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Endocrine Abstracts (2023) 91 CB4 | DOI: 10.1530/endoabs.91.CB4

Maidstone Hospital, Hermitage Lane, Maidstone, Kent, United Kingdom

Introduction: Amiodarone is a widely used antiarrhythmic drug for refractory atrial or ventricular tachyarrhythmias. Amiodarone-induced thyrotoxicosis (AIT) occurs in up to 6% of patients taking this medication in iodine-sufficient areas of the world and in up to 10% in iodine deficient areas. AIT is of two types: type 1 is a form of iodine-induced hyperthyroidism whereas type 2 is a drug-induced destructive thyroiditis. Type 1 AIT tends to occur in patients with underlying thyroid autonomy in a nodular goitre, or Graves’ disease, while type 2 AIT appears because of direct damage or induction of apoptosis in thyrocytes by amiodarone.

Case report: A 68-year-old man presented to our emergency department with worsening palpitations and shortness of breath. He was known to have a paroxysmal atrial fibrillation and had been on Amiodarone for about two years. Amiodarone was discontinued about a month prior to presentation when his thyroid function test results were found to be abnormal. He denied previous personal or familiar history of thyroid dysfunction. On examination, he was tachycardic with a heart rate of 150 bpm. An ECG showed in was in a fast atrial fibrillation. Thyroid function tests showed a TSH <0.02 μU/l, FT3 9.1 pmol/l, FT4 71.0 pmol/l. Given the previous medical history of amiodarone use, a diagnosis of amiodarone-induced thyrotoxicosis was made. He was started on bisoprolol by the Cardiologist for rate control. He was then started on Carbimazole 40 mg mg and 30 mg of prednisolone daily. An iodine uptake scan was not performed as patient had already been started on carbimazole. His TSH-receptor antibody result came later to be < 0.3IU/l. We stopped carbimazole as this was likely a Type 2 AIT, while he continued prednisolone. Prednisolone was gradually tapered and stopped over the next three months while monitoring his thyroid function. About four months post-steroid cessation, biochemical re-evaluation showed TSH 16.2 μU/ml and FT4 11.4 pmol/land similar picture persisted on a repeat follow up sample. He was then started on Levothyroxine replacement. He is presently under endocrine follow

Conclusion: This case highlights the effects of Amiodarone on the thyroid gland and demonstrates the possible spontaneous evolution of amiodarone induced thyrotoxicosis into hypothyroidism.

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