SFEEU2023 Society for Endocrinology Clinical Update 2023 Workshop C: Disorders of the thyroid gland (16 abstracts)
Western General Hospital, Edinburgh, United Kingdom
A 56 year old man came to the attention of the endocrine service during an admission with COVID 19. Due to persistent tachycardia he had thyroid function tests (TFTs) which showed TSH <0.01mU/land free T4 of 58 pmol/l. He had reported weight loss over the past couple of months and occasional palpitations but no other features of thyrotoxicosis. He had no personal or family history of thyroid or autoimmune disease. On examination his pulse was 90 beats per minute, had no goitre or thyroid tenderness and no signs of thyroid eye disease. In addition to COVID 19, he also had acute hepatitis and required NG feeding. His past medical history is of Marfan syndrome, aortic valve replacement, aortic repair complicated by T