Alopecia areata after denosumab treatment for osteoporosis

AA: alopecia areata RANK: receptor activator of nuclear factor kappa RANKL: receptor activator of nuclear factor kappa b ligand TNF: tumor necrosis factor INTRODUCTION In the last 2 decades, various biologic agents have been developed to treat autoimmune disorders. Along with their high clinical efficacy, these agents have been associated with several paradoxical proinflammatory or autoimmune reactions, such as autoimmune hepatitis, drug-induced lupus erythematosus, psoriasiform eruptions, and alopecia areata (AA). New cases of AA become more frequent in patients undergoing treatment with biologic therapies, especially antietumor necrosis factor (TNF)alpha agents, including infliximab, adalimumab, and etanercept. Development of AA also has been noted with other biologic agents such as efalizumab, ustekinumab, and daclizumab. Denosumab is a new biologic agent that suppresses osteoclastmediated bone resorption. This agent was recently approved by the US Food and Drug Administration for treatment of osteoporosis in postmenopausal women at high risk of fracture and prevention of skeletal-related events in patients with bone metastases and unresectable giant cell tumors. Denosumab is a fully human monoclonal antibody to receptor activator of nuclear factor kappa b ligand (RANKL) that belongs to a group of anti-TNF agents. We describe a case of extensive AA after treatment with denosumab.