Introduction Prurigo nodularis (PN) is a chronic, inflammatory skin condition characterized by intensely pruritic, hyperkeratotic nodules most commonly showing a symmetric distribution on arms, legs, and torso. PN is divided into an early-onset atopic and a late-onset nonatopic form. 1 The pathogenic mechanisms behind PN remain unclear, but patients’ skin exhibits alterations in nerve density and inflammation including activation of various proinflammatory pathways such as interleukin (IL) 4, IL-13, IL-31, and neuropeptides. 2 Dupilumab is a fully human monoclonal antibody blocking the IL-4 receptor α thereby inhibiting IL-4/IL-13 signaling and is used in the treatment of moderate-to-severe atopic dermatitis (AD), moderate-to-severe asthma, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, and PN. IL-4, IL-13, and IL-31 are all part of type 2 inflammation driven by the T helper (Th)2 cells. It has been suggested that inhibition of IL-4 and IL-13 can lead to increased IL-17 activity, which has been proposed as the mechanism behind paradoxical development of both psoriasis 3 and arthritis 4 after dupilumab treatment. Paradoxical development of psoriasis after dupilumab treatment has been described previously, 5 , 6 particularly in patients with AD, but to our knowledge only one case of scalp psoriasis has been reported after dupilumab treatment of PN. 7 Here, we describe a patient with PN, who experienced widespread psoriasis after dupilumab treatment, but obtained complete resolution of all symptoms after subsequent treatment with adalimumab.
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Sørensen et al. (2024) studied this question.
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