[Challenges in the management of amiodarone-induced thyrotoxicosis]

Amiodarone, a benzofuranic iodine-rich pan antiarrhythmic drug, is frequently associated with thyroid dysfunction. This side effect is heterogeneous and unpredicted, motivating regular evaluation of thyroid function tests. In contrary to hypothyroidism, amiodarone-induced thyrotoxicosis (AIT) is a challenging situation owing to the risk of deterioration of the general and cardiac status of such debilitating patients. Classically, AIT is either an iodine-induced thyrotoxicosis in patients with an abnormal thyroid (type I), or due to a subacute thyroiditis on a "healthy" thyroid (type II). Even if many studies tried to better identify the types of AIT, the diagnostic dilemma of type of AIT could be present, and many patients are treated by an association of antithyroid drugs (useful for type I AIT) with corticoids (useful for type II AIT). Being the main etiological factor in AIT, amiodarone is supposed to be stopped, but it could remain the only anti-arrhythmic option that is needed to be either continued or reintroduced to improve the cardiovascular survival. Recently, many studies demonstrated that amiodarone could be continued or reintroduced in patients with history of type II AIT. Nevertheless, in the other patients, amiodarone maintenance complicates the therapeutic response to the antithyroid drugs and increases the risk of AIT recurrence. Thus, amiodarone therapy is preferred to be interrupted. In such patients, thyroid ablation is recommended once AIT is under control.