ABSTRACT
Amiodarone-induced thyrotoxicosis (AIT) is a challenging complication occurring on average in 10% of patients during chronic therapy. Two main forms of AIT may be identied: type 1, occurring in patients with underlying thyroid diseases, and type 2 occurring in patients with normal glands. Type 1 AIT is a form of true iodine-induced hyperthyroidism triggered by excess iodine released by amiodarone metabolism unveiling latent Graves’ disease or functional autonomy. Type 2 AIT is a drug-induced destructive thyroiditis arising from the cytotoxic effect of amiodarone on thyroidal follicular cells. The co existence of destructive phenomena and increased thyroid hormone (TH) synthesis are key features of the mixed (or undened) forms of AIT.1,2
Amiodarone is a benzofuranic iodine-rich class III anti arrhythmic drug used for treating various arrhythmic disturbances. Its structural formula is similar to that of thyroid hormone (Figure 21.1) and, as expected, amiodarone and its main metabolite, desethylamiodarone, exert thyromimetic action. In fact, amiodarone and desethylamiodarone can bind to thyroid hormone receptor as a weak competitor, thus reducing thyroid hormone effect. These actions contribute to the hypothyroid-like effect observed in euthyroid subjects tasking this therapy, including transient increase of TSH and reduced expression of thyroid hormone-sensitive genes.
