ESPE Abstracts

İntroduction: Amiodarone, an iodine-rich antiarrhythmic agent, is associated with thyroid dysfunction in 15-20% of patients, potentially leading to amiodarone-induced thyrotoxicosis. The etiology of amiodarone-induced hyperthyroidism encompasses two distinct mechanisms: iodine-induced hyperthyroidism (Type 1) prevalent in patients with Graves' disease or nodular goiter, and destructive thyroiditis-induced hyperthyroidism (Type 2) observed in individuals with normal thyroid glands. This report aims to present a case of thyrotoxicosis arising from amiodarone use for supraventricular tachycardia treatment and discuss the implications for management based on etiology.

Case: A sixteen-month-old male patient with a history of recurrent hospitalizations for arrhythmia in infancy presented with elevated sT4 levels. Neurological follow-up for motor mental retardation resulting from hypoxic-ischemic encephalopathy at birth was ongoing. There were no consanguineous relationships among parents, and no significant familial medical history was reported. Physical examination revealed normal thyroid gland size and no palpable goiter. Laboratory investigations demonstrated elevated ST4 levels and urinary iodine concentration, while thyroid autoantibodies were negative. Thyroid ultrasonography depicted normal thyroid gland morphology. The patient's thyrotoxicosis was attributed to amiodarone therapy for refractory supraventricular tachycardia. Management involved monitoring thyroid function tests and clinical status without initiating specific treatment for tachycardia or hyperthyroidism.

Conclusion: Regular monitoring of thyroid function tests is imperative in patients receiving amiodarone therapy, both prior to treatment initiation and during the course of therapy. This case highlights the occurrence of Type 2 amiodarone-induced hyperthyroidism in the absence of pre-existing thyroid pathology. Prompt recognition and appropriate management of amiodarone-induced hyperthyroidism are essential to mitigate associated complications and optimize health outcomes, particularly in patients with concomitant cardiac morbidities.

Keywords: Amiodarone, hyperthyroidism, thyrotoxicosis