Sequential Amiodarone‐Induced Thyroid Dysfunction: From Myxedema Coma to Late‐Onset Type 1 Thyrotoxicosis After Drug Withdrawal

ABSTRACT Amiodarone therapy may induce thyroid dysfunction in approximately 20% of patients, either amiodarone‐induced hypothyroidism (AIH) or thyrotoxicosis (AIT). Both situations may occur at any time during treatment or even months to years after drug withdrawal due to tissue storage with slow systemic release. The sequential occurrence of severe AIH followed by late‐onset AIT, particularly type 1, is exceptionally uncommon. We report the case of a 76‐year‐old woman, with long‐standing amiodarone therapy for atrial fibrillation who presented in the emergency department with lethargy, hypothermia, bradycardia, respiratory and renal failure, and severe biochemical hypothyroidism. A Popoveniuc score of 90 points supported the diagnosis of myxedema coma, and intravenous levothyroxine plus hydrocortisone therapy was initiated. She presented favorable evolution with all dysfunctions' resolution and was discharged under 150 μg levothyroxine; amiodarone was discontinued after Cardiology's assessment. Thyroid function normalized under gradually reduced levothyroxine dosing, which was ultimately suspended fourteen months later. Thirty‐two months after amiodarone suspension, the patient developed persistent biochemical hyperthyroidism with negative thyroid autoimmunity. 99m Tc‐pertechnetate scintigraphy showed diffuse uptake, compatible with type 1 AIT. Methimazole therapy was initiated, and the patient presented a gradual recovery of thyroid function. This case illustrates the full spectrum of amiodarone‐induced thyroid dysfunction, from life‐threatening AIH to late‐onset type 1 AIT long after drug withdrawal. It underscores the prolonged metabolic consequences of amiodarone exposure, the possibility of sequential opposing thyroid dysfunction states, and the necessity for extended surveillance even years after cessation.