ArticleCase reports in dermatology
Trauma-Induced Psoriatic Arthritis: A Deep Köbner Phenomenon.
Article in Case reports in dermatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Understanding Enthesitis in Psoriatic Disease: Insights and Implications.American journal of clinical dermatology · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: 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. Case Presentation: 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. Conclusion: 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.
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Registered trials
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