Giant cell arteritis: update on pathogenesis and clinical implications DOI
H. Ibrahim, Cosimo De Bari

Current Opinion in Rheumatology, Journal Year: 2024, Volume and Issue: 37(1), P. 72 - 79

Published: Aug. 28, 2024

Purpose of review Giant cell arteritis (GCA) is an age-related autoimmune disease with a complex pathogenesis that involves several pathogenic mechanisms. This provides recent critical insights into novel aspects GCA pathogenesis. Recent findings The use approaches, including multiomic techniques, has uncovered notable broaden the understanding TCF1 hi CD4 + T cells have been identified as stem-like residing in tertiary lymphoid structures adventitia aortic tissues, which likely supply effector present vasculitic lesions. Studies demonstrated fibroblasts GCA-inflamed arteries are not innocent bystanders, but they contribute to arterial inflammation via maintenance Th1 and Th17 polarisation, cytokine secretion (IL-6, IL-1B, IL-12, IL-23) antigen presentation. Additionally, deregulated cellular senescence programs accumulation IL-6 matrix metalloproteinase 9-producing senescent Summary studies unravelled interesting potentially significant clinical relevance. Stem-like key contributors vascular persistence, targeted depletion or modulation these holds promise management. Fibroblast-targeting therapies senotherapeutics also exciting prospects treatment GCA.

Language: Английский

Imaging to predict early relapses after treatment discontinuation in patients with large vessel giant cell arteritis – A cohort study DOI
Andrea Katharina Hemmig, Christof Rottenburger,

Luan Baruti

et al.

Seminars in Arthritis and Rheumatism, Journal Year: 2024, Volume and Issue: 66, P. 152425 - 152425

Published: Feb. 28, 2024

Language: Английский

Citations

8
Association between vascular FDG uptake during follow-up and the development of thoracic aortic aneurysms in giant cell arteritis DOI Creative Commons
Daniël Blockmans, Lien Moreel, Albrecht Betrains

et al.

Frontiers in Medicine, Journal Year: 2024, Volume and Issue: 11

Published: March 20, 2024

Background A positive PET scan at diagnosis was associated with a greater yearly increase in ascending and descending aortic diameter thoracic volume patients giant cell arteritis (GCA). Radiologic histopathologic vascular abnormalities persist subset of treated despite clinical remission. The aim this study to evaluate the association between FDG uptake during follow-up development aneurysms. Methods We recently performed prospective cohort 106 GCA patients, who underwent CT imaging for maximum 10 years. In post hoc analysis, also have had were included. scans visually scored (0–3) 7 areas. considered case ≥grade 2 any large vessel. Results Eighty-eight repeat 52 out included original cohort. Fifty-five (63%) done time relapse 33 (38%) while Nine ten an incident aneurysm both follow-up. Conclusion addition intensity extent initial inflammation, ongoing inflammation may contribute aneurysms GCA. However, hypothesis should be confirmed trial predefined points

Language: Английский

Citations

4
Vascular disease persistence in giant cell arteritis: are stromal cells neglected? DOI Creative Commons
Maira Karabayas, H. Ibrahim, Anke J. Roelofs

et al.

Annals of the Rheumatic Diseases, Journal Year: 2024, Volume and Issue: unknown, P. ard - 225270

Published: April 29, 2024

Giant cell arteritis (GCA), the most common systemic vasculitis, is characterised by aberrant interactions between infiltrating and resident cells of vessel wall. Ageing breach tolerance are prerequisites for GCA development, resulting in dendritic T-cell dysfunction. Inflammatory cytokines polarise T-cells, activate macrophages synergistically enhance vascular inflammation, providing a loop autoreactivity. These events originate adventitia, commonly regarded as biological epicentre wall, with additional recruitment that infiltrate migrate towards intima. Thus, GCA-vessels exhibit infiltrates across layers, various growth factors amplifying pathogenic process. ineffective repair mechanisms, where dysfunctional smooth muscle fibroblasts phenotypically shift along their lineage colonise While high-dose glucocorticoids broadly suppress these inflammatory events, they cause well known deleterious effects. Despite emerging targeted therapeutics, disease relapse remains common, affecting >50% patients. This may reflect discrepancy local mediators inflammation. Indeed, temporal arteries aortas GCA-patients can show immune-mediated abnormalities, despite treatment induced clinical remission. The mechanisms persistence remain elusive. Studies other chronic diseases point to (and including myofibroblasts) possible orchestrators or even effectors chronicity through immune cells. Here, we critically review contribution stromal pathogenesis analyse molecular which would underpin disease.

Language: Английский

Citations

4
Histological pattern of non-infectious thoracic aortitis impacts mortality DOI Creative Commons
Olivier Espitia, Patrick Bruneval, É. Liozon

et al.

Journal of Autoimmunity, Journal Year: 2025, Volume and Issue: 151, P. 103360 - 103360

Published: Jan. 18, 2025

Non-infectious aortitis encompasses various histological patterns, but their specific cardiovascular outcomes remain unclear. To evaluate the mortality associated with non-infectious surgical thoracic aortitis. This retrospective multicenter study included patients who underwent aortic surgery and had evidence of The analyzed characteristics presenting either a granulomatous/giant cell pattern or lymphoplasmacytic pattern. Factors were identified using multivariate analysis. Among 5666 surgery, 197 found to have (n = 138) 59). overall standardized rate (SMR) for was 1.61 (95 % CI: 1.05; 2.39), 31.5 dying within 10 years initial procedure. After median follow-up 3.5 [IQR: 0.5-6.8] post-surgery, 31 deaths due dissection rupture. 10-year cumulative incidence death 40.1 CI, 17.7-61.8) 14.4 2.6-35.6) those Granulomatous/giant (HR 4.71 [vs pattern]; 95 1.37-16.2; p 0.023) at diagnosis 6.07 aneurysm]; 2.89-12.7; < 0.0001) independently increased mortality. that are expected die surgery. is higher

Language: Английский

Citations

0
Giant Cell Arteritis DOI Creative Commons
Е. В. Шевченко, A. M. Izmailova, Е. А. Ковалева

et al.

