciag158","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"category","value":"Infectious Diseases","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"condition","value":"Adult-Onset Still Disease","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"condition","value":"Fever of Unknown Origin","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"condition","value":"Inflammation of Unknown Origin","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"condition","value":"Tuberculosis","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"generic","value":"fluorodeoxyglucose F-18","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"modality","value":"Interferon-Gamma Release Assay","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"modality","value":"Molecular Diagnostics (Next-Generation Sequencing)","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"modality","value":"PET/CT Imaging","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"study_design","value":"State-of-the-Art Review / Expert Consensus (Modified Delphi)","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"warning","value":"Level of evidence assigned as 5 (expert consensus/narrative review); individual meta-analyses cited within the paper carry higher evidence levels for specific questions.","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"warning","value":"No sample size tag applied — this is a narrative/consensus review, not a single primary study with one N. Individual cited studies range from 51 to 19,390 participants.","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"warning","value":"Study design label reflects dual nature: state-of-the-art review plus modified Delphi consensus; clinicians should weigh recommendations accordingly.","value_numeric":null},{"paper_doi":"10.1093/cid/ciag158","tag_type":"warning","value":"The paper is dated 2026; some cited guideline documents (e.g., EANM 2024, Delphi 2024) are recent and may not yet be universally adopted.","value_numeric":null}],"summaries":{"what_studied":"This state-of-the-art review synthesizes evidence on the ambulatory diagnostic and management approach to classic fever of unknown origin (FUO) in immunocompetent adults, incorporating recommendations from a modified Delphi consensus panel and the Society of Nuclear Medicine and Molecular Imaging, with input from infectious disease, rheumatology, and oncology specialists.","key_result":"Key findings include: (1) Qualitative FUO criteria (requiring a minimal standard diagnostic workup) yield 15.3% more undiagnosed cases and 19.7% fewer infectious diagnoses than time-based criteria alone. (2) *Mycobacterium tuberculosis* complex is the leading infectious cause globally (34.3% of infections across 19 prospective studies, n=2667). (3) 18F-FDG-PET/CT has a pooled diagnostic yield of 84–98%; a negative result correlates with spontaneous fever remission ~6× more often than a positive result (RR=5.6; 95% CI: 3.4–9.2). (4) Undiagnosed FUO patients generally have a favorable prognosis; mortality in a recent expert-center cohort was 2.1%.","limitations":"- Review is limited to immunocompetent adults; findings do not apply to children, adolescents, or immunocompromised patients.\n- Epidemiologic data are sparse for Africa and the Americas, limiting geographic generalizability.\n- No rigorous head-to-head studies directly compare 18F-FDG-PET/CT to the currently recommended minimal imaging investigations.","practice_takeaway":"Use the updated Delphi-based FUO criteria (fever ≥38.3°C on >3 occasions, >3 weeks, without explanation despite a minimal standard workup) to define patients before pursuing advanced imaging. Reserve 18F-FDG-PET/CT for after criteria are met—especially in patients with unintentional weight loss ≥5% and anemia—since a negative scan predicts spontaneous remission and a positive scan guides targeted biopsy or therapy."}},{"doi":"10.1136/rmdopen-2026-006866","pmid":"42414038","title":"Glucocorticoid in giant cell arteritis: real-world treatment patterns over time and associated burden in a nationwide hospital-based study within the French health insurance database","journal_title":"RMD Open","journal_issn":"2056-5933","published_at":"2026-07-07T00:00:00.000Z","url":"https://doi.org/10.1136/rmdopen-2026-006866","source_score":10,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-14T13:24:15.561Z","updated_at":"2026-07-14T13:24:15.561Z","tags":[{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"brand","value":"Actemra","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"generic","value":"methotrexate","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"generic","value":"prednisone","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"generic","value":"tocilizumab","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"modality","value":"Disease-Modifying Antirheumatic Drug","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"modality","value":"Glucocorticoid","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"modality","value":"IL-6 Receptor Inhibitor","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"sample_size","value":"n=18301","value_numeric":18301},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"warning","value":"GC exposure is likely underestimated because IV methylprednisolone pulses given in hospital were not captured in the claims data.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"warning","value":"The association at the lowest dose category (≤5 mg/day) with MACE and infection has wide confidence intervals, suggesting limited precision at this end of the dose range.