Amiodarone-Induced Thyrotoxicosis in a Patient with Autonomously Functioning Nodular Goiter (original) (raw)

2009, Annals of Pharmacotherapy

A miodarone is an effective antiarrhythmic agent for treatment and prophylaxis of life-threatening ventricular arrhythmias. It contains 37% organic iodine in its molecular mass, or about 75 mg of iodine per 200-mg tablet, 10% of which is released as unbound iodide. 1 A dosage of 200 mg of amiodarone daily provides roughly 50 times the recommended iodine requirement determined by the World Health Organization (150 µg/day for adults). 2-4 Amiodarone is also highly lipophilic and accumulates in adipose tissue after ingestion, leading to its long elimination half-life (~100 days). 3,5 This "iodine-rich" characteristic is believed to be the major etiology of amiodarone-induced thyroid dysfunction, which includes failure to escape from the Wolff-Chaikoff effect, iodine-induced potentiation of thyroid autoimmunity, and unregulated hormone synthesis (Jod-Basedow effect). In addition, amiodarone inhibits type 1 5'-deiodinase activity, thereby decreasing the peripheral conversion of thyroxine (T 4 ) to triiodothyronine (T 3 ) and the clearance of both T 4 and reverse T 3 . Amiodarone can act as a competitive antagonist of T 3 and inhibit the entry of thyroid hormones into peripheral tissues. Cytotoxic effects that cause lysis of thyroid follicles have also been described. 1,3, Adverse reactions to amiodarone are complex and include amiodarone-induced thyrotoxicosis (AIT) and hy-pothyroidism (AIH). In iodine-sufficient geographic areas, AIT is less common than AIH. 1,7 Although the overall incidence of thyroid dysfunction by amiodarone is about 2-24%, 3,8 AIT should be considered in patients taking amiodarone who develop symptoms and signs of thyrotoxicosis including weight loss, tremors, restlessness, and tachycardia. Laboratory tests usually demonstrate depressed thyroid-stimulating (TSH) levels with elevated T 4 and T 3 levels. AIT is further classified as type 1 or type 2 based on different etiologies. Type 1 AIT is due to unregulated hor-Author information provided at the end of the text.