34888 Refractory pustular psoriasis treated successfully with IL-23 inhibitors. Report of 1 patient with generalized pustular psoriasis and 4 patients with palmoplantar pustulosis

Abstract

Introduction: It is known that the key inflammatory cytokines in plaque psoriasis are TNF-a/IL-23/IL-17/IL-22. Conversely, recent data demonstrate that pustular psoriasis is mainly characterized by a neutrophil-driven inflammatory response following “hyperactivation” of the IL-36 axis. However, it appears that these 2 pathways cross-talk to each other and act synergistically in the pathophysiologic mechanism of pustule formation. In terms of guidance to treatment, no robust data exist. Considering the advances into the pathophysiology, arises the question whether the novel IL-23 antagonists could lead to clinical improvement. Methods: We present a 75-year-old female patient with generalized-pustular-psoriasis for 10 years and 4 patients (2 females and 2 males) 53, 58, 60, and 62 years old with palmoplantar-pustulosis for 3, 5, 5, and 6 years, respectively. The former had unsuccessfully undergone every available at that point systemic therapy (both conventional and biologic) whereas the laters had failed acitretin, MTX/acitretin, apremilast/acitretin, acitretin/MTX/apremilast respectively. All five had PGA score >3. We initiated an IL-23 inhibitor. Patient with the generalized-pustular form and 2 patients with the palmoplantar form received risankizumab whereas the other 2 guselkumab. Results: All 4 had reached PPPGA 0/1 by week 12, whereas the patient with generalized pustular form had reached PGA 1 by week 16. Formers are currently undergoing the sixth month of therapy, whereas the later the eighteenth month and still present great response. Conclusions: Il-23 might be a key operator in the interconnection of the complex pathogenetic pathways in pustular psoriasis. Therefore, IL-23 inhibition could be a therapeutic option. More data are required.