Amiodarone is used to treat life-threatening ventricular arrhythmias with an additional off-label indication for intractable atrial fibrillation. Amiodarone toxicity occurs in about 23% of patients. This may be a clinical or laboratory diagnosis. Amiodarone-induced thyrotoxicosis (AIT) occurs in 3% of all the patients treated and is subclassified into type 1 and 2. Amiodarone is a long-acting benzofuran with iodine accounting for 39.3% of its molecular weight. The half-life is 200 days, accounting for AIT lasting around 8 months. Patients with ventricular arrhythmias who need to remain on amiodarone are treated with thyroidectomy. Radioiodine ablation of the thyroid gland does not work for AIT. Amiodarone itself helps prevent conversion of T4 to the more active T3. Hence stopping the amiodarone may often allow the hyperthyroidism to progress to AIT. When treating AIT, propylthiouracil is usually started at 700 mg tid, with prednisone 30 mg daily. Other treatments include iopanoic acid (oragraphin), which prevents the conversion of T4 to the more potent T3. The use of iopanoic may reduce the use of steroids, with their complications. However, the iopanoic acid does not prevent the destructive thyroiditis that is seen with type 2 AIT. Iopanoic acid contains 66.68% iodine, and a prolonged course can lead to hyper- or hypothyroidism. The production of iopanoic acid for human use was discontinued 5 years ago. However, iopanoic acid is still available from compounding pharmacies and may continue to be indicated for this complication.
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