SAT-398 - Amiodarone-Induced Thyrotoxicosis in the Era of Weight Loss

Introduction
Amiodarone, a lipophilic medication with substantial iodine content, is used in the management of cardiac arrhythmias. However, its use is associated with thyroid dysfunction, including hypothyroidism and amiodarone-induced thyrotoxicosis (AIT). AIT can manifest in individuals with pre-existing thyroid conditions such as autoimmune thyroid disease or thyroid nodules (AIT1) or as a result of destructive thyroiditis (AIT2). If left untreated, AIT is linked to a higher incidence of cardiovascular events and increased mortality. In the current era of weight loss strategies involving pharmacological or surgical interventions, significant weight reduction may theoretically enhance the mobilization of stored amiodarone into the systemic circulation. We report a case of AIT in a patient undergoing concurrent treatment with amiodarone and semaglutide.

Case Report
74-year-old male with history of type 2 diabetes mellitus, obesity, atrial fibrillation, and congestive heart failure (CHF), started on amiodarone in 2022. In 2025, he was admitted for CHF exacerbation and reported experiencing dyspnea, diarrhea, tremors, palpitations, and weight loss over the previous month. Thyroid function tests revealed suppressed TSH and elevated free T4 level of 7.02 ng/dL (range: 0.8-1.7 ng/dL). Notably, he started semaglutide in 2024 and subsequently lost 57 pounds (13%) over 14 months. His thyroid function tests had been within the normal range for more than two years while on amiodarone, prior to the initiation of weight loss therapy. A thyroid ultrasound showed heterogeneous echotexture without increased vascularity or thyroid nodules. Given the acute nature of his presentation, and while awaiting thyroid autoimmune lab results, he was started on both methimazole and prednisone. Significant clinical and biochemical improvements were noted. Most recent free T4 normalized to 1.64 ng/dL, although TSH remains suppressed. Thyroid autoimmune antibodies are negative. The patient is currently stable from a cardiovascular standpoint.

Discussion
This case emphasizes the clinical need to recognize the potential complication of thyrotoxicosis in patients treated with amiodarone who are also undergoing significant weight loss in the setting of treatment. Due to its high lipophilicity, amiodarone and its active metabolite accumulates in adipose tissue, resulting in significantly higher concentrations in fat tissue compared to plasma levels. Substantial weight loss, as observed in our patient, can lead to rapid reductions in adipose tissue, resulting in the increased mobilization of stored amiodarone from fat depots into the systemic circulation. This can potentially precipitate iodine overload and AIT. This case highlights the necessity for close clinical follow-up to facilitate early detection of AIT, thereby reducing the risk of cardiovascular complications.

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