Objective: To review the amiodarone-associated alterations in thyroid hormone metabolism and thyroid function and compare them with the effects of inorganic iodide. To clarify the pathophysiologic features and treatment of amiodarone-associated hypothyroidism and thyrotoxicosis.

Conclusions: Amiodarone, an iodinated benzofuran, is an important antianginal and antiarrhythmic medication. It also alters thyroid hormone metabolism and may precipitate hypothyroidism or hyperthyroidism. Amiodarone-associated hypothyroidism (AAH) is similar to iodine-induced hypothyroidism. Amiodarone-associated thyrotoxicosis (AAT) has a complex pathophysiology. Type I AAT is due to increased thyroid hormone synthesis and release and occurs in patients with multinodular goiter or Graves' disease. Therapeutic interventions may include discontinuation of amiodarone, thionamide therapy, perchlorate, or surgery. In type II AAT, hyperthyroidism is the consequence of a destructive thyroiditis with release of preformed thyroid hormone. Prednisone therapy is the treatment of choice. The distinction between these two entities is of considerable clinical and therapeutic importance.