Endocrine Abstracts

Introduction: Amiodarone-induced thyrotoxicosis (AIT) occurs in up to 6% of patients taking this medication in iodine sufficient areas and in up to 10% of patients in iodine deficient areas and has a high rate of mortality, that can reach 50% in untreated severe forms. There are two main types (1 and 2) described, although usually we find mixed types, with both components. Below, we describe the cases of two brothers that developed severe mixed forms of amiodarone-induced thyrotoxicosis.

Case-Report: The first case was a 61-year-old male with ischemic cardiomyopathy and atrial fibrillation which was successfully ablated in 2017 and was treated with amiodarone until September 2018. In April 2019, he was admitted to hospital because of a severe mixed AIT with initially good response to medication, which enabled discharge home with continued medical management. However, he was immediately re-admitted to the hospital due to worsening symptoms and increasing levels of thyroid hormones and required amiodarone continuous infusion and urgent total thyroidectomy. The second case was a 60-year-old male with recurrence of atrial fibrillation successfully ablated a few years prior and also treated with amiodarone until December 2020. In August 2021 he began to experience palpitations and independently decided to start amiodarone for 2 weeks. Two months later he was admitted with severe AIT, despite medical treatment. He was treated with amiodarone continuous infusion and two sessions of plasmapheresis before total thyroidectomy.

Discussion: We report two cases in the same family with severe mixed AIT. They both needed urgent thyroidectomy and amiodarone continuous infusion, useful four days before surgery to rapidly block conversion between T4 and T3, decreasing the active form of the hormone. Furthermore, in one of the cases plasmapheresis was used, being a procedure that decreases blood levels of thyroid hormone up to 40-50%.

Although both cases could be explained by underlying thyroid autonomy or iodine deficiency and a Job-Basedow phenomenon, we can’t rule out the existence of familiar predisposition to AIT. There is not literature describing genetic alterations potentially involved in increasing production of thyroid hormones secondary to amiodarone administration. For that reason, it would be useful to report those familiar cases of AIT, from now on, so that we can investigate which factors are involved.