Amiodarone-induced thyroid dysfunction in clinical practice.

Amiodarone is a potent class III anti-arrhythmic drug used in clinical practice for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxismal atrial fibrillation to life threatening ventricular tachyarrhythmias. Amiodarone often causes changes in thyroid function tests mainly related to the inhibition of 5'-deiodinase activity resulting in a decrease in the generation of T3 from T4 with a consequent increase in rT3 production and a de- crease in its clearance. In a group of amiodarone- treated patients there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT). The pathogenesis of AIH is related to a failure to escape from the acute Wolff- Chaikoff effect due to defects in thyroid hormono- genesis, or, in patients with positive thyroid au- toantibody test, to concomitant Hashimoto's thy- roiditis. Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting, clinically silent abnormalities. AIT is more common in iodine-deficient regions of the world, whereas AIH is usually seen in iodine- sufficient areas. In contrast to AIH, AIT is a diffi- cult condition to diagnose and treat, and discon- tinuation of amiodarone is usually recommended. In this review we analyse, according to data from current literature, the alterations in thyroid labora- tory tests seen in euthyroid patients under treat- ment with amiodarone and the epidemiology and treatment options available of amiodarone-in- duced thyroid dysfunctions (AIT and AIH).