Amiodarone-induced thyroid dysfunction represents a serious complication of treatment with amiodarone, a frequently used potent antiarrhythmic drug. In clinical practice, there are two main forms: hypothyroidism and hyperthyroidism. Amiodarone-induced thyrotoxicosis is further divided into type 1 and type 2 with different pathogenesis, diagnostic findings and, most importantly for the patient, therapeutic approach. Due to frequent diagnostic overlap, a mixed form of amiodarone-induced thyrotoxicosis is also recognized, requiring a combination of both distinct treatment strategies, antithyroid drugs and glucocorticoids. Amiodarone-induced type 1 thyrotoxicosis necessitates prospective discontinuation of amiodarone therapy; in type 2 this step is usually not warranted. In hypothyroidism, substitution therapy with levothyroxine is sufficient without the need to stop antiarrhythmic treatment with amiodarone. Amiodarone-induced thyrotoxicosis may significantly increase the incidence of cardiovascular complications. If amiodarone treatment is discontinued solely for cardiological indications, patients without a history of thyroid disease usually experience restoration of normal thyroid function. However, in predisposed individuals, dysfunction may persist or recur following repeated iodine exposure.
Keywords: amiodarone, thyroid gland; thyroid dysfunction, hypothyroidism, thyrotoxicosis.