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"warning","value":"The study is observational with time-varying confounding; causal inference about GC dose and adverse outcomes should be made cautiously.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2026-006866","tag_type":"warning","value":"Upadacitinib is mentioned in the discussion as a GC-sparing agent but was not part of the exposure analysis; its real-world uptake is not described in this dataset.","value_numeric":null}],"summaries":{"what_studied":"This nationwide retrospective cohort study used the French health insurance database (SNDS) to characterize oral glucocorticoid (GC) use trajectories in the 2 years following GCA diagnosis among 18,301 incident cases (2010–2022), and assessed associations between cumulative GC exposure and mortality, serious infections, MACE, and osteoporotic fractures.","key_result":"Four GC trajectories were identified; mean 2-year cumulative dose fell from 9.4 g (2010) to 7.6 g (2022) but remained high. Each additional gram of GC was linked to higher all-cause mortality (HR 1.024, 95% CI 1.021–1.027). Even the lowest dose category (≤5 mg/day) was associated with increased serious infection (HR 1.13, 95% CI 1.00–1.29) and MACE (HR 1.04, 95% CI 1.01–1.08). Tocilizumab use exceeded 25% of patients diagnosed in 2022.","limitations":"- Claims data lacked clinical/biological variables (e.g., disease activity, CRP values), so residual confounding by indication is possible.\n- In-hospital IV methylprednisolone pulses were not captured, likely underestimating true cumulative GC exposure.\n- Vertebral fractures are known to be under-reported in administrative databases, so GC-related fracture burden is probably underestimated.","practice_takeaway":"Clinicians should prioritize early GC-sparing therapy (tocilizumab or methotrexate) in all GCA patients, especially those who are older, female, hypertensive, or have kidney or neurocognitive disease—groups that taper more slowly and face the greatest toxicity risk. Even maintenance doses ≤5 mg/day carry measurable cardiovascular and infection risk, reinforcing the goal of full GC withdrawal."}},{"doi":"10.1016/s2665-9913(26)00142-6","pmid":"42379213","title":"Trends in autoimmune rheumatic disease diagnoses before and after the COVID-19 pandemic in England: a population-based cohort study using OpenSAFELY","journal_title":"The Lancet Rheumatology","journal_issn":"2665-9913","published_at":"2026-06-30T00:00:00.000Z","url":"https://doi.org/10.1016/s2665-9913(26)00142-6","source_score":5,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-05T13:38:35.585Z","updated_at":"2026-07-05T13:38:35.585Z","tags":[{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Autoimmune Rheumatic Disease","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Axial Spondyloarthritis","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Connective Tissue Disease","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Rheumatoid Arthritis","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"condition","value":"Small Vessel Vasculitis","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"sample_size","value":"n=23353040","value_numeric":23353040},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"study_design","value":"Population-Based Cohort Study","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"warning","value":"Level of evidence assigned as 3 (large observational cohort); no randomization or intervention was performed. Causal claims about the pandemic driving diagnostic changes cannot be confirmed from this design alone.","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"warning","value":"Socioeconomic and ethnicity subgroup findings are described in the abstract but specific numerical results are not reported; clinical interpretation of these subanalyses should be cautious.","value_numeric":null},{"paper_doi":"10.1016/s2665-9913(26)00142-6","tag_type":"warning","value":"The study covers adults in England registered with TPP-software GP practices only — approximately 40% of England's population — which may introduce selection bias.","value_numeric":null}],"summaries":{"what_studied":"This population-based cohort study used OpenSAFELY to evaluate incident diagnosis rates for 10 autoimmune rheumatic diseases in England (April 2016–March 2025), comparing observed post-pandemic rates to Prophet time-series–modelled expected rates across age, sex, ethnicity, and socioeconomic status.","key_result":"Five years after pandemic onset, cumulative diagnosis deficits persist for psoriatic arthritis (−12,320 diagnoses; −24.9%), rheumatoid arthritis (−11,690; −9.8%), and giant cell arteritis (−5,660; −15.2%); axial spondyloarthritis bucked the trend with a net increase (+2,040 diagnoses; +8.9%), driven notably by women surpassing men in diagnosis rates from 2023 onward.","limitations":"Observational design limits causal inference; data restricted to practices using TPP software, which may not be fully representative of all England; ethnicity and socioeconomic subgroup analyses may be underpowered for rarer conditions.","practice_takeaway":"Clinicians should actively screen for undiagnosed psoriatic arthritis, rheumatoid arthritis, and giant cell arteritis, as cumulative diagnostic backlogs from COVID-19 disruption remain substantial 5 years on. The unexpected rise in axial spondyloarthritis diagnoses in women warrants heightened clinical suspicion in this group."