Pos0389 Low Incidence of Late-Onset Gca During the First Year in Patients With Polymyalgia Rheumatica — An Imaging-Based Study

Background: Recent research has indicated that 23% of newly diagnosed polymyalgia rheumatica (PMR) patients exhibit subclinical giant cell arteritis (GCA) 1,2. However, typically only a small proportion of patients with PMR are evaluated in specialist care, therefore previous studies may represent highly selected PMR populations with an increased risk of GCA. Furthermore, the precise incidence of late-onset GCA remains to be determined. Existing studies reporting the occurrence of PMR throughout the disease course did not systematically employ imaging to evaluate for subclinical GCA both at baseline and during follow-up 3.Consequently, it remains unclear whether GCA emerging during the PMR disease course represents a delayed onset or an initially overlooked diagnosis. Objectives: This study aimed to investigate the incidence of late-onset GCA in newly diagnosed PMR patients without cranial symptoms, applying imaging at baseline, 8 weeks, 10 weeks and 52 weeks to exclude GCA at baseline and diagnose GCA during follow-up. Methods: In this one-year prospective cohort study, treatment-naïve individuals newly diagnosed with PMR and without cranial symptoms of GCA underwent baseline assessments, including vascular ultrasonography and 2-18Ffluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) with computed tomography (CT). Subsequently, prednisolone treatment was initiated, with a gradual 8-week taper, followed by a short-term discontinuation until week 10. Clinical visits at weeks 8 and 10 included vascular ultrasonography and FDG-PET/CT. Prednisolone was subsequently reintroduced and tapered in accordance with standard care. Patients were monitored for cranial symptoms throughout the study, and confirmatory imaging was conducted as needed. After one year, a follow-up visit was conducted to confirm the PMR diagnosis and perform vascular ultrasonography. Results: At baseline (Table 1), 2/64 patients (3%) exhibited subclinical GCA. During the one year follow-up, two PMR patients developed late-onset GCA corresponding to an incidence rate of 32 per 1000 person years. One patient developed symptomatic cranial GCA 14 weeks after the PMR diagnosis, exhibiting cranial symptoms and elevated CRP. The diagnosis was subsequently confirmed with vascular ultrasonography. In contrast, the second patient was diagnosed with subclinical GCA during the one-year visit using vascular ultrasonography, affecting both temporal and axillary arteries, coupled with the recurrence of shoulder and pelvic symptoms and an elevated CRP of 45. A subsequent FGD-PET/CT was performed, showing vasculitis encompassing the same arteries as identified with vascular ultrasonography (Figure 1). Neither of these patients exhibited signs of vasculitis at week 8 or week 10 on FDG-PET/CT or vascular ultrasonography. Conclusion: This study is the first to demonstrate a low incidence rate of late-onset GCA in patients with PMR during the first year, employing imaging to exclude GCA at baseline and diagnose GCA during follow-up. Additionally, it provides evidence of a low prevalence of subclinical GCA in an unselected PMR population, suggesting that previous reported prevalence rates of subclinical GCA might have been overestimated across the entire PMR population. REFERENCES: 1 Hemmig AK, Gozzoli D, Werlen L, et al. Subclinical giant cell arteritis in new onset polymyalgia rheumatica A systematic review and meta-analysis of individual patient data. Semin Arthritis Rheum 2022;55:152017. 2 De Miguel E, Macchioni P, Conticini E, et al. Prevalence and characteristics of subclinical giant cell arteritis in polymyalgia rheumatica. Rheumatology (Oxford) 2023. 3 Nielsen AW, Frølund LL, Våben C, et al. Concurrent baseline diagnosis of giant cell arteritis and polymyalgia rheumatica - A systematic review and meta-analysis. Semin Arthritis Rheum 2022;56:152069. Acknowledgements: NIL. Disclosure of Interests: Andreas Wiggers Nielsen: None declared, Ellen-Margrethe Hauge EMH has received personal fees unrelated to this manuscript from AbbVie, Sanofi, SOBI, Merck Sharp & Dohme and Union Chimique Belge., EMH has received grants unrelated to this manuscript from Novo Nordic Foundation, Roche and Novartis, Ib Hansen: None declared, Berit Dalsgaard NIelsen BDN has received speaking fees unrelated to this manuscript from Novartis an AbbVie, Gøren Geil Kjær: None declared, Jesper Blegvad-Nissen: None declared, Kate Rewers: None declared, Christian Møller Sørensen: None declared, Lars Christian Gormsen: None declared, Kresten Keller: None declared.