Abstract

Immune checkpoint inhibitors (ICIs) are associated with a variety of immune-related cutaneous adverse events (irCAEs), including Sweet syndrome and psoriasis. PD-1 inhibitors have rarely been associated with immunotherapy-induced hidradenitis suppurativa (HS). We report a case of a 73-year-old female patient with stage IVB small-cell lung cancer who developed erythematous nodules in her axillae and inguinal folds three months following initiation of atezolizumab (PD-L1 inhibitor). Histopathology demonstrated a perivascular and periadnexal mixed inflammatory infiltrate composed of neutrophils, plasma cells and lymphocytes, and a suppurative folliculitis with fibrosis. She had concomitant obesity and Graves’ disease and was a former smoker (>50 pack-year smoking history). The patient’s lesions improved following cessation of atezolizumab and treatment with doxycycline. The latency period between drug initiation and onset of HS lesions in our case was similar to those of previously reported cases of PD-1-inhibitor-induced HS – one to three months. IL-17 is a key cytokine in HS pathogenesis, with lesional and perilesional HS skin demonstrating increased Th17 cells. The Th17 pathway has been implicated in the pathogenesis of ICI-induced colitis and PD-1-inhibitor-induced psoriasis. Thus, the Th17 pathway has been suggested in the pathogenesis of PD-1-inhibitor-induced HS. Similarly, the Th17 pathway is likely involved in the pathogenesis of PD-L1-inhibitor-induced HS. Pre-existing risk factors, including obesity and smoking, may contribute to the development of immunotherapy-induced HS in patients receiving PD-1-inhibitor or PD-L1-inhibitor therapy. With increasing use of immunotherapies in the treatment of metastatic malignancies, it is important to characterize and manage the spectrum of irCAEs that may arise.