}},{"doi":"10.1016/j.berh.2026.102164","pmid":"42248698","title":"Pneumocystis prophylaxis in rheumatic disease","journal_title":"Best Practice & Research Clinical Rheumatology","journal_issn":"1521-6942","published_at":"2026-06-05T00:00:00.000Z","url":"https://doi.org/10.1016/j.berh.2026.102164","source_score":3,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:12.738Z","updated_at":"2026-06-10T14:24:12.738Z","tags":[{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"ANCA-Associated Vasculitis","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"Dermatomyositis","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"Pneumocystis Jirovecii Pneumonia","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"Rheumatic Disease","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"condition","value":"VEXAS Syndrome","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"generic","value":"trimethoprim-sulfamethoxazole","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"modality","value":"Antibiotic Prophylaxis","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"modality","value":"Glucocorticoid","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"warning","value":"No sample size is reported; this is a review article without a primary patient cohort.","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"warning","value":"Study design tagged as 'Narrative Review' based on abstract language ('this review examines'); formal systematic review methodology is not confirmed.","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"warning","value":"The anti-MDA5 antigen is referenced in the abstract as 'anti-MD5' which appears to be a typo for anti-MDA5 (melanoma differentiation-associated protein 5); interpreted accordingly.","value_numeric":null},{"paper_doi":"10.1016/j.berh.2026.102164","tag_type":"warning","value":"Trimethoprim-sulfamethoxazole is inferred as the primary prophylaxis agent based on general clinical context; the abstract does not explicitly name the agent used.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates PJP prophylaxis in rheumatic diseases, examining efficacy, adverse effects, and risk factors across conditions to support a risk-stratified, individualized approach to prophylaxis decisions.","key_result":"Routine PJP prophylaxis is warranted in high-risk conditions (ANCA-associated vasculitis during induction, anti-MDA5+ dermatomyositis, VEXAS syndrome) especially with high-dose glucocorticoids, while low-risk conditions like Giant Cell Arteritis do not justify routine prophylaxis. PJP mortality in rheumatic disease exceeds that seen in HIV-infected patients.","limitations":"Evidence-based guidelines specific to rheumatic disease are lacking; the review is narrative in design without systematic pooled data or meta-analysis, limiting quantitative conclusions.","practice_takeaway":"Use a risk-stratified framework: prioritize PJP prophylaxis for patients with ANCA-associated vasculitis on induction therapy, anti-MDA5+ dermatomyositis, or VEXAS syndrome receiving high-dose glucocorticoids. Routine prophylaxis is not needed for all rheumatic disease patients — tailor decisions to individual risk."}},{"doi":"10.1093/rheumatology/keag285","pmid":"42226006","title":"Prevalence and characteristics of subclinical polymyalgia rheumatica in patients with giant cell arteritis","journal_title":"Rheumatology","journal_issn":"1462-0324","published_at":"2026-06-02T00:00:00.000Z","url":"https://doi.org/10.1093/rheumatology/keag285","source_score":2,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-09T13:50:10.200Z","updated_at":"2026-06-09T13:50:10.200Z","tags":[{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"generic","value":"fluorodeoxyglucose F-18","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"modality","value":"PET-CT Imaging","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"sample_size","value":"n=168","value_numeric":168},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"warning","value":"GCA is predominantly a disease of older adults, but the paper does not explicitly report mean age — the 'older_adult' age group tag is inferred from the known epidemiology of GCA.","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"warning","value":"The PET-based definition of subclinical PMR used here (grade ≥2 uptake at specific sites) is not universally standardised; results may vary with different diagnostic criteria.","value_numeric":null},{"paper_doi":"10.1093/rheumatology/keag285","tag_type":"warning","value":"The study population is from a single centre, so the 56% prevalence of subclinical PMR may not generalise broadly.","value_numeric":null}],"summaries":{"what_studied":"A single-centre retrospective cohort of 168 newly diagnosed GCA patients who underwent 18F-FDG PET-CT at diagnosis; patients with apparently isolated GCA (n=102) were classified as subclinical PMR, clinical PMR, or pure GCA based on PET uptake patterns and symptoms.","key_result":"56% (57/102) of apparently isolated GCA patients had PET findings consistent with subclinical PMR. This subgroup showed greater large-vessel involvement than pure GCA (thoracic aorta p=0.023, abdominal aorta p=0.0001, supra-aortic trunks p=0.007), but no significant differences in cranial manifestations, severe ischaemic events, or relapse rates across groups.","limitations":"Single-centre retrospective design limits generalisability. PET-CT was performed at diagnosis only, so longitudinal musculoskeletal evolution is unknown. Subclinical PMR definition relied on PET grade ≥2 uptake thresholds, which are not yet universally standardised.","practice_takeaway":"Clinicians evaluating apparently isolated GCA should be aware that over half may have subclinical PMR detectable only on PET-CT, suggesting a GCA-PMR disease spectrum rather than distinct entities. This finding does not appear to alter cranial ischaemic risk or relapse rates, but may have implications for understanding large-vessel involvement."