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Long-term follow-up of 89 patients with giant cell arteritis: a retrospective observational study on disease characteristics, flares and organ damage

Yazar
Artim-Esen, Bahar
Yalcinkaya, Yasemin
Inanc, Murat
Gül, Ahmet
Ocal, Lale
Ince, Burak
Artan, Selay
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Özet
The objective of the study is to investigate the clinical characteristics and long-term prognosis including flares and organ damage in patients with giant cell arteritis (GCA) from a tertiary referral centre and compare these features in different subgroups. In this retrospective observational study, patients with GCA who were followed up in our vasculitis clinic between 1998 and 2018 were evaluated by a predefined protocol. Patients with and without cranial symptoms were compared for clinical and laboratory features, flares and permanent damage findings. Vasculitis Damage Index and Large Vessel Vasculitis Index of Damage were used for damage assessment. Records of 89 patients (median follow-up time 46 months) were analysed; mean time to diagnosis after initial symptom was longer in patients with acute vision loss (11 +/- 4 vs. 4.8 +/- 1.1 months p = 0.002). EGG (n = 19) was younger (63 +/- 2 vs. 69 +/- 1 years old p = 0.01); had higher mean CRP (141.8 +/- 107.3 vs. 76.6 +/- 67.9 mg/dL p = 0.023) and ESR (120.8 +/- 25.1 vs. 99.3 +/- 24.3 mm/h p = 0.004) at diagnosis. PET-CT detected large vessel vasculitis in 42/48 (87.5%) cases of the entire cohort. Thirty-one patients had flares and proportion of flared patients was significantly higher in patients with cranial symptoms. At least one damage item (DI) was present in 54 (60.7%) patients. The development of damage was found to be associated with flares. Evaluation of our cohort revealed the importance of early diagnosis for prevention of vision loss in GCA. Patients without cranial symptoms were younger, present with higher inflammatory response and for these, PET-CT was the main diagnostic tool. Relapse rate was higher in patients with cranial symptoms. Flares and accompanying corticosteroid treatment may contribute to organ damage in GCA.
Bağlantı
http://hdl.handle.net/20.500.12627/84650
https://doi.org/10.1007/s00296-020-04730-1
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