Amiodarone, a benzofuranic iodine-rich pan-anti-arrhythmic drug, induces amiodarone-induced thyrotoxicosis (AIT) in 7-15% of patients. AIT is a major issue due to its typical severity and resistance to anti-thyroid measures, and to its negative impact on cardiac status. Classically, AIT is either an iodine-induced thyrotoxicosis in patients with abnormal thyroid (type 1), or due to acute thyroiditis in a "healthy" thyroid (type 2). Determination of the type of AIT is a diagnostic dilemma, as characteristics of both types may be present in some patients. As it is the main etiological factor in AIT, it is recommended that amiodarone treatment should be stopped; however, it may be the only anti-arrhythmic option, needing to be either continued or re-introduced to improve cardiovascular survival. Recently, a few studies demonstrated that amiodarone could be continued or re-introduced in patients with history of type-2 AIT. However, in the other patients, it is recommended that amiodarone treatment be interrupted, to improve response to thioamides and to alleviate the risk of AIT recurrence. In such patients, thyroidectomy is recommended once AIT is under control, allowing safe re-introduction of amiodarone.
Keywords: Amiodarone; Amiodarone re-introduction; Amiodarone-induced thyrotoxicosis; Hyperthyroïdie induite par l’amiodarone; Recurrence; Reprise d’amiodarone; Récidive.
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