Abstract
Denosumab is a human monoclonal antibody that inhibits RANKL, thereby suppressing osteoclast-mediated bone resorption and increasing bone mass in patients with osteoporosis. Although generally well tolerated, denosumab is associated with hypocalcemia, particularly in individuals with impaired calcium and vitamin D homeostasis. We report the case of a 40-year-old woman with a history of sleeve gastrectomy who developed severe, symptomatic hypocalcemia following a single dose of denosumab despite receiving vitamin D supplementation. She presented with neuromuscular symptoms, QTc prolongation, profound hypocalcemia, severe vitamin D deficiency, and marked secondary hyperparathyroidism. Her clinical course was notable for delayed onset, resistance to standard therapy, recurrent hypocalcemia after discharge, and the need for prolonged hospitalization with high-dose intravenous calcium, active vitamin D, and aggressive oral supplementation. This case highlights bariatric surgery as a major and underrecognized risk factor for severe and prolonged denosumab-induced hypocalcemia and underscores the importance of correcting nutritional deficiencies and implementing close biochemical monitoring when initiating denosumab in high-risk patients.