Delayed-Onset Amiodarone Induced Thyrotoxicosis After Glucagon-Like Peptide-1 Agonist–Related Weight Loss

Abstract Amiodarone is known to cause thyroid dysfunction, due to both direct cytotoxicity and high iodine content. Due to its lipophilic properties, amiodarone gets stored in the adipose tissue and may induce delayed amiodarone-induced thyrotoxicosis (AIT), months after discontinuation. We present the case of a 60-year-old man admitted with new-onset atrial fibrillation. He had a history of ventricular tachycardia, treated with amiodarone that was discontinued 14 months earlier. On admission, thyrotropin was undetectable, with markedly elevated free thyroxine and total triiodothyronine. He had no previous history of thyroid dysfunction or recent exposure to iodinated contrast. Additional history revealed that the patient had been taking tirzepatide 10 mg weekly resulting in a 54-kg weight loss over the previous 12 months. With this information, a spot urine iodine/creatinine (Cr) was measured and found to be significantly increased at 2323 µg/g Cr (SI: 2075 µmol/mol Cr) (normal reference range 584 µg/g Cr, SI: 521 µmol/mol Cr). He was treated with prednisone and methimazole with eventual resolution of hyperthyroidism. Delayed AIT should be considered in the differential diagnosis of new-onset thyrotoxicosis in patients previously treated with amiodarone who experience significant weight loss.