Amiodarone is a benzofuranic derivative containing 37.2 mg iodine per 100 mg of active drug. It is widely used for the treatment of cardiac arrhythmias and angina pectoris (1,2), and has a prolonged half-life up to 2–4 months. Amiodarone inhibits the outer ring deiodination (5’-deiodinase) of thyroxine (T4) and 3,3’,5’-triiodothyronine (rT3) resulting in an increase in the concentration of serum T4, a decrease in the concentration of serum triiodothyronine (T3) and an increase in the concentration of serum rT3 (3–12). These changes are associated during the first few months of therapy by an increase in basal serum thyrotropin (TSH) concentration and the TSH response to thyrotropin-releasing hormone (TRH) (3,5). Although a tendency toward normalization after more prolonged therapy is usually observed, changes in these parameters of thyroid function may persist to some extent. Moreover, the development of hyperthyroidism and hypothyroidism may also occur with variable frequency (4,6,13–21). The mechanisms by which thyroid dysfunction is induced are not completely clear and the reasons why some patients become hyperthyroid and others hypothyroid remain to be elucidated. In view of the multiple and variable changes of thyroid function tests occurring in euthyroid, hyperthyroid, and hypothyroid amiodaronetreated patients, the precise evaluation of thyroid status often represents a difficult clinical challenge. Moreover, difficult therapeutic problems arise in the presence of amiodarone-associated thyrotoxicosis (AT) and, to a lesser extent, in the presence of amiodarone-associated hypothyroidism (AAH).
KeywordsIodine Deficiency Nodular Goiter Serum Thyroglobulin Serum Thyroid Hormone Toxic Diffuse Goiter
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