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Amiodarone is a type III antiarrhythmic agent that has some structural similarity to thyroid hormone and has a high iodine content. Amiodarone treatment leads to substantial iodine overload and is associated with (1) acute, transient suppression of thyroid function, (2) hypothyroidism, or (3) thyrotoxicosis. These effects are only partially attributable to iodine overload. Hypothyroidism can occur in pts with preexisting thyroid disease, with an inability to escape from the suppressive effect of excess iodine. Pts with hypothyroidism can be easily managed with levothyroxine replacement therapy, without a need to stop amiodarone. There are two major forms of amiodarone-induced thyrotoxicosis (AIT). Type 1 AIT is associated with an underlying thyroid abnormality (preclinical Graves’ disease or nodular goiter). Thyroid hormone synthesis becomes excessive as a result of increased iodine exposure. Type 2 AIT occurs in pts with no intrinsic thyroid abnormalities and is the result of destructive thyroiditis. Differentiation between type 1 and type 2 AIT may be difficult as the high iodine load interferes with thyroid scans. The drug should be stopped, if possible, although this is often difficult to achieve without compromising the arrhythmia management. Amiodarone has a long biologic half-life, and its effects persist for weeks following discontinuation. Therapy of type 1 AIT consists of high-dose antithyroid drugs, but efficacy may be limited. In type 2 AIT, sodium ipodate (500 mg/d) or sodium tyropanoate (500 mg, 1–2 doses/d) can be used to rapidly lower thyroid hormone levels. Potassium perchlorate (200 mg every 6 h) can be used to deplete the thyroid of iodine, but long-term use carries a risk of agranulocytosis. Glucocorticoids in high doses are partially effective. Lithium can be used to block thyroid hormone release. In some cases, subacute thyroidectomy may be necessary to control thyrotoxicosis.