Double Trouble: Acquired QTc Prolongation in a Patient on Denosumab and Amiodarone
Abstract
Introduction Denosumab is a monoclonal antibody used to treat osteoporosis. Due to its impact on bone metabolism, it can precipitate hypocalcemia potentially leading to QTc prolongation on electrocardiogram (EKG), increasing the risk of life-threatening arrhythmias. Amiodarone, a Class III antiarrhythmic, is also known to prolong QTc via its effects on cardiac conduction. We present a unique case of acquired QTc prolongation in a patient on concurrent Denosumab and Amiodarone therapy. Case Presentation A 70-year-old female with atrial fibrillation on Amiodarone and osteoporosis on Denosumab, presented to ED complaining of dizziness without syncope, palpitations, or chest pain. She was hemodynamically stable with negative orthostatic vitals. Neurologic examination revealed a positive Romberg without other cerebellar deficits. MRI showed an incidental vascular loop within the internal auditory canal without acute ischemic changes. Benign paroxysmal positional vertigo, Meniere’s disease, vestibular neuritis, and giant cell arteritis were ruled out based on history and physical examination. Laboratory tests revealed hypocalcemia (8.3 mg/dL) with reduced ionized calcium (1.05 mg/dL). EKG showed a QTc interval >550 ms, suggesting acquired long QT syndrome due to hypocalcemia. Given the patient's recent Denosumab infusion (administered less than a week before presentation) and ongoing Amiodarone use, drug-induced QTc prolongation was suspected. She was treated with IV calcium gluconate, leading to symptomatic improvement and calcium normalization. Amiodarone was replaced with metoprolol. Following these interventions, QTc improved to 486 ms. The patient was advised to transition from Denosumab to an alternative osteoporosis therapy during outpatient followup. Discussion Denosumab inhibits RANKL, disrupting osteoclast and osteoblast maturation and leading to hypocalcemia in 3–10% of patients, with severe cases occurring in <1–3%. Hypocalcemia-induced QTc prolongation is rare, but can be exacerbated by concurrent medications such as Amiodarone, which prolongs QTc through potassium channel blockade. This case highlights the importance of evaluating side effect profiles in polypharmacy patients, particularly those on multiple QT-prolonging agents.
Start Time
16-4-2025 1:30 PM
End Time
16-4-2025 4:00 PM
Presentation Type
Poster
Presentation Category
Health
Student Type
Clinical Doctoral Student (e.g., medical student, pharmacy student)
Faculty Mentor
Krishna Pulivarthi MD
Faculty Department
Internal Medicine
Double Trouble: Acquired QTc Prolongation in a Patient on Denosumab and Amiodarone
Introduction Denosumab is a monoclonal antibody used to treat osteoporosis. Due to its impact on bone metabolism, it can precipitate hypocalcemia potentially leading to QTc prolongation on electrocardiogram (EKG), increasing the risk of life-threatening arrhythmias. Amiodarone, a Class III antiarrhythmic, is also known to prolong QTc via its effects on cardiac conduction. We present a unique case of acquired QTc prolongation in a patient on concurrent Denosumab and Amiodarone therapy. Case Presentation A 70-year-old female with atrial fibrillation on Amiodarone and osteoporosis on Denosumab, presented to ED complaining of dizziness without syncope, palpitations, or chest pain. She was hemodynamically stable with negative orthostatic vitals. Neurologic examination revealed a positive Romberg without other cerebellar deficits. MRI showed an incidental vascular loop within the internal auditory canal without acute ischemic changes. Benign paroxysmal positional vertigo, Meniere’s disease, vestibular neuritis, and giant cell arteritis were ruled out based on history and physical examination. Laboratory tests revealed hypocalcemia (8.3 mg/dL) with reduced ionized calcium (1.05 mg/dL). EKG showed a QTc interval >550 ms, suggesting acquired long QT syndrome due to hypocalcemia. Given the patient's recent Denosumab infusion (administered less than a week before presentation) and ongoing Amiodarone use, drug-induced QTc prolongation was suspected. She was treated with IV calcium gluconate, leading to symptomatic improvement and calcium normalization. Amiodarone was replaced with metoprolol. Following these interventions, QTc improved to 486 ms. The patient was advised to transition from Denosumab to an alternative osteoporosis therapy during outpatient followup. Discussion Denosumab inhibits RANKL, disrupting osteoclast and osteoblast maturation and leading to hypocalcemia in 3–10% of patients, with severe cases occurring in <1–3%. Hypocalcemia-induced QTc prolongation is rare, but can be exacerbated by concurrent medications such as Amiodarone, which prolongs QTc through potassium channel blockade. This case highlights the importance of evaluating side effect profiles in polypharmacy patients, particularly those on multiple QT-prolonging agents.