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EJD, vol. 31, n◦ 5, September-October 2021 The second case is a 23-year-old Japanese man with AD since infancy who was started on dupilumab due to insufficient control of skin lesions by topical corticosteroids (EASI 16.8). The skin lesions improved with dupilumab, however, after 1.5 years of dupilumab administration, the patient developed well-demarcated, slightly elevated scaly erythematous lesions on his face (figure 1F). A biopsy specimen showed psoriasiform acanthosis with intracorneal microabscesses (figure 1H). Immunohistochemically, positive immunostaining for p-STAT3 was found in the nucleus in keratinocytes (figure 1I, J). Topical corticosteroids (hydrocortisone butyrate) and 0.1 % tacrolimus ointment were ineffective, however, delgocitinib ointment markedly improved his skin lesions within three weeks (figure 1G). Currently, the psoriasiform eruption is well controlled with delgocitinib ointment even under dupilumab treatment. AD is mainly caused by type 2 cytokines, such as IL-4 and IL-13, while psoriasis is a condition involving IL-23 and Th17-related cytokines [7]. It is postulated that psoriasiform dermatitis in AD patients receiving dupilumab therapy is due to the immunological shift from Th2 to Th17 by the blockade of IL-4/IL-13 signalling. In fact, an elevation of IL-23 in dupilumab-induced psoriasiform lesions has been reported [8]. Although we did not confirm the upregulation of IL-23 or Th17-related cytokines in our cases, the strong expression of p-STAT3 in keratinocytes is consistent with psoriasis [6], suggesting that the Th17-related cytokine milieu was induced by dupilumab in our patients. Currently, various JAK inhibitors including delgocitinib (a pan-JAK inhibitor) and baricitinib (a JAK inhibitor mainly targeting JAK1 and JAK2) are used clinically for AD. Upadacitinib (a JAK inhibitor mainly targeting JAK1) also showed a significant therapeutic effect on AD in a Phase III clinical trial [9]. JAK inhibitors, upadacitinib and PF06826647 (a JAK inhibitor mainly targeting TYK2) may also be used to treat psoriasis, as well as AD, as these drugs are currently being tested under clinical trials with promising therapeutic effects [10]. Since the JAK-STAT pathway is involved in the signalling of various Th17related cytokines, including IL-23 and IL-22, delgocitinib may have regulated the effects of these cytokines more effectively than steroid or tacrolimus ointments in our patients. Given the potential efficacy of JAK inhibitors for psoriasis and the possible immunological shift from Th2 to Th17 by dupilumab, it may be reasonable to use JAK inhibitors specific to the Th17 pathway for the treatment of dupilumab-induced psoriasiform dermatitis.