POS0950 FIRST PROFILING OF THE SWISS NATIONAL SCQM GIANT CELL ARTERITIS AND POLYMYALGIA RHEUMATICA COHORT

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Background: Giant cell arteritis (GCA) and Polymyalgia rheumatica (PMR) constitute the giant cell arteritis spectrum disease (GPSD) [1]. Disease and risk stratification within this spectrum is an unmet need. The Swiss Clinical Quality Management in Rheumatic Diseases (SCQM) foundation (https://www.scqm.ch/en/) runs since 1997 national registries for inflammatory arthropathies. Objectives: The primary aim of this cohort profile is to describe patient characteristics, comorbidities, laboratory investigation results, imaging findings, and treatment data. Methods: In 2020, we established a registry for patients with PMR and GCA within the framework of SCQM. Results: Since its establishment in 2020 until January 6, 2024, a total of 436 patients, 337 with GCA and 99 with PMR have been included in the cohort. Of the GCA patients 51%, and of the PMR patients 30% were newly diagnosed (within 14 days), while the rest of the patients had an established disease. Patients were enrolled across Switzerland, from tertiary hospitals (74%), regional hospitals (12%) and rheumatologists in private practice (14%). Median age of GCA patients at diagnosis was 72 (IQR: 65-77) years, with 64% of the patients being female. For PMR patients median age at diagnosis was 71 (IQR: 63-77) years, 56% female. The median duration of symptoms prior to diagnosis was shorter (40 vs. 52 days; p=0.04) for GCA compared to PMR patients. At diagnosis, 81% (124/153) of the GCA patients reported cranial symptoms, 31% (48/156) visual symptoms and 43% (39/91) polymyalgia (Table 1). At diagnosis, 95 % of the PMR patients stated shoulder girdle pain, 85% pelvic girdle pain, 44% neck pain and 96 % had elevated inflammatory markers. For 193 out of 337 GCA patients we had information on the diagnostic imaging modality used within the first 2 months after diagnosis. The majority of patients 76% (147/193) underwent vascular ultrasound, followed by PET-CT in 59% (114/193) and MRI in 40% (77/193) of cases. The majority of the patients (85%) underwent two imaging modalities: ultrasound+ PET in 40% (78/193), ultrasound + MRI in 33% (63/193) or PET-CT + MRI in 11% (22/193) of the cases. Temporal artery biopsy was performed in 29% (97/337) of the patients and was diagnostic in 66%. PMR patients underwent shoulder ultrasound in 49% (36/73) of the cases, hip ultrasound in 23% (16/71) and screening for vasculitis by PET/CT in 16% (16/99) of patients. Six months after the GCA diagnosis, 79% (116/147) of the patients were still on corticosteroids, after 12 months 50% (70/140) and after 24 months still 37% of the patients were on corticosteroids (Figure 1). The median duration of steroid treatment was 377 days, 95% CI [338–420]. Of all GCA patients, 77% (231/300) received a steroid sparing treatment: 73% Tocilizumab, 14% Methotrexate, 5% Abatacept. The median time from the GCA diagnosis to initiation of Tocilizumab was 87 days, IQR [31, 247]. 