No need to change the drug class: ixekizumab- following secukinumab-therapy in psoriasis

Abstract

Abstract Background: Regarding treatment of psoriasis, dermatologists now use new, highly effective targeted therapies. Among such, biologic therapies have become a mainstay in patients with moderate to severe psoriasis; yet, a substantial proportion of patients show insufficient or no treatment response. Current literature has insufficient evidence for successful treatment when switching biologics after multiple failures, in particular when the biologics share a common mechanism of action. Objectives: To compile a case series of patients with moderate to severe psoriasis who had primary or secondary loss of response to multiple previous systemic treatments. We specifically focused on patients recently treated with the anti-IL-17A antibody secukinumab, who further received the anti-IL-17A antibody ixekizumab as subsequent therapy. Patients and methods: We performed a retrospective cohort analysis. Inclusion criteria were patients with moderate to severe psoriasis vulgaris (as defined by European consensus and the German guidelines), who have previously been treated with systemic therapies including three or more biological therapies. All patients treated with anti-IL-17A antibody secukinumab experienced a primary and/or secondary treatment failure and subsequently received the anti-IL-17A antibody ixekizumab. The primary outcome was treatment response to ixekizumab using PASI score; the secondary outcome was incidence of adverse events. Results: Twelve patients were included. At week 6 of ixekizumab treatment, PASI 75 was achieved in 91.7%, PASI 90 in 66.7%, PASI 100 in 8.3% of patients. At week 12, PASI 75 was achieved in 100%, PASI 90 in 100%, PASI 100 in 58.3% of the cohort. Throughout the observation period, no severe adverse events were observed. Conclusions: Ixekizumab proved to be an effective and safe therapeutic option for patients with prior systemic therapies, including biological treatments with the same mechanism of action. Thus, failure of secukinumab does not preclude future therapy success with a second IL-17A-directed therapy.