Endocrine Abstracts

Amiodarone is an effective anti-arrhythmic drug but is associated with significant side effects, including thyroid dysfunction due to its high iodine content and direct toxic effects on the thyroid. We present a 74-year-old gentleman with asymptomatic hyperthyroidism (TSH < 0.01 mU/L, free T3 6.1 pmol/L, free T4 30.2 pmol/L) while on long-term amiodarone therapy. His medical history included ventricular tachycardia (VT), atrial fibrillation, implanted cardioverter defibrillator (ICD), myocardial infarction, and coronary artery bypass grafting (CABG). He had been on amiodarone for five years, with unsuccessful attempts at discontinuation due to arrhythmia recurrence necessitating its reintroduction. Initially managed with carbimazole for suspected amiodarone-induced thyroiditis (AIT), further investigations revealed negative TSH receptor antibody and thyroid peroxidase (TPO) antibodies (0.63 IU/mL, reference range 0–5 IU/mL). ESR was moderately raised while awaiting interleukin-6 results. Inflammatory thyroiditis with normal vascularity was identified on thyroid ultrasound. Thyroid uptake scan was deemed unreliable due to ongoing amiodarone therapy, which was continued per cardiology recommendations to mitigate the risk of recurrent VT. On clinical suspicion, prednisolone 40 mg/day was initiated, leading to very good initial response, further supporting the diagnosis of amiodarone-induced thyroiditis (AIT) type 2. However, patient admitted discontinuing prednisolone after taking only 20 mg/day for two weeks. His thyroid function worsened after stopping the steroids. Prednisolone was subsequently restarted with a plan for close monitoring of thyroid function tests. This case highlights the diagnostic and management challenges of amiodarone-induced thyroiditis in patients requiring ongoing amiodarone therapy due to high risk of VT recurrence.