DOI: 10.1093/bjd/ljag086.484 ISSN: 0007-0963

BI30 First UK-reported case of pembrolizumab-induced reactive perforating collagenosis

Sulaiman Tomy, Hamza Ahmed, Sarah Mohamadein, Mini Varghese, Helen Joyce, Minh Lam

Abstract

Immunotherapeutic options including programmed-cell death (PD)-1 inhibitors have revolutionized cancer therapy. Meanwhile, PD-1 inhibitors have been associated with multisystem adverse effects including a plethora of cutaneous manifestations: pruritus, vitiligo, eczematous, psoriasiform, morbilliform, lichenoid reactions, bullous disorders, Stevens–Johnson syndrome, toxic epidermal necrolysis and drug rash with eosinophilia and systemic symptoms. Yet, only three cases of acquired perforating dermatosis (APD) associated with PD-1 inhibitors have been reported in literature, with only one involving pembrolizumab therapy (Gu Y, de Silva D, Henderson CJA, Sebaratnam DF. Pembrolizumab-induced acquired perforating dermatosis. JEADV Clin Pract 2024; 3: 1611–14). A 66-year-old man with a background of metastatic colon adenocarcinoma, who had previously been treated with a right hemicolectomy and hemihepatectomy, was commenced on systemic treatment with the PD-1 inhibitor, pembrolizumab, following previous adjuvant chemotherapy (oxaliplatin and capecitabine). His past medical history included type 2 diabetes mellitus (glycated haemoglobin 51 mmol mol−1). He developed a pruritic rash that began on his arms and back, subsequently spreading to his legs within 2 months of commencing pembrolizumab. Clinical examination revealed widespread erythematous lesions with plugged follicular changes. His rash improved with oral steroids and briefly pausing his pembrolizumab therapy but flared immediately on recommencement. He then underwent a diagnostic biopsy, demonstrating a punched-out ulcer with a cup-shaped plug of degenerate material admixed with collagen bundles and acute inflammatory cells comprised predominantly of neutrophils. These findings were in keeping with an acquired reactive perforating collagenosis, a subtype of APD. His acquired reactive perforating collagenosis was well controlled following a prompt diagnosis and treatment with topical and oral corticosteroids alongside antihistamines and emollients. This allowed his key pembrolizumab therapy to continue. We report the first UK case and second global case of APD associated with pembrolizumab therapy. Similarly, we postulate given the time course that pembrolizumab acted as a trigger in a patient with an underlying susceptibility to APD.

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