Russian Sklifosovsky Journal Emergency Medical Care, Journal Year: 2025, Volume and Issue: 13(4), P. 641 - 649

Published: Jan. 28, 2025

Giant cell arteritis is a disease characterized by granulomatous inflammation of large and medium-sized arteries. The aorta its branches are most susceptible to pathological changes in this arteritis. course giant often complicated ischemia the blood supply basin artery involved process. Variants such complications may be ischemic optic neuropathy retinopathy, limb ischemia, acute cerebrovascular accident. This review presents current data on etiology pathogenesis arteritis, prevalence, sensitivity, specificity clinical instrumental signs disease, as well practical recommendations for various treatment methods during exacerbation remission.

Language: Английский

Citations

0
Aortic Disease in Giant Cell Arteritis DOI
Kenneth J. Warrington

Seminars in Arthritis and Rheumatism, Journal Year: 2025, Volume and Issue: unknown, P. 152677 - 152677

Published: Feb. 1, 2025

Language: Английский

Citations

0
Repeated Cranial and Large‐Vessel Positron Emission Tomography/Computed Tomography Scans and the Association With Structural Aortic Disease in Giant Cell Arteritis: A Five‐Year Observational Study DOI Creative Commons
Anthony M. Sammel, Ivan Ho Shon, Daniel Moses

et al.

ACR Open Rheumatology, Journal Year: 2025, Volume and Issue: 7(3)

Published: Feb. 26, 2025

Objective Giant cell arteritis (GCA) is characterized by cranial ischemia at diagnosis and late aortic structural disease. Repeated combined large‐vessel fluoro‐2‐deoxyglucose (FDG) positron emission tomography (PET)/computed (CT) scans were performed to assess the distribution of vasculitis activity over time relationship with clinical outcomes. Methods Patients eligible if they enrolled in a 64‐patient inception suspected GCA cohort 2016 2017 had positive temporal artery biopsy and/or PET/CT scan diagnosis. At five years, patients underwent scan, magnetic resonance aortogram, assessment. Scans reported for overall metabolic disease visual FDG avidity grade each vascular territory. Results Sixteen met inclusion criteria, 11 attended five‐year visit. Median age was 75 73% women, all remission. 4 (36%) dilatation (range 40–43 mm), (45%) globally active scans. Cranial resolved between but aortitis developed four who previously PET‐inactive aortas. Disease‐modifying rheumatic drug (DMARD) use years associated inactivity ( P = 0.02). There trend toward higher mean diameter those (40.2 mm vs 36.0 mm, 0.06) not Conclusion Vasculitis changed from large vessel exclusively years. This may explain preponderance early complications GCA. The potential role long‐term DMARDs mitigate smoldering warrants further study.

Language: Английский

Citations

0
Update in imaging for large vessel vasculitis DOI Creative Commons
Berit Dalsgaard Nielsen, Luca Seitz, Wolfgang Schmidt

et al.

Best Practice & Research Clinical Rheumatology, Journal Year: 2025, Volume and Issue: unknown, P. 102060 - 102060

Published: April 1, 2025

Language: Английский

Citations

0
Precision Over Prednisone: Innovative Treatment Strategies for Giant Cell Arteritis DOI Creative Commons
Andrea D. Gloor, M. Sørensen, Francesco Muratore

et al.

Current Treatment Options in Rheumatology, Journal Year: 2025, Volume and Issue: 11(1)

Published: May 22, 2025

Language: Английский

Citations

0
Current management of giant cell arteritis and its complications DOI
Elena Galli, Francesco Muratore, Kenneth J. Warrington

et al.

Current Opinion in Rheumatology, Journal Year: 2024, Volume and Issue: unknown

Published: June 26, 2024

Purpose of the review This provides an update on current management strategies for giant cell arteritis (GCA), emphasizing need alternative therapies to reduce disease relapses and mitigate glucocorticoid (GC)-related morbidity. Recent Findings The standard care GCA has traditionally involved prolonged use GC, recent studies are exploring faster GC tapering regimens in effort adverse effects while maintaining control. Randomized clinical trials have highlighted efficacy tocilizumab (TCZ), interleukin-6 receptor inhibitor, reducing flares sparing GCs. However, optimal treatment duration with TCZ is unknown patients remain at risk relapse after discontinuation. An unmet therapeutic persists who not candidates TCZ, those inadequate response this biologic. Therefore, investigations into such as targeting interleukin-17A, blocking T-cell activation or inhibiting Janus kinase–signal transducer activator transcription pathway, showcase potential avenues tailored treatments. Summary While GCs cornerstone therapy, emerges a promising GC-sparing agent. Ongoing research different pathways implicated pathogenesis led encouraging results. preliminary nature these findings necessitates larger randomized controlled establish their conclusively.

Language: Английский

Citations

2