Alopecia Areata in a Patient Receiving Cemiplimab for Metastatic Cutaneous Squamous Cell Carcinoma

ABSTRACT Introduction Alopecia areata (AA) is an autoimmune disease characterized by non‐scarring hair loss of the scalp and/or body, with an unpredictable and variable clinical course. Its etiology is not entirely understood, although evidence suggests that environmental, immunological, and genetic factors contribute to disease development. In patients with locally advanced or metastatic cutaneous squamous cell carcinoma (cSCC) who are not candidates for surgery or radiotherapy, immune checkpoint inhibitors—including the anti‐Programmed Death‐1 (PD‐1) agent cemiplimab—have been successfully employed, demonstrating significant clinical benefit. Despite the overall favorable safety profile of cemiplimab, adverse events of any grade have been reported in nearly 50% of patients, with asthenia, diarrhea, anemia, and pruritus being the most common. Nevertheless, less frequent side effects may occur, including rare cutaneous immune‐related manifestations. Case report We report the case of a 77‐year‐old woman who was treated with cemiplimab for cSCC of the nose with metastatic involvement of the locoregional cervical lymph nodes. After eight infusions and local radiation therapy, due to the achievement of a complete clinical and radiological response, the immunotherapic treatment was discontinued. Shortly after treatment interruption, she developed diffuse alopecia involving the entire scalp, along with diffuse fingernail dystrophy. A diagnosis of AA was established based on clinical and trichoscopic evaluation. Treatment with prednisone 0.5 mg/kg/day and topical corticosteroids was started, leading to complete hair regrowth and satisfactory improvement of nail changes. At 2‐year follow‐up after cemiplimab discontinuation, the complete oncologic response has been maintained. Discussion The onset of AA following cemiplimab therapy can be considered an immune‐related adverse event, with only a few cases reported to date in the literature. This reaction is thought to result from the breakdown of the hair follicle's immune privilege, triggered by the immune response boost induced by checkpoint inhibitors, possibly reflecting systemic immune activation potentially enhanced by concomitant radiotherapy.