Ogawa Youichi, Maejima Eri, Takeichi Takuya, Okamoto Takashi, Mitsui Hiroshi, Shimada Shinji, Akiyama Masashi, Kawamura Tatsuyoshi
Department of Dermatology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Department of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
J Dermatol. 2025 Jan;52(1):167-170. doi: 10.1111/1346-8138.17464. Epub 2024 Sep 20.
Generalized pustular psoriasis (GPP) is a recurrent and sometimes life-threatening sterile pustular disease. Because interleukin (IL)-36 is the central cytokine in disease formation, spesolimab, which interferes with IL-36 receptor signaling, is highly effective. Here, we report a patient with GPP with a heterozygous hypomorphic MPO variant refractory to intravenous spesolimab. Although spesolimab showed excellent clinical efficacy in resolving pre-existing pustules and erythema, it did not suppress the emergence of new pustules and erythema, which did not decrease the peripheral blood neutrophil count, therefore bimekizumab, an anti-IL-17A/IL-17F antibody, was administered after the second spesolimab infusion, which resolved the pustules and erythema. We discuss the possible reasons for the resistance mechanism to spesolimab.
泛发性脓疱型银屑病(GPP)是一种复发性且有时会危及生命的无菌性脓疱病。由于白细胞介素(IL)-36是疾病形成中的核心细胞因子,干扰IL-36受体信号传导的司库奇尤单抗具有高效性。在此,我们报告1例携带杂合性低表达MPO变异的GPP患者,该患者对静脉注射司库奇尤单抗难治。尽管司库奇尤单抗在消退已有的脓疱和红斑方面显示出优异的临床疗效,但它并未抑制新脓疱和红斑的出现,且外周血中性粒细胞计数未降低,因此在第二次输注司库奇尤单抗后给予抗IL-17A/IL-17F抗体比美吉珠单抗,后者消退了脓疱和红斑。我们讨论了对司库奇尤单抗产生耐药机制的可能原因。