Adriana Dokupilová, Juraj Payer
Amiodarone is a potent antiarrhythmic drug that is used to treat ventricular and supraventricular tachyarrhythmias. It is a benzofuran- derived, iodine-rich compound with some structural similarity to thyroxine (T4). The elimination half-life of amiodarone is highly variable, ranging from 50-100 days. Thyroid abnormalities have been noted in up to 14-18% of patients receiving long-term amiodarone therapy. The effects range from abnormal thyroid function test findings to overt thyroid dysfunction, which may be either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Two forms of AIT have been described. Type 1 usually affects patients with latent or preexisting thyroid disorders and is more common in areas of low iodine intake. Type 2 occurs in patients with a previously normal thyroid gland and is caused by a destructive thyroiditis that leads to the release of preformed thyroid hormones from the damaged thyroid follicular cells. Differentiation of these two types of thyrotoxicosis is essential for determining of the best disease management.
Keywords: amiodarone, thyroid, hyperthyreosis, type 1, type 2, treatment