}},{"doi":"10.1002/ijgo.71103","pmid":"42223974","title":"Rare vasculitis types and obstetric and neonatal outcomes – A population‐based study","journal_title":"International Journal of Gynecology & Obstetrics","journal_issn":"0020-7292","published_at":"2026-06-01T00:00:00.000Z","url":"https://doi.org/10.1002/ijgo.71103","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:23:55.399Z","updated_at":"2026-06-10T14:23:55.399Z","tags":[{"paper_doi":"10.1002/ijgo.71103","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Hypertensive Disorders of Pregnancy","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Kawasaki Disease","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Polyarteritis Nodosa","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Preterm Delivery","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Takayasu Arteritis","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Vasculitis","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"condition","value":"Wegener's Granulomatosis","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"sample_size","value":"n=9096788","value_numeric":9096788},{"paper_doi":"10.1002/ijgo.71103","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"warning","value":"ICD-9 coding is used for diagnosis; rare conditions may be under-coded or miscoded in administrative databases.","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"warning","value":"No information on vasculitis disease activity, flares during pregnancy, or specific immunosuppressive medications is available in the dataset, limiting causal inference.","value_numeric":null},{"paper_doi":"10.1002/ijgo.71103","tag_type":"warning","value":"The vasculitis group is very small (n=335 out of >9 million), so individual subtype-level analyses are not reported and estimates should be interpreted cautiously.","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study used the HCUP-NIS database (2004–2014) to compare obstetric and perinatal outcomes in pregnant US women with rare vasculitis subtypes (polyarteritis nodosa, Kawasaki disease, hypersensitivity angiitis, Wegener's granulomatosis, giant cell arteritis, Takayasu arteritis) versus those without, among 9,096,788 deliveries.","key_result":"Only 335 women (3.7/100,000) had rare vasculitis. Compared to controls, they had significantly higher rates of hypertensive disorders of pregnancy (aOR 1.89), preterm delivery (aOR 1.76), blood transfusion (aOR 3.68), cesarean delivery (aOR 1.31), and congenital anomalies (aOR 4.1); placental abruption, hysterectomy, and VTE were comparable between groups.","limitations":"- Extremely small vasculitis group (n=335) limits statistical power and subgroup analysis by vasculitis type.\n- Retrospective ICD-9 coding may misclassify or undercount rare vasculitis diagnoses.\n- Database lacks disease activity, medication use (e.g., immunosuppressants), and disease severity data, which are key confounders.","practice_takeaway":"Pregnant women with rare vasculitis should be counseled about elevated risks of hypertensive disorders, preterm birth, cesarean delivery, and fetal congenital anomalies, and managed with close maternal-fetal medicine surveillance. Blood transfusion risk is notably high (aOR 3.68), warranting proactive hemorrhage planning."}},{"doi":"10.1016/j.semarthrit.2026.153003","pmid":"42247731","title":"Adherence to dietary recommendations and the risk of developing giant cell arteritis: A nested Case-Control study","journal_title":"Seminars in Arthritis and Rheumatism","journal_issn":"0049-0172","published_at":"2026-05-29T00:00:00.000Z","url":"https://doi.org/10.1016/j.semarthrit.2026.153003","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-11T13:42:39.137Z","updated_at":"2026-06-11T13:42:39.137Z","tags":[{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"modality","value":"Dietary Intervention","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"sample_size","value":"n=193","value_numeric":193},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"study_design","value":"Nested Case-Control Study","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"warning","value":"The 'impact_flag' of practice_changing is used cautiously: the finding is counterintuitive and hypothesis-generating rather than immediately practice-directing, but it materially challenges current assumptions about diet and GCA risk.","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"warning","value":"The study population is from a Swedish cohort (Malmö Diet and Cancer Study), which may limit generalizability to other ethnic or geographic populations.","value_numeric":null},{"paper_doi":"10.1016/j.semarthrit.2026.153003","tag_type":"warning","value":"The total sample size of 193 cases is provided, but the exact number of controls (nominally ~772 at 4:1 matching) is not explicitly stated in the abstract — the sample_size tag reflects cases only.","value_numeric":null}],"summaries":{"what_studied":"This nested case-control study examined whether adherence to dietary recommendations (measured by the Swedish Dietary Guidelines Score, SDGS) and intake of specific dietary components were associated with the risk of developing giant cell arteritis (GCA) in participants from the Malmö Diet and Cancer Study cohort, with 193 incident GCA cases matched to 4 controls each.","key_result":"High diet quality (SDGS 4–5 vs. 0–1) was independently associated with a **2.70-fold increased risk** of GCA (adjusted OR 2.70; 95% CI 1.43–5.10). Adherence to recommendations for added sugar, fish/shellfish, and vegetables/fruit were each linked to higher GCA risk; higher quantified added sugar intake was associated with *reduced* risk, while higher fiber and fish/shellfish intake were associated with *increased* risk.","limitations":"- Observational nested case-control design limits causal inference.