Endocrine Abstracts

Introduction: Amiodarone is a highly effective drug, used for the treatment of arrhythmias. However, it can cause either hypothyroidism or thyrotoxicosis. It leads to alterations in thyroid gland function or thyroid hormone metabolism, due to its high iodine content. Amiodarone-induced hypothyroidism is common in countries with high iodine dietary intake, and Amiodarone-induced thyrotoxicosis is more prevalent in regions with low iodine dietary intake. A large amount of iodide released during the metabolism of Amiodarone causes the so-called Wolff-Chaikoff effect, in which there is a blockage of thyroidal iodide uptake and thyroid hormone biosynthesis. Here we report two cases of Amiodarone-induced thyrotoxicosis and one case of Amiodarone-induced hypothyroidism.

Cases: 1) A 65-year-old male patient with a background of long-standing atrial fibrillation was on treatment with Amiodarone. He was subsequently diagnosed with dilated cardiomyopathy resulting in cardiac failure. A year later, the patient presented with thyrotoxicosis (likely secondary to Amiodarone) blood test showed FT4 20pmol/l, TSH<0.01 mIU/l. He was treated with carbimazole, and Amiodarone was discontinued. 2) A 72-year-old man presented to the hospital with palpitations, tremors, and dizziness. He was found to be thyrotoxic: T4>100pmol/l, TSH<0.01 mIU/l. His background includes atrial fibrillation, chronic obstructive pulmonary disease, Type 2 diabetes, hypertension, and high cholesterol. He was taking Amiodarone to manage atrial fibrillation. Amiodarone was then discontinued. 3) An 80-year-old man developed hypothyroidism after being started on Amiodarone. He was known to have ischemic heart disease, atrial fibrillation, and episodes of ventricular tachycardia. Amiodarone was continued as his implantable cardioverter-defibrillator was removed, and he was commenced on thyroxine.

Discussion: Amiodarone is used in some patients to treat arrhythmias. Amiodarone is no longer given as a first-line treatment due to the serious side effects caused by long-term therapy. Common side effects include QT prolongation leading to arrhythmias (Torsades de Pointes), hepatic dysfunction, and thyroid disorders. Amiodarone-induced thyrotoxicosis (AIT) is divided into type 1 and type 2. AIT type 1 occurs in patients with underlying unmasked thyroid disease such as Graves’ disease or toxic nodule. Type 2 AIT is due to destructive thyroiditis. Amiodarone-induced hypothyroidism is likely due to the inhibition of thyroid hormone synthesis and is more common in patients with underlying subclinical hypothyroidism.

Conclusion: Patients commencing Amiodarone therapy should have their baseline thyroid function tests checked and then reviewed every six months for early detection of thyroid dysfunction thus avoiding severe episodes of both hypo- and hyperthyroidism.