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Tomelleri, A; Bond, M; Marvisi, C; Campochiaro, C; Farina, N; Venerandi, B; Matucci-Cerinic, M; Salvarani, C; Dejaco, C; Dagna, L.
Secukinumab is effective and safe for patients with giant cell arteritis after tocilizumab failure.
Rheumatology (Oxford). 2025;
Doi: 10.1093/rheumatology/keaf250
PubMed
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- Co-authors Med Uni Graz
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Dejaco Christian
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- Abstract:
- OBJECTIVES: To evaluate the effectiveness and safety of secukinumab in patients with giant cell arteritis (GCA) who experienced an inadequate response to tocilizumab. METHODS: This is a case series of six patients with GCA started on secukinumab after tocilizumab failure from three centres in Italy. Tocilizumab failure was defined as disease relapse, indicated by clinical symptoms and/or vascular inflammation on imaging. Secukinumab was administered subcutaneously at 300 mg weekly for four weeks, subsequently at 300 mg monthly. Clinical response was assessed at six months based on symptoms resolution and normalisation of inflammatory markers. Imaging was used to confirm remission in cases where it had previously documented relapse. RESULTS: The cohort consisted exclusively of women, with a median age of 72 years (IQR, 67-73). At disease onset, all patients had cranial symptoms, and four experienced constitutional symptoms. Tocilizumab failure occurred after a median of 14 months (IQR, 11-22). Following secukinumab initiation, all patients achieved clinical and laboratory remission within six months. Imaging confirmed complete resolution of vasculitis in the four patients with documented active disease before start of secukinumab. Three patients successfully discontinued glucocorticoids within four months, while the remaining three continued low-dose prednisone (1.25, 2.5, 5 mg daily). No adverse events were reported during secukinumab treatment. CONCLUSIONS: Secukinumab demonstrated effectiveness in achieving clinical and imaging remission in patients with GCA failing tocilizumab. These preliminary real-world findings support the potential role of interleukin-17A inhibition in GCA management, particularly in cases of inadequate response to interleukin-6 blockade. Larger studies are warranted to confirm these observations.