Amiodarone is a highly effective agent for the prophylaxis and treatment of many cardiac rhythm disturbances, ranging from paroxysmal atrial fibrillation to life threatening ventricular tachyarrhythmias.1 Unlike many other antiarrhythmic drugs, amiodarone appears to be safe in patients with significant left ventricular dysfunction,2-5 and may confer prognostic benefit in some patient subgroups.6 ,7

Amiodarone bears a remarkable structural resemblance to thyroid hormones. The free base contains 39% iodine by weight (fig 1), and chronic treatment is associated with 40-fold increases in plasma and urinary iodide levels.8 Amiodarone has complex effects on thyroid physiology in all patients taking the drug, and chronic treatment is associated with substantial changes in the results of standard thyroid function tests. Although most patients remain clinically euthyroid, a significant minority (up to 15% of patients in the UK and the USA) develop amiodarone induced hypothyroidism or thyrotoxicosis.9-12 Unfortunately, amiodarone induced thyroid dysfunction is rarely manageable by discontinuation of amiodarone alone, partly because it has an extremely long terminal half life (up to four months).13 The purposes of this review are to summarise expected and abnormal changes in thyroid function in patients taking amiodarone, and to suggest guidelines for the diagnosis and management of amiodarone induced thyroid dysfunction.