Adalimumab-induced paradoxical psoriasis treated with biologics targeting the IL-17/IL-23 axis in patients with hidradenitis suppurativa.

Background Paradoxical psoriasis (PP) has been mainly described in patients receiving tumor necrosis factor-α (TNFα)-inhibitors for inflammatory bowel disease or psoriasis vulgaris, while such data in the context of hidradenitis suppurativa (HS) are scarce. The purpose of this study was to demonstrate the course of PP and the underlying HS upon switching from adalimumab to a biologic agent targeting the interleukin (IL)-17/IL-23 axis. Methods The electronic medical database of the outpatient department for HS of a tertiary hospital for skin diseases was searched to identify patients with moderate to severe HS under treatment with adalimumab, who developed PP and were switched to biological therapy with an IL-17 or IL-23 inhibitor between February 2016 and January 2022. Disease assessment scores were evaluated at baseline, at time of PP development as well as six and twelve months thereafter. Results Among the 83 patients who received adalimumab the treatment of HS between February 2016 and January 2022, 10 patients (12%) developed paradoxical psoriasiform skin reactions after a median time of seven (range, 2-48) months. There were four females (40%) and six males (60%) with a median age of 42,5 (range, 33-56) years. Five patients presented with plaque psoriasis and five with palmoplantar pustulosis, while four had intertriginous and three nail involvement. In most of the patients the HS responded well to adalimumab at onset of PP. Eight patients were changed to secukinumab, one to ustekinumab and one to rizankizumab. The HS further improved in all but two patients, one receiving secukinumab and one receiving rizankizumab. In addition, all patients achieved improvement of PP. Conclusion Despite the small number of patients, this study provides support that patients with adalimumab-induced PP may benefit from biologics targeting IL-17/IL-23 axis. Further studies are needed, to establish the optimal therapeutic strategy of the anti-TNFα-induced PP in the context of HS.