Treatment with
amiodarone is associated with changes in thyroid function tests, but also with thyroid dysfunction (
amiodarone-induced
hypothyroidism, AIH, and
amiodarone-induced
thyrotoxicosis, AIT). Both AIH and AIT may develop in apparently normal thyroid glands or in the presence of underlying thyroid abnormalities. AIH does not require
amiodarone withdrawal, and is treated with
levothyroxine replacement if overt, whereas subclinical forms may be followed without treatment. Two main types of AIT are recognized: type 1 AIT (AIT 1), a form of
iodine-induced
hyperthyroidism occurring in nodular goitres or latent
Graves disease, and type 2 AIT (AIT 2), resulting from destructive
thyroiditis in a normal thyroid gland. Mixed/indefinite forms exist due to both pathogenic mechanisms. AIT 1 is best treated with thionamides that may be combined for a few weeks with
sodium perchlorate to make the thyroid gland more sensitive to thionamides. AIT 2 is treated with oral
glucocorticoids. Once euthyroidism has been restored, AIT 2 patients are followed up without treatment, whereas AIT 1 patients should be treated with
thyroidectomy or radioiodine. Mixed/indefinite forms of AIT are treated with thionamides. Oral
glucocorticoids can be added from the beginning if a precise diagnosis is uncertain, or after a few weeks if response to thionamides alone is poor. The decision to continue or to stop
amiodarone in AIT should be individualized in relation to cardiovascular risk stratification and taken jointly by specialist cardiologists and endocrinologists. In the presence of rapidly deteriorating cardiac conditions, emergency
thyroidectomy may be required for all forms of AIT.