Abstract
Amiodarone is an antiarrhythmic drug, containing 37% iodine by weight, and with structural similarities to thyroid hormones. Amiodarone-induced thyroid dysfunction occurs in 15–20% of patients and includes amiodarone-induced hypothyroidism (AIH) and amiodarone-induced thyrotoxicosis (AIT). AIH is due to failure to escape from the acute Wolff-Chaikoff effect and is easily treated with levothyroxine replacement without requiring amiodarone withdrawal. There are two types of AIT: type 1 AIT, a form of iodine-induced thyrotoxicosis that develops in patients with underlying thyroid disease exposed to the high iodine content of amiodarone, and type 2 AIT, a drug-induced destructive thyroiditis caused by a direct cytotoxic effect of amiodarone. In some cases both pathogeneses coexist and these forms are called mixed forms. Differential diagnosis between AIT types is important since therapy differs. Type 1 AIT is treated with thionamide and in some cases by adding potassium perchlorate; type 2 AIT is treated with glucocorticoids; mixed forms may benefit from the combination of thionamide and glucocorticoids. Patients who are resistant to the other forms of treatment or who need a rapid restoration of euthyroidism should be treated by thyroidectomy. Radioactive iodine is usually not feasible, since these patients have a low radioiodine uptake. Monitoring of thyroid function should be performed before starting amiodarone and then every 3 months during amiodarone therapy and up to at least 2 years after amiodarone withdrawal.
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De Leo, S., Braverman, L.E. (2019). Amiodarone-Induced Thyroid Dysfunction. In: Luster, M., Duntas, L., Wartofsky, L. (eds) The Thyroid and Its Diseases. Springer, Cham. https://doi.org/10.1007/978-3-319-72102-6_30
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