Track: Clinical Studies

Abstract:

Programmed cell death-1 (PD-1) inhibitors have significantly improved cancer survival outcomes. Up to 70% of patients develop cutaneous immune-related complications. We retrospectively reviewed 75 biopsy-confirmed cases of PD-1 inhibitor-associated dermatoses from our departmental pathology database between September 2014 and June 2025. Clinical data, histopathologic features, and treatment outcomes were analyzed. Among 75 patients (mean age 67.0 years; 52% female) with diverse malignancies, most developed reactions within 6 months of initiating therapy: 8 shortly after initiation, 11 within 1 month, 15 within 3 months, 5 within 6 months, 10 within 12 months, 9 beyond 12 months, and 17 with unknown timing. Histopathologic categories were type IV hypersensitivity (T4HS) lichenoid (N = 29), T4HS eczematoid (N=10), other T4HS patterns (N=6) including one case of toxic epidermal necrolysis, vesiculobullous (N=12) encompassing bullous pemphigoid (N=7) and lichen planus pemphigoides (N=5), psoriasis-like (N=4), reversible epitheliotropic T cell dyscrasia (pityriasis lichenoides-like [N=2] and mycosis fungoides-like [N=2]), autoimmune sclerodermoid (N=3), and miscellaneous (N=6). Miscellaneous included Sweet syndrome (N=3), eosinophilic granulomatosis with polyangiitis (N=1), subacute cutaneous lupus erythematosus (N=1), and folliculitis (N=1). Almost all patients’ lesions improved or stabilized with management, with one fatal case of toxic epidermal necrolysis. In closing, PD-1 inhibitor-associated dermatoses resemble established standard cutaneous adaptive B and T cell-driven dermatoses such as eczema, lichen planus, and bullous pemphigoid. Inhibition of regulatory T cells, thereby allowing the emergence of autoreactive B cells and T cells or unmasking subclinical hypersensitivity, is likely pathogenetically key to these cutaneous immune adverse effects.

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Christina Del Guzzo