Double Trouble: Acquired QTc Prolongation in a Patient on Denosumab and Amiodarone

Prolongation of the corrected QT (QTc) interval is a known risk factor for life-threatening ventricular arrhythmias and can result from medications, electrolyte imbalances, or both. We report the case of a 70-year-old female with atrial fibrillation on amiodarone and osteoporosis treated with denosumab who presented with dizziness, but without syncope, palpitations, or chest pain. She was hemodynamically stable with negative orthostatic vitals, and neurologic examination revealed a positive Romberg sign. Brain imaging was unremarkable. ECG demonstrated marked QTc prolongation >550 ms (reference range: <460 ms for women). Laboratory testing revealed hypocalcemia with total calcium of 8.3 mg/dL (reference: 8.5-10.5 mg/dL) and ionized calcium of 1.05 mg/dL (reference: 4.5-5.3 mg/dL). Given her recent denosumab infusion within the prior week and ongoing amiodarone use, acquired long QT syndrome secondary to drug-induced hypocalcemia was suspected. The patient received intravenous calcium gluconate, with resolution of symptoms and normalization of calcium levels. Amiodarone was discontinued and replaced with metoprolol. Her QTc improved to 486 ms on repeat ECG. The patient was advised to discontinue denosumab and follow up for alternative osteoporosis management. This report illustrates a rare but clinically significant interaction between denosumab-induced hypocalcemia and amiodarone, resulting in acquired long QT syndrome. It highlights the importance of monitoring electrolytes and cardiac conduction in patients receiving QT-prolonging and calcium-altering therapies. Early recognition and intervention are essential to prevent potentially fatal arrhythmic complications.