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Psoriasiform keratosis shows abnormal keratinization and increased number of T‐helper 17 cells in psoriasiform keratosis implying a pathogenic link to psoriasis

decided to initiate the therapy with secukinumab 15 days after admission, and the rashes rapidly improved. We assessed for secondary adrenal insufficiency and performed rapid adrenocorticotropic hormone test and found that the serum cortisol was 2.41 lg/dL. As the cortisol level was not elevated (8.0 lg/dL), we made the diagnosis of secondary adrenal insufficiency. Therapy with hydrocortisone at 5 mg/day was initiated. After 2 months, the patient obtained a PASI score of 0 (Fig. 1c). To date, the patient has been undergoing treatment and maintaining a PASI score of 0 with no reported sideeffects for 2 years. The mechanism of PE is elusive, but the excessive interleukin (IL)-17 signaling is presumed to be important in the pathogenesis of psoriasis. Recently, Saeki et al. reported the efficacy of ixekizumab treatment in a small number of patients with PE in Japan. Yamasaki et al. also reported the efficacy of brodalumab for PE. It is known that T-helper 17 cells accumulate in PE pathological sections similar to that in pustular psoriasis. Mugheddu et al. reported two cases whereby secukinumab improved PE. Furthermore, Tsai et al. reported a series of 10 cases in which secukinumab was prescribed for PE. Their data showed that at week 16, four out of 10 patients and seven out of 10 patients were able to achieve PASI-90 and PASI-75, respectively. It is expected that secukinumab might improve PE by IL-17 inhibition. We experienced a case of PE that was successfully treated with secukinumab for 2 years. Thus, secukinumab may be an effective and safe option for the treatment of PE. CONFLICT OF INTEREST: None declared.