BI03 Erythrodermic psoriasis following second cycle of cemiplimab: a case report

Abstract Programmed cell death protein-1 (PD-1) and its ligand PD-L1 are key immune checkpoints that play a crucial role in regulating immune responses. In oncology, immune checkpoint inhibitors (ICIs) targeting PD-1/PD-L1 enhance antitumour immunity by preventing tumour cells from evading immune detection. Cemiplimab, a PD-1 inhibitor, has demonstrated efficacy in treating metastatic squamous cell carcinoma (SCC), significantly improving patient outcomes. However, ICIs are increasingly recognized for their potential to induce novel immune-related adverse events (irAEs), particularly dermatological toxicities. Reported cutaneous irAEs include lichenoid eruptions, alopecia areata and vitiligo, among others. Here, we present a case of erythrodermic psoriasis following a second cycle of cemiplimab. A patient undergoing cemiplimab treatment for metastatic SCC developed a widespread scaly rash following their second cycle of therapy. Clinical examination revealed islands of sparing within an erythematous and scaly eruption. This was managed initially with topical treatment and oral prednisolone. Over the subsequent 8 weeks, the rash progressed to a severe erythrodermic presentation, characterized by diffuse erythema, desquamation and marked hyperkeratosis, including prominent palmoplantar hyperkeratosis. The patient was admitted and commenced on intravenous methylprednisolone, leading to symptom resolution within 7 days. Upon discharge, he was transitioned to a tapering regimen of oral prednisolone, starting at 100 mg with weekly dose reductions. At follow-up, there was no evidence of disease flare. Histopathological analysis from two punch biopsies revealed a psoriasiform reaction pattern, supporting a diagnosis of psoriasis rather than pityriasis rubra pilaris. Cutaneous toxicities from immune checkpoint inhibitors are increasingly recognized, often mimicking primary dermatological disorders. Reports of ICI-induced alopecia, vitiligo and lichenoid dermatoses highlight the spectrum of immune-mediated skin reactions. Our case underscores the potential for cemiplimab to trigger psoriasis, which may theoretically be associated with aberrant expression of IL-17 and IL-23, further illustrating the diversity of cutaneous irAEs. Understanding the pathophysiological mechanisms underlying these toxicities is essential for optimizing treatment strategies, minimizing adverse effects without compromising ICI efficacy, and ultimately prolonging patient access to immunotherapy. Further research into immune-related dermatological conditions may also provide valuable insights into the molecular mechanisms governing endogenous dermatological diseases, offering new avenues for targeted dermatological therapies.