Mima Yoshihito, Yamamoto Masako, Nishida Naoki, Norimatsu Yuta, Iozumi Ken
Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Department of Dermatology, Tokyo Metropolitan Police Hospital, Tokyo, Japan.
Case Rep Dermatol. 2025 Apr 3;17(1):137-142. doi: 10.1159/000545694. eCollection 2025 Jan-Dec.
Psoriasis is a chronic systemic inflammatory disorder resulting from complex interactions between genetic and environmental factors. In addition to cutaneous manifestations, psoriasis is associated with psoriatic arthritis (PsA). Among the recognized mechanisms of disease exacerbation, the Köbner phenomenon (KP) plays a crucial role. KP refers to the appearance of new psoriatic lesions on previously healthy skin following trauma. A deeper variant of this phenomenon, the deep Köbner phenomenon (DKP), involves severe trauma triggering systemic inflammation, including the onset of PsA. Trauma-induced DKP represents unique disease mechanisms, linking external mechanical stress to immune-mediated joint pathology.
We present a case of a 60-year-old male with psoriasis, who initially responded well to ixekizumab, an IL-17A inhibitor but subsequently developed PsA following a wrist injury. The PsA exacerbation was attributed to increased mechanical stress from daily activities and rehabilitation efforts. Adjustments were made to rehabilitation intensity and joint movement restrictions, leading to gradual symptom improvement over 3 months without intensifying biological therapy.
This case highlights the pathophysiological relationship between trauma, DKP, and PsA. The rapid onset of PsA following trauma suggests that inflammatory mediators and neuropeptides triggered by DKP play significant roles. Given that rehabilitation plays crucial roles in recovery but may also exacerbate symptoms if improperly managed, tailored rehabilitation strategies are essential in managing trauma-induced PsA. This case also underscores the importance of comprehensive management, including biological therapy and personalized rehabilitation approaches. Further studies are needed to optimize inflammation control and joint function in patients experiencing post-trauma PsA.
银屑病是一种慢性全身性炎症性疾病,由遗传和环境因素之间的复杂相互作用引起。除皮肤表现外,银屑病还与银屑病关节炎(PsA)相关。在公认的疾病加重机制中,同形反应(KP)起着关键作用。KP是指先前健康的皮肤在受到创伤后出现新的银屑病皮损。这种现象的一种更严重变体,即深部同形反应(DKP),涉及严重创伤引发全身炎症,包括PsA的发作。创伤诱导的DKP代表了独特的疾病机制,将外部机械应力与免疫介导的关节病理联系起来。
我们报告一例60岁男性银屑病患者,该患者最初对IL-17A抑制剂司库奇尤单抗反应良好,但随后在手腕受伤后发展为PsA。PsA的加重归因于日常活动和康复训练带来的机械应力增加。对康复强度和关节活动限制进行了调整,症状在3个月内逐渐改善,且未强化生物治疗。
该病例突出了创伤、DKP和PsA之间的病理生理关系。创伤后PsA的迅速发作表明,DKP触发的炎症介质和神经肽起了重要作用。鉴于康复在恢复过程中起着关键作用,但如果管理不当也可能加重症状,因此定制的康复策略对于管理创伤诱导的PsA至关重要。该病例还强调了综合管理的重要性,包括生物治疗和个性化康复方法。需要进一步研究以优化创伤后PsA患者的炎症控制和关节功能。