背景 逆行性银屑病（PP）主要出现在接受肿瘤坏死因子-α（TNFα）抑制剂治疗炎症性肠病或寻常型银屑病的患者中，而在汗腺脓肿（HS）背景下的相关数据较少。本研究旨在证明从阿达木单抗转换为靶向白细胞介素（IL）-17/IL-23轴的生物制剂后PP和潜在HS的病程。 方法 通过检索一个皮肤疾病三级医院HS门诊部的电子病历数据库，从2016年2月至2022年1月之间确定了接受阿达木单抗治疗中度至重度HS的患者，他们出现了PP，并在之后转换为抑制剂IL-17或IL-23的生物治疗。 在基线、PP发展时以及之后的6个和12个月，对疾病评估得分进行了评估。 结果 在2016年2月至2022年1月接受阿达木单抗治疗的83名患者中，有10名患者（12%）在中位数为7（范围为2-48）个月后发展出逆行性银屑病反应。其中有四名女性（40%）和六名男性（60%），中位年龄为42.5（范围为33-56）岁。五名患者表现为银屑病斑块型，五名患者表现为掌跖角化症，而四名患者表现为腹股沟和三名患者有指甲受累。在大多数患者中，HS在出现PP时对阿达木单抗的反应良好。 八名患者转换为塞库珂单抗，一名患者转换为乌斯特可单抗，一名患者转换为里珍卡单抗。 所有患者除了一名接受塞库珂单抗治疗和一名接受里珍卡单抗治疗的患者外，HS进一步得到改善。 此外，所有患者的PP都有所改善。 结论 尽管患者数量较少，但本研究支持接受阿达木单抗后发生PP的患者可能会从靶向IL-17/IL-23轴的生物制剂中获益。 需要进一步的研究来确定HS背景下抗TNFα引起的PP的最佳治疗策略。 S. Karger AG, Basel.

Background Paradoxical psoriasis (PP) has been mainly described in patients receiving tumor necrosis factor-α (TNFα)-inhibitors for inflammatory bowel disease or psoriasis vulgaris, while such data in the context of hidradenitis suppurativa (HS) are scarce. The purpose of this study was to demonstrate the course of PP and the underlying HS upon switching from adalimumab to a biologic agent targeting the interleukin (IL)-17/IL-23 axis. Methods The electronic medical database of the outpatient department for HS of a tertiary hospital for skin diseases was searched to identify patients with moderate to severe HS under treatment with adalimumab, who developed PP and were switched to biological therapy with an IL-17 or IL-23 inhibitor between February 2016 and January 2022. Disease assessment scores were evaluated at baseline, at time of PP development as well as six and twelve months thereafter. Results Among the 83 patients who received adalimumab the treatment of HS between February 2016 and January 2022, 10 patients (12%) developed paradoxical psoriasiform skin reactions after a median time of seven (range, 2-48) months. There were four females (40%) and six males (60%) with a median age of 42,5 (range, 33-56) years. Five patients presented with plaque psoriasis and five with palmoplantar pustulosis, while four had intertriginous and three nail involvement. In most of the patients the HS responded well to adalimumab at onset of PP. Eight patients were changed to secukinumab, one to ustekinumab and one to rizankizumab. The HS further improved in all but two patients, one receiving secukinumab and one receiving rizankizumab. In addition, all patients achieved improvement of PP. Conclusion Despite the small number of patients, this study provides support that patients with adalimumab-induced PP may benefit from biologics targeting IL-17/IL-23 axis. Further studies are needed, to establish the optimal therapeutic strategy of the anti-TNFα-induced PP in the context of HS.S. Karger AG, Basel.