\n- Dietary assessment was performed at cohort entry, potentially years before GCA diagnosis, raising concerns about temporal relevance and dietary change over time.\n- Potential residual confounding from unmeasured lifestyle or metabolic factors cannot be excluded.","practice_takeaway":"These findings challenge the assumption that a healthy diet protects against all immune-mediated diseases — GCA risk was paradoxically higher in those with the best diet quality. Clinicians should be aware that a 'healthy metabolic profile' may not confer protection against GCA, though causality remains unestablished."}},{"doi":"10.1007/s10067-026-08183-y","pmid":"42207464","title":"Temporal artery biopsy in polyarteritis nodosa: a case-based narrative literature review","journal_title":"Clinical Rheumatology","journal_issn":"0770-3198","published_at":"2026-05-28T00:00:00.000Z","url":"https://doi.org/10.1007/s10067-026-08183-y","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-05T13:26:35.253Z","updated_at":"2026-06-05T13:26:35.253Z","tags":[{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"condition","value":"Central Retinal Artery Occlusion","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"condition","value":"Polyarteritis Nodosa","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"modality","value":"Temporal Artery Biopsy","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"sample_size","value":"n=21","value_numeric":21},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"sex","value":"male","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"study_design","value":"Case-Based Narrative Review","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"warning","value":"All identified cases may have been biopsied because GCA was suspected, introducing significant selection bias that limits generalizability to unselected PAN patients.","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"warning","value":"Study design is labeled 'Case-Based Narrative Review' rather than a standard systematic review; level of evidence is correspondingly low (4).","value_numeric":null},{"paper_doi":"10.1007/s10067-026-08183-y","tag_type":"warning","value":"The 21-case series includes the index case itself; this is a narrative review without systematic pooling or quantitative meta-analysis, so effect estimates are not available.","value_numeric":null}],"summaries":{"what_studied":"This case-based narrative review examined the diagnostic role of temporal artery biopsy (TAB) in polyarteritis nodosa (PAN), anchored by a 27-year-old Japanese man with visceral aneurysms, central retinal artery occlusion, and medullary infarction whose TAB confirmed PAN. A literature review identified 21 TAB-confirmed PAN cases in total.","key_result":"In 21 TAB-confirmed PAN cases identified, most biopsies were performed because GCA was initially suspected; histopathology was heterogeneous, but a neutrophil-predominant necrotizing pattern with fibrinoid change and absence of multinucleated giant cells was the key distinguishing feature pointing away from GCA toward PAN.","limitations":"- Evidence is limited entirely to case reports and TAB-based cohorts; no prospective or controlled data exist.\n- The diagnostic yield of TAB in unselected PAN patients has not been studied.\n- Publication bias likely inflates the apparent utility of TAB in PAN.","practice_takeaway":"When standard biopsy sites (e.g., kidney, nerve/muscle) are impractical or high-risk in suspected PAN, TAB is a pragmatic alternative—especially if the patient has temporal artery induration or cranial ischemic events. A neutrophil-rich necrotizing arteritis with fibrinoid change and no giant cells on TAB should prompt reconsideration of PAN over GCA."}},{"doi":"10.1038/s41584-026-01379-1","pmid":"42162376","title":"Treatment strategies in giant cell arteritis and polymyalgia rheumatica: beyond glucocorticoids","journal_title":"Nature Reviews Rheumatology","journal_issn":"1759-4790","published_at":"2026-05-20T00:00:00.000Z","url":"https://doi.org/10.1038/s41584-026-01379-1","source_score":21,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-23T13:24:53.743Z","updated_at":"2026-05-23T13:24:53.743Z","tags":[{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"modality","value":"Glucocorticoid","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"modality","value":"IL-6 Receptor Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"warning","value":"Age group tagged as 'older_adult' based on well-established epidemiology of GCA/PMR; not explicitly stated in the abstract.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"warning","value":"No specific trial names, patient numbers, or effect sizes are cited in the abstract; summary reflects qualitative conclusions only.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01379-1","tag_type":"warning","value":"The review covers both GCA and PMR together, but some therapeutic findings (e.g., JAK inhibition) appear to apply primarily to GCA — clinicians should interpret condition-specific applicability carefully.