Amiodarone-induced thyrotoxicosis and hypothyroidism

Amiodarone is an antiarrhythmic medication that contains more than 35% iodine by weight. Amiodarone can cause iodine overload up to 100 times the normal daily intake.

Amiodarone-induced thyrotoxicosis

Amiodarone-induced thyrotoxicosis (AIT) can occur during amiodarone therapy or even long after amiodarone withdrawal. AIT is associated with increased mortality, especially in elderly patients with left ventricular dysfunction.

Two types of AIT have been described. Type I occurs in patients with underlying thyroid disease, and reflects increased function triggered by the iodine load of amiodarone. The mechanism is referred to as the Jod-Basedow effect: hyperthyroidism following administration of iodine or iodide. It is treated using potassium perchlorate (decreases uptake of iodine into the thyroid) and methimazole (inhibits addition of iodine to thyroglobulin).

Type II AIT, on the other hand, occurs in patients with no underlying thyroid disease and is thought to be caused by destruction of the thyroid gland by iodine or amiodarone or one of its metabolites. The destruction of the thyroid gland leads to leakage of preformed hormones from damaged follicles. Type II AIT is treated with steroids.

The scintigraphic findings are similar to those seen with destructive (subacute) thyroiditis: Low activity in the gland with low (less than 2% at 24 hours) uptake.

Amiodarone-induced hypothyroidism

Amiodarone-induced hypothyroidism (AIH) is thought to occur via the Wolff-Chaikoff effect (inhibition of thyroid hormone production due to iodine overload). AIH is treated with L-T4.

references

Martino E, Bartalena L, Bogazzi F & Braverman LE. The effects of amiodarone on the thyroid. Endocrine Reviews 2001; 22:240–254.
O'Sullivan AJ, Lewis M & Diamond T. Amiodarone-induced thyrotoxicosis: left ventricular dysfunction is associated with increased mortality. European Journal of Endocrinology 2006; 154:533–536.