Endocrine Abstracts

Introduction: Amiodarone is an effective drug in the management of supraventricular arrhythmias. Due to its composition rich in iodine and pharmacological properties can cause thyroid dysfunction in 15–20% of the treated patients. Clinically it can present in the form of amiodarone-induced hypothyroidism or amiodarone-induced thyrotoxicosis. This latter situation may result from an excess of iodine supply, glandular destruction or both pathogenic mechanisms.

Clinical case: A 58-year-old male with a history of ischemic stroke with cardioembolic etiology, paroxysmal atrial fibrillation requiring ablative therapy and electrical cardioversion, who has been treated with amiodarone for three years. He started with exuberant tremor of extremities, tachycardia, palpitations, irritability, heat intolerance and asthenia with about 6 weeks of evolution associated with involuntary weight loss of 13 pounds in 4 months, initially requiring hospitalization for control and monitoring of symptoms. In thyroid function tests, thyroid stimulating hormone (TSH) < 0.008 μUI/ml (0.4–4.0), triiodothyronine-L (T3L) > 20 pg/ml (1.8–4.2), thyroxine-L (T4L) > 6.0 ng/dl (0.8–1.9), anti-TSH receptor antibodies (TRABS) 2.4 U/l (<1.0) and anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) antibodies were negative. The Colour-flow Doppler sonography showed a gland of increased dimensions, heterogeneous texture, without thyroid nodules, with reduced vascularity but not negligible. He started therapy with thiamazol a daily dose of 30 mg, prednisolone 40 mg, bisoprolol 2.5 mg and stopped amiodarone. During the 6 months of treatment, there was a symptomatic improvement, with reestablishment of euthyroidism – TSH 0.008; 0.012; 2.3; 1.6 uUI/ml; T3L> 20; 9.7; 5.0 pg/ml; T4L 6.0; 5.0; 2.4; 1.0 ng/dl; TRABS 2.4; 1.9; 1.4; 0.6 U/l. It is currently asymptomatic, without treatment with thionamides or glucocorticoids. He did not restart treatment with amiodarone and maintains an annual monitoring of thyroid function tests.

Conclusion: This case is an example of the approach of amiodarone-induced thyrotoxicosis of mixed/indefinite cause, in which the best therapeutic strategy remains controversial.