Endocrine Abstracts

Amiodarone has been used widely for treating resistant tachyarrhythmias in the past three decades. It is an iodinated benzofuran derivative with a structural formula that closely resembles that of thyroid hormones and contains about 37% of organic iodine by weight, from which 10% is deiodinated to yield free iodide. Given the daily maintenance dose of amiodarone between 100–600 mg daily, about 3.5–21 mg of iodide are released into the systemic circulation, equivalent to 35–140 fold excess of iodine reference daily intake of 100–150 mg. Amiodarone and its main metabolically active metabolite desethylamiodarone (DEA) cause adverse effects on a number of organs including the thyroid. These effects range from subclinical to overt thyroid dysfunction, either amiodarone-induced hypothyroidism (AIH) or amiodarone-induced thyrotoxicosis (AIT). Between 15–28% of patients develop thyroid dysfunction after 2–3 years of treatment, and this risk increases with higher cumulative doses. The pathogenesis of amiodarone-induced thyroid dysfunction is complex but the inherent effects of amiodarone itself as well as its high iodine content appear to play a central role. The underlying thyroid status of the individuals and their environment (reflecting iodine intake) predispose them to a specific amiodarone-induced thyroid dysfunction. This session will review the biochemistry of amiodarone including its pharmacology and the physiology necessary for the understanding of the cellular mechanisms involved in its actions. The effects of amiodarone on thyroid action will be described together with recommendations for management of amiodarone-induced thyroid dysfunction.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.