Radiation-triggered psoriasiform rash with systemic dissemination after prolonged PD-1 inhibitor therapy: A case report.

[RATIONALE] Psoriasiform rash associated with programmed cell death protein 1 (PD-1) inhibitors typically occurs during the early phase of treatment. However, systemic dissemination triggered by radiotherapy after more than 2 years of immunotherapy is rarely reported. This case aims to highlight the potential for delayed and severe cutaneous immune-related adverse events following combined immunotherapy and radiotherapy, which has significant implications for long-term patient monitoring. Herein, we present a case of a patient with driver-negative lung adenocarcinoma who, after 25 months of tislelizumab monotherapy without cutaneous toxicity, subsequently developed a unique clinical course of psoriasiform rash. The rash initially emerged at the irradiation site (right iliac crest) 1 month after local radiotherapy and progressively disseminated systemically.

[PATIENT CONCERNS] An elderly patient with lung adenocarcinoma, having received tislelizumab for 2 years, developed a right iliac bone metastasis and subsequently underwent stereotactic body radiotherapy (45 Gy in 5 fractions), achieving complete pain relief. However, 1 month post-radiotherapy (25 months after initiating immunotherapy), well-demarcated scaly plaques initially appeared at the irradiation site, followed by centrifugal dissemination to the scalp, trunk, and limbs.

[DIAGNOSES] Psoriasis as a cutaneous immune-related adverse event.

[INTERVENTIONS] PD-1 inhibitor therapy was discontinued, and treatment with oral prednisone (0.5 mg/kg/day) combined with topical halometasone was initiated.

[OUTCOMES] After 4 weeks of treatment with oral prednisone (0.5 mg/kg/day) and topical halometasone, the psoriasiform rash showed marked regression, with > 80% reduction in erythema and scaling. The patient reported significant relief from pruritus and no new lesions emerged. PD-1 inhibitor therapy remained discontinued, and the patient continued under dermatological surveillance.

[LESSONS] This case supports the "two-hit hypothesis": prolonged PD-1 inhibition establishes a subclinical autoimmune state (first hit), and radiotherapy acts as a second hit, ultimately culminating in systemic toxicity. These findings underscore the necessity for long-term cutaneous surveillance during immunotherapy and rigorous dermatological assessment when combined with radiotherapy.