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates treatment strategies for giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) beyond glucocorticoids, focusing on IL-6 pathway inhibitors and JAK inhibitors — their efficacy in reducing relapse risk and enabling glucocorticoid sparing.","key_result":"IL-6 receptor inhibitors reduce disease relapse risk and allow glucocorticoid dose reduction in both GCA and PMR; JAK inhibitors enable glucocorticoid sparing and lower relapse risk in GCA specifically.","limitations":"This is a narrative review without systematic meta-analytic methodology, so effect sizes and absolute risk reductions are not directly quantified. Evidence for some emerging therapies remains preliminary.","practice_takeaway":"For patients with GCA or PMR who relapse on glucocorticoids or accrue treatment-related toxicity, consider adding an IL-6 receptor inhibitor or JAK inhibitor to reduce relapse risk and lower steroid burden. Management should be individualized with close monitoring of both disease activity and treatment-related adverse effects."}},{"doi":"10.1002/art.70203","pmid":"42045811","title":"Higher complement\n \n C4\n \n gene copy number constitutes a shared genetic risk factor for giant cell arteritis and\n IgA\n vasculitis","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2026-04-27T00:00:00.000Z","url":"https://doi.org/10.1002/art.70203","source_score":6,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-07T22:49:29.698Z","updated_at":"2026-05-07T22:49:29.698Z","tags":[{"paper_doi":"10.1002/art.70203","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"condition","value":"IgA Vasculitis","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"modality","value":"Complement Pathway","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"sample_size","value":"n=20,649","value_numeric":20649},{"paper_doi":"10.1002/art.70203","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"study_design","value":"Genetic Association Study","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"warning","value":"C4 CN was computationally imputed from genotypic arrays, not directly sequenced; imputation accuracy is assumed but not validated in this paper.","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"warning","value":"IgAV subgroup analyses (especially sex-stratified) should be interpreted cautiously given the small sample size (n=284).","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"warning","value":"The 'practice_changing' impact flag reflects a novel mechanistic finding rather than a direct change to treatment protocols — no therapeutic intervention was tested.","value_numeric":null},{"paper_doi":"10.1002/art.70203","tag_type":"warning","value":"The study population ancestry is not explicitly described in the abstract, which may limit generalizability.","value_numeric":null}],"summaries":{"what_studied":"This study evaluated whether copy number (CN) variation in complement C4 isoforms (C4A, C4B) and retroviral HERV-K elements confers genetic risk for giant cell arteritis (GCA) and IgA vasculitis (IgAV), including sex-stratified analyses and comparison with classical HLA alleles, using imputed genotypic data from 3,498 GCA patients, 284 IgAV patients, and 16,867 controls.","key_result":"Unlike most immune-mediated inflammatory diseases where low C4 CN drives risk, **higher C4 CN increased risk** for both vasculitides: in GCA, higher C4B CN was a male-specific risk factor (OR = 1.23, 95% CI 1.07–1.42, p = 4.52×10⁻³); in IgAV, elevated C4A CN raised overall disease risk (OR = 1.68, 95% CI 1.22–2.30, p = 1.49×10⁻³), with a male-biased C4B trend (OR = 1.46). All associations were independent of classical HLA alleles.","limitations":"- The IgAV cohort was small (n = 284), limiting statistical power for sex-stratified analyses.\n- C4 CN was imputed rather than directly measured, which may introduce imputation error.\n- Causal mechanisms linking higher C4 CN to vascular inflammation are not established by this study.","practice_takeaway":"Complement C4 copy number variation is a novel, HLA-independent genetic risk factor for GCA and IgAV, with male patients showing a particularly strong signal — this supports a role for complement dysregulation in these vasculitides and may inform future biomarker or therapeutic research targeting complement pathways."}},{"doi":"10.1016/j.ajo.2026.01.004","pmid":"41525816","title":"Exploring the Association Between Autoimmune and Inflammatory Diseases and Uveitis","journal_title":"American Journal of Ophthalmology","journal_issn":"0002-9394","published_at":"2026-01-13T00:00:00.000Z","url":"https://doi.org/10.1016/j.ajo.2026.01.004","source_score":10,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-11","doi":"10.1016/j.ajo.2026.01.004","days":"7","issn":"0002-9394","rank":"5","field":"Clinical Medicine","score":"10","category":"Ophthalmology","categories":["Ophthalmology"],"_categories":["Ophthalmology"]},"pubmed":{"doi":"10.1016/j.ajo.2026.01.004","title":"Exploring the Association Between Autoimmune and Inflammatory Diseases and Uveitis.","journal":"American journal of ophthalmology","methods":"","results":"Patients with all 12 IMIDs had a significantly increased risk of developing uveitis. Highest risks were observed in ankylosing spondylitis (RR=7.71, 95% CI: 5.84-10.19), JIA (RR=5.13, 95% CI: 3.51-7.49), and systemic vasculitis (RR=4.61, 95% CI: 3.73 to 5.69). Increased risk was