Tocilizumab in Giant Cell Arteritis: A Real-Life Retrospective Study

Angiology ◽  
2018 ◽  
Vol 69 (9) ◽  
pp. 763-769 ◽  
Author(s):  
Gianfranco Vitiello ◽  
Carolina Orsi Battaglini ◽  
Giulia Carli ◽  
Anna Radice ◽  
Andrea Matucci ◽  
...  

This study aims to evaluate (1) the efficacy and safety of tocilizumab (TCZ) as a steroid-sparing agent in patients with giant cell arteritis (GCA) and (2) the usefulness of 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) in the follow-up and to detect disease activity. We retrospectively evaluated 12 patients with GCA treated with TCZ (8 mg/kg/mo). Pre- and posttherapy data about clinical signs and symptoms, laboratory results, FDG-PET imaging study, and the mean glucocorticoid (GC) dose were used to assess disease activity. Tocilizumab achieved complete disease remission in all patients. Mean FDG-PET-detected standard uptake value decreased from 2.05 ± 0.64 to 1.78 ± 0.45 ( P = .005). In 2 patients in whom temporal arteries color Doppler sonography examination was consistent with temporal arteritis, the hypoechoic halo disappeared after TCZ treatment. Mean GC dose was tapered from 26.6 ± 13.4 mg/d to 3.3 ± 3.1 mg/d ( P < .0001). One-half of the patients discontinued GC therapy. Three patients experienced severe adverse reactions and had to stop TCZ therapy. In accordance with previous reports, TCZ is an effective steroid-sparing agent for GCA, although careful monitoring of adverse drug reactions is needed. 18F-fluorodeoxyglucose positron emission tomography could be used to monitor disease activity in TCZ-treated patients, but prospective studies are needed to confirm these data.

Author(s):  
Mariella Baldini ◽  
◽  
Sara Giannoni ◽  
Elisa Cioffi ◽  
Elisa Grifoni ◽  
...  

Giant Cell Arteritis (GCA) is an immune-mediated vasculitis of large- and medium-sized vessels. Stroke happens in 3% to 7% of the cases, and identifying GCA properly is important because potentially curative treatment exists. We present a case of an 83-year-old woman, in whom suspected GCA was revealed by stroke caused by Vertebral Artery (VA) inflammation. The uncommon stroke localization and the ultrasound findings suggested vasculitic etiology of lesions. 18-Fluorodeoxyglucose-Positron Emission Tomography (18-FDG-PET) confirmed inflamed VA walls. Patient was treated with oral steroids and antiplatelet therapy, with improvement of clinical and ultrasonographic status. In our patient clinical diagnosis of GCA was challenging due to limited classical symptoms. Arguments in favor of arteritis were the symmetric and bilateral involvement of the VA, the sonographic halo sign and atypical stroke localization. Abbreviations: VA: Vertebral Artery; MRI: Magnetic Resonance Imaging; 18-FDG-PET: 18-Fluorodeoxyglucose-Positron Emission Tomography; AICA: Anterior Inferior Cerebellar Artery; PICA: Posterior Inferior Cerebellar Artery; GCA: Giant Cell Arteritis.


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