Delayed Release of Amiodarone Causing Late-Onset Thyrotoxicosis

Abstract

Introduction: Amiodarone is an antiarrhythmic medication associated with a wide range of adverse effects, including thyroid dysfunction.1 Thyrotoxicosis without underlying Graves' disease or nodules is classified as Type II, or destructive, amiodarone-induced thyrotoxicosis (AIT).2 However, few cases have been reported in whom AIT occurs months after cessation of medication use. We describe a case of late-onset Type II AIT, diagnosed in the setting of atrial fibrillation (AF), 10 months after last known dose of amiodarone. Description of the Case: A 51-year-old man presented with palpitations and an electrocardiogram showing AF with rapid ventricular response. His history was notable for a diagnosis of AF, treated with ablation and multiple courses of amiodarone, most recently 1 year prior with a cumulative dose of 22.4 g for 12 weeks. Serum laboratory tests showed newly suppressed thyroid-stimulating hormone <0.02 (0.3–4.7 mcIU/mL) and elevated free thyroxine 1.9 (0.8–1.7 ng/dL). Thyroid autoantibodies to thyroid peroxidase and thyrotropin receptor and thyroid-stimulating immunoglobulins were absent. He had no recent exposure to biotin or iodinated contrast and reported no recent viral illness or neck pain. He had a 9 kg weight loss in the preceding few months secondary to decreased appetite. Family history was significant for mother and nephew with autoimmune thyroid disease. Thyroid ultrasonography showed no nodules. An iodine-123 uptake scan showed homogeneous bilateral decreased uptake most consistent with destructive thyroiditis. Methimazole treatment, started empirically at presentation, was discontinued. Thyroid function tests normalized within 3 months with no therapy needed. Discussion: Delayed-onset AIT may occur after cessation of amiodarone therapy. To our knowledge, only one case series of eight patients has been reported in whom late-onset thyrotoxicosis occurred after amiodarone cessation.3 Amiodarone contains a significant amount of iodine and releases about 100 to 300 times of the recommended daily intake. It is a lipophilic complex primarily stored within adipose tissue, with a long half-life of up to 100 days. Our patient's rapid weight loss may have contributed to a delayed release of amiodarone from lipid stores, thereby triggering Type II AIT. This case emphasizes the importance of considering AIT in all patients with history of amiodarone use, even months after cessation of therapy, when supported by presentation and diagnostic tests. Patient Consent: Authors have received and archived patient consent for video recording/publication in advance of video recording of procedure. No competing financial interests exist for any of the authors. Runtime of video: 4 mins 12 secs