also found in sarcoidosis (RR=3.67, 95% CI: 3.02 to 4.47), GCA (RR=3.24, 95% CI: 2.58-4.07), and ANCA vasculitis (RR=3.18, 95% CI: 1.84-5.48). In addition, in patients with uveitis, both the odds of a prior IMID diagnosis and the risk of a future IMID diagnosis were significantly increased for all 12 IMIDs.","abstract":"$30","keywords":["Autoimmune","Inflammatory","Uveitis","Vasculitis"],"pubmed_id":"41525816","conclusions":"","publication_date":"2026-01-13T00:00:00"},"crossref":{"DOI":"10.1016/j.ajo.2026.01.004","URL":"https://doi.org/10.1016/j.ajo.2026.01.004","ISSN":["0002-9394"],"link":[{"URL":"https://api.elsevier.com/content/article/PII:S0002939426000115?httpAccept=text/xml","content-type":"text/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https://api.elsevier.com/content/article/PII:S0002939426000115?httpAccept=text/plain","content-type":"text/plain","content-version":"vor","intended-application":"text-mining"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Exploring the Association Between Autoimmune and Inflammatory Diseases and Uveitis"],"author":[{"given":"Nitesh","family":"Mohan","sequence":"first","affiliation":[]},{"given":"Sunil K.","family":"Srivastava","sequence":"additional","affiliation":[]},{"given":"Matthew J.","family":"Schulgit","sequence":"additional","affiliation":[]},{"given":"Rula A.","family":"Hajj-Ali","sequence":"additional","affiliation":[]},{"given":"David C.","family":"Kaelber","sequence":"additional","affiliation":[]},{"given":"Sumit","family":"Sharma","sequence":"additional","affiliation":[]}],"funder":[{"id":[{"id":"10.13039/100012729","id-type":"DOI","asserted-by":"publisher"}],"DOI":"10.13039/100012729","name":"Case Western Reserve University Clinical and Translational Science Collaborative","doi-asserted-by":"publisher"}],"issued":{"date-parts":[[2026,1]]},"member":"78","prefix":"10.1016","source":"Crossref","volume":null,"created":{"date-time":"2026-01-10T07:36:43Z","timestamp":1768030603000,"date-parts":[[2026,1,10]]},"indexed":{"date-time":"2026-01-16T22:54:24Z","timestamp":1768604064151,"date-parts":[[2026,1,16]]},"license":[{"URL":"https://www.elsevier.com/tdm/userlicense/1.0/","start":{"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000,"date-parts":[[2026,1,1]]},"delay-in-days":0,"content-version":"tdm"},{"URL":"https://www.elsevier.com/legal/tdmrep-license","start":{"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000,"date-parts":[[2026,1,1]]},"delay-in-days":0,"content-version":"tdm"},{"URL":"http://creativecommons.org/licenses/by-nc-nd/4.0/","start":{"date-time":"2026-01-09T00:00:00Z","timestamp":1767916800000,"date-parts":[[2026,1,9]]},"delay-in-days":8,"content-version":"vor"}],"subject":[],"abstract":null,"language":"en","relation":{},"resource":{"primary":{"URL":"https://linkinghub.elsevier.com/retrieve/pii/S0002939426000115"}},"subtitle":[],"assertion":[{"name":"publisher","label":"This article is maintained by","value":"Elsevier"},{"name":"articletitle","label":"Article Title","value":"Exploring the Association Between Autoimmune and Inflammatory Diseases and Uveitis"},{"name":"journaltitle","label":"Journal Title","value":"American Journal of Ophthalmology"},{"name":"articlelink","label":"CrossRef DOI link to publisher maintained version","value":"https://doi.org/10.1016/j.ajo.2026.01.004"},{"name":"content_type","label":"Content Type","value":"article"},{"name":"copyright","label":"Copyright","value":"© 2026 The Author(s). 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and case-control components; design label simplified.","value_numeric":null},{"paper_doi":"10.1016/j.ajo.2026.01.004","tag_type":"warning","value":"Timeframe, setting, and adjustment methods were not specified in the provided text.","value_numeric":null}],"summaries":{"what_studied":"Retrospective cohort and case-control analyses of electronic health records assessed associations between 12 immune‑mediated inflammatory diseases (IMIDs) and uveitis, estimating risk of uveitis in IMID patients, odds of prior IMIDs among those with uveitis, and risk of developing an IMID after uveitis.","key_result":"All 12 IMIDs were linked to higher uveitis risk; the largest relative risks were ankylosing spondylitis RR 7.71 (95% CI 5.84–10.19), juvenile idiopathic arthritis RR 5.13 (95% CI 3.51–7.49), and systemic vasculitis RR 4.61 (95% CI 3.73–5.69), with increased risks also in sarcoidosis RR 3.67 (95% CI 3.02–4.47), giant cell arteritis RR 3.24 (95% CI 2.58–4.07), and ANCA‑associated vasculitis RR 3.18 (95% CI 1.84–5.48). In patients with uveitis, both the odds of prior IMIDs and the risk of future IMIDs were increased for all 12 IMIDs.","practice_takeaway":"IMIDs have strong, bidirectional associations with uveitis; patients with IMIDs should receive ophthalmologic evaluation when appropriate, and patients with uveitis should be monitored for subsequent IMID development."