Upadacitinib as a treatment for co-existent allergic contact dermatitis and psoriasis
Peter Ch’en, Miriam Al-Saedy, Eingun James Song
Abstract
Atopic dermatitis (AD) and psoriasis have divergent and antagonistic immune mechanisms, explaining the rarity of the presence of both diseases in the same individual. AD has been primarily shown to be a helper T cell (Th)2-driven disease, whereas psoriasis is caused by Th17 immune activation.1 Biologic therapies that selectively target the Th2 and Th17 immune pathways have been transformative in treating these conditions. However, rare cases of the development of eczema in patients receiving psoriasis biologics or development of de novo psoriasiform dermatitis in patients receiving dupilumab (Dupixent), which is an interleukin 4 (IL-4) receptor subunit antagonist that blocks Th2-mediated cytokines, have been reported in the literature and referred to as “phenotypic switching” by some.