13% of the GCA patients received more than one steroid sparing agents. In the PMR cohort, 30% of the patients received methotrexate, 15% tocilizumab and 3% leflunomide. At the inclusion visit, both GCA and PMR patients reported the following comorbidities: hypertension (51% in GCA vs. 44% in PMR), diabetes (15% in GCA vs. 12% in PMR), myocardial infarction (3.8% GCA vs. 3.3% PMR), and stroke (7% GCA vs. 1% PMR). More GCA patients (19%) were active smokers compared to PMR patients (2.6%), p=0.001. At the inclusion visit, infections were reported more frequently in GCA, 11.2% (32/286) vs. 1.2% (1/84) in PMR patients (p= 0.002). Infections occurred at a median of 17 days IQR [-2, 1100] after GCA diagnosis. At inclusion, 26% (67/256) of the GCA patients had osteoporosis vs. 15% (12/79) of the PMR patients. Among the newly diagnosed GCA patients, 11.7% (20/171) developed osteoporosis during follow-up and 43.2% (129/299) of the GCA patients received an osteoporosis specific therapy (bisphosphonates 38.5%, denosumab 4% or teriparatide 1%). Future research objectives encompass characterization of the GPSD, the role of longitudinal imaging, search for disease biomarkers and identifying predictive factors for response to new therapies. Figure 1Kaplan- Meier curve: steroid retention in new diagnosed GCA patients, n=152. Conclusion: The GCA/PMR registry is used in many regions and in different institutions in Switzerland. Our data confirms the diverse manifestations of the GPSD spectrum. Comorbidities are present in a substantial proportion of patients. US is the diagnostic method of choice for GCA in this cohort. A proportion of patients with GCA received treatment with corticosteroids beyond 2 years. Tocilizumab has been used as steroid sparing treatment in around 75% of GCA patients. The SCQM GCA-PMR database facilitates future research in GPSD in the era of new steroid sparing treatments. REFERENCES: [1] Tomelleri, A. et al. Disease stratification in GCA and PMR: state of the art and future perspectives. Nat. Rev. Rheumatol. 19 , 446–459 (2023). Table 1Disease features of the newly diagnosed GCA patients, N=171.VariableFrequencyn/reported (%)Cranial symptoms including ocular124/153 (81%)Headache92/159 (57.9%)Headache VAS (0-10) (median [IQR])6.00 [4.00, 8.00]Scalp tenderness45/138 (32.6%)Jaw claudication57/149 (38.3%)Painful or indurated temporal arteries41/137 (29.9%)Ocular involvement48/156 (30.8%)Diplopia16/156 (10.3%)Blurring vision22/156 (14.1%)Vision loss unilateral12/156 (7.7%)Vision loss bilateral4/156 (2.6%)General SymptomsNight sweats47/141 (33.3%)Fever24/143 (16.8%)Weight loss75/147 (51%)Polymyalgic symptoms (%)39/91 (42.9%)Laboratory parametersMedian [IQR]ESR, mm/h58 [30, 87]CRP, mg/l55 [19, 109]Abbreviations: ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; VAS, visual analog scale; Anti-CCP, anti-Cyclic Citrullinated Peptide antibodies Acknowledgements: NIL . Disclosure of Interests: Mihaela Stegert Novartis AG Switzerland, Jonas Brändli: None declared, Christoph Blapp: None declared, Alfred Mahr: None declared, Lisa Christ Novartis, Bristol-Myers Squibb, Vifor, Gilead Sciences, F. Hoffmann-La Roche, Novartis, Gilead Sciences, F. Hoffmann-La Roche, Pfizer, Thomas Neumann Vifor Phrarma, Switzerland, GlaxoSmithKline AG, Amgen Switzerland AG, GlaxoSmithKline AG, AstraZeneca GmbH, Vifor Phrarma, Switzerland, Vifor Phrarma, Switzerland, Michele Iudici Vifor Pharma, Boehringher Ingelheim, Giorgio Tamborrini: None declared, Christoph Berger: None declared, Christoph Iking-Konert Abbvie, Amgen, AstraZeneca, CSL Vifor, GSK, Janssen, Lilly, Novartis, Pfizer, Abbvie, AstraZeneca, GSK, Sanofi, Vifor, Almut Scherer MSD, Pfizer, Abbvie, Pfister, Roche, Novartis, Sanofi, Mike O. Becker GSK, Amgen, Novartis, Vifor, Amgen, Vifor, EMDO Foundation, Novartis foundation for medical-biological research, Innovative Medicines Initiative (IMI), Peter Villiger Roche, Vifor, Vifor, Sanofi, Astra, GSK, Thomas Daikeler Sanofi, Novartis, Vifor, Novartis, Abbvie. © The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.

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