}},{"doi":"10.1177/1759720x251414122","pmid":"41523797","title":"Imaging-guided stratification in giant cell arteritis: prognostic and therapeutic implications","journal_title":"Therapeutic Advances in Musculoskeletal Disease","journal_issn":"1759-720X","published_at":"2026-01-12T00:00:00.000Z","url":"https://doi.org/10.1177/1759720x251414122","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-10","doi":"10.1177/1759720x251414122","days":"7","issn":"1759-720X","rank":"10","field":"Clinical Medicine","score":"1","category":"Rheumatology","categories":["Rheumatology"],"_categories":["Rheumatology"]},"pubmed":{"doi":"10.1177/1759720X251414122","title":"Imaging-guided stratification in giant cell arteritis: prognostic and therapeutic implications.","journal":"Therapeutic advances in musculoskeletal disease","methods":"","results":"","abstract":"Imaging has become a cornerstone in the clinical management of giant cell arteritis (GCA), with its role extending beyond diagnosis to include disease monitoring, risk stratification of relapse, and therapeutic decision-making. While imaging modalities have been well-established for diagnostic purposes, growing evidence supports their utility in tracking disease activity and stratifying the risk of relapse. In this narrative review, we discuss the available evidence on the prognostic and therapeutic implications of imaging-guided stratification in GCA, and highlight areas that require further research. Ultrasound assessment of intima-media thickness shows measurable improvement following treatment. While this response is relatively rapid in the cranial arteries, it occurs slowly or very slowly in extracranial vessels. Moreover, ultrasound signs and quantitative indices may be useful for distinguishing remission from relapse. 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RT-qPCR analysis confirmed that secukinumab decreased mRNA encoding IL-6, CCL20, and GM-CSF in positive-TABs, while IL-17 upregulated them in negative-TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL-17 receptor chains were expressed on MFs, and their expression was enhanced by IFN-γ. RT-qPCR and Luminex® analyses confirmed IL-17-driven upregulation of IL-6, CCL20, CCL2, GM-CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN-γ to the culture increased the expression level of IL-17 receptor chains, resulting in a synergistic effect. Additionally, IL-17 pre-treated MFs promoted Th17 polarization.","abstract":"$32","keywords":[],"pubmed_id":"41524618","conclusions":"","publication_date":"2026-01-12T00:00:00"},"crossref":{"DOI":"10.1002/art.70051","URL":"https://doi.org/10.1002/art.70051","ISSN":["2326-5191","2326-5205"],"link":[{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70051","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70051","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["In synergy with interferon‐gamma, interleukin‐17 activates vascular stromal cells towards a pro‐inflammatory profile in giant cell arteritis"],"author":[{"given":"Hélène","family":"Greigert","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases (MAIS), Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Department of Vascular Medicine, Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"André","family":"Ramon","sequence":"additional","affiliation":[{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"},{"name":"Department of Rheumatology, Dijon University Hospital Université EPE Bourgogne Europe Dijon France"}]},{"given":"Claudie","family":"Cladiere","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases (MAIS), Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"Baptiste","family":"Lamarthée","sequence":"additional","affiliation":[{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"Corentin","family":"Richard","sequence":"additional","affiliation":[{"name":"Unit of Molecular Biology, Department of Biology and Pathology of Tumors, Georges‐François Leclerc Cancer Center, UNICANCER, Dijon, France ; 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In myofibroblasts, IL-17 increased IL-6, CCL20, CCL2, GM-CSF, and VEGF (reversed by secukinumab), IFN-γ upregulated IL-17 receptor chains and synergized with IL-17, and IL-17–pretreated myofibroblasts promoted Th17 polarization.","limitations":"Findings are from ex vivo/in vitro models without clinical outcomes or in vivo validation. 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In the prospective cohort (n=40), 7/40 (17.5%) developed ascending aortic aneurysms over a mean 54 months (95% CI 43.7–64.6); all had large-vessel involvement (2 LV-GCA, 5 mixed-GCA).","limitations":"Ultrasonography and CT were performed up to six months apart, not simultaneously. The prospective follow-up included only 40 patients, limiting precision.","practice_takeaway":"In GCA, ultrasonography aligns closely with CT for ascending aorta sizing and may be used for longitudinal monitoring and screening. About 18% developed ascending aortic aneurysms over ~4.5 years, supporting regular aortic screening in this population."}},{"doi":"10.1002/art.43358","pmid":"40826980","title":"Genome‐Wide\n DNA\n Methylation Study Reveals Specific Signatures in the Affected Arterial Tissue of Patients With Giant Cell Arteritis","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2025-08-19T00:00:00.000Z","url":"https://doi.org/10.1002/art.43358","source_score":38,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-01-16","doi":"10.1002/art.43358","days":"7","issn":"2326-5191","rank":"1","field":"Clinical Medicine","score":"38","category":"Rheumatology","categories":["Rheumatology"],"_categories":["Rheumatology"]},"pubmed":{"doi":"10.1002/art.43358","title":"Genome-Wide DNA Methylation Study Reveals Specific Signatures in the Affected Arterial Tissue of Patients With Giant Cell Arteritis.","journal":"Arthritis & rheumatology (Hoboken, N.J.)","methods":"","results":"EWAS identified 3,644 DMPs (P","abstract":"$35","keywords":[],"pubmed_id":"40826980","conclusions":"Our study identified GCA-specific DNA methylation signatures in arterial tissue, revealing disrupted inflammatory and vascular pathways and suggesting the involvement of exhausted T cells in this condition. 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