LAUSR

Programmed cell death–1 receptor (PD-1) inhibitors enhance the antitumoral immune response via immune checkpoint inhibition. In a healthy immune system, the binding of ligands to PD-1 induces T-cell inactivation and prevents overactive immune responses. However, PD-1 ligands are also expressed by a variety of tumors, including melanomas, renal cell carcinomas, and brain tumors, in an effort to evade the host immune response. Although immune checkpoint inhibitors have revolutionized care for cancer patients, new cutaneous and systemic toxicities are still being discovered. Nivolumab is a humanized IgG4 anti–PD-1 monoclonal antibody that is currently approved by the US Food and Drug Administration for the treatment of melanoma, non–small cell lung cancer, renal cancer, and classical Hodgkin lymphoma.1 Several adverse effects of immune-targeting therapies are described and are referred to as immune-related adverse events (irAEs). Systemic irAEs include enterocolitis, pneumonitis, hepatitis, nephritis, hypophysitis, and autoimmune thyroid disease. In addition, dermatologic toxicity is the most common irAE of checkpoint inhibitors and ranges from pruritus and mild dermatoses to severe reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis.2 Vitiligo-like depigmentation is well described in melanoma patients receiving immunotherapy with PD-1 inhibitors and may be associated with favorable outcomes.3 Here we report a case of vitiligo-like depigmentation in a patient with acute myeloid leukemia (AML) receiving nivolumab as part of a phase II clinical trial. To our knowledge, this is the first reported case of vitiligo-like depigmentation associated with PD-1 inhibitor treatment in a patient with a nonmelanoma malignancy. Previous reports of PD-1 inhibitor–associated vitiligo-like depigmentation have been exclusively described in patients being treated for melanoma.