Endocrine Abstracts

Background: Amiodarone induced thyroid dysfunction can be either thyrotoxicosis (AIT) or hypothyroidism (AIH). AIT is classified as Type 1 and Type 2. Type 1 occurs in patients with underlying thyroid pathology and Type 2 AIT is a destructive thyroiditis. We describe a patient with severe Type 2 AIT with a protracted course.

>Case History: A 40 year old male with Atrial Fibrillation, Obesity and Obstructive Sleep Apnoea had been on Amiodarone from October 2020 till July 2022. His TSH in March 2022 was normal. In December 2022, he saw the GP for abdominal pain. The investigations showed supressed TSH with FT4>100 pmol/l and FT3 21 pmol/l. Carbimazole was started in the primary care. Three weeks later, patient was admitted with abdominal pain and vomiting. His FT3 >50 pmol/l, FT4>100 pmol/l, ALT 218IU/l and calcium 2.99mmol/l. He was treated with IV fluids and antiemetics. Once vomiting settled and calcium normalised, he was discharged. A week later he was readmitted and referred to Endocrinology as persistently high TFT despite high dose Carbimazole. The US and Technetium uptake scans were compatible with thyroiditis. TRAb was negative. The diagnosis of AIT Type 2 was made. Prednisolone 40 mg was started and Carbimazole discontinued. Thyroid function improved gradually and returned to normal after 4 months. Attempts to reduce steroids caused a relapse hence protracted course.

Discussion: Amiodarone induced thyrotoxicosis can occur months after discontinuing Amiodarone due to its long half-life but usually occurs whilst on Amiodarone. Our patient had severe thyrotoxicosis due to Type 2 AIT leading to deranged liver functions and hypercalcaemia. He had a protracted recovery leading to increased cardiovascular risk. He is on high dose corticosteroids with risk of weight gain, diabetes and osteoporosis. This presentation highlights the importance of regular monitoring of thyroid function on Amiodarone, accurate diagnosis and urgency of referral in severe thyrotoxicosis.