CƯỜNG GIÁP DO AMIODARON: CA LÂM SÀNG THỂ HỖN HỢP

Abstract

Introduction: Amiodarone is a benzofuranic acid derivative and a potent class III antiarrhythmic drug indicated for the treatment of ventricular tachycardia and supraventricular tachyarrhythmias. It is an iodine-rich compound, containing approximately 37% iodine by weight, and has a molecular structure similar to thyroid hormones¹. Deiodination of amiodarone releases a large amount of iodine, which may disrupt thyroid function and lead to hypothyroidism or hyperthyroidism, with an estimated incidence of about 15–20%^2–4. In addition to iodine overload, amiodarone itself (or its metabolite desethylamiodarone) may induce thyroid dysfunction through direct cytotoxic effects on thyroid follicular cells. Here, we report a clinical case of a 72-year-old female with a history of hypertension, ventricular premature beats, GERD, dyslipidemia, and bilateral thyroid nodules. Her medications included Cordarone 200 mg once daily from June 2023 to the end of June 2024. In July 2024 she was admitted due to fatigue, palpitations, weight loss and anxiety. Laboratory evaluation showed suppressed TSH, elevated FT4, and positive TRAb. The patient initially received antithyroid therapy with poor response; however, after the addition of corticosteroid, both clinical status and biochemical parameters improved significantly. Conclusion: Patients receiving amiodarone require regular monitoring of thyroid function, because amiodarone-related thyroid dysfunction may occur at any time during therapy and even after drug discontinuation. When thyroid dysfunction occurs, distinguishing between type 1, type 2, or mixed-type amiodarone-induced thyrotoxicosis is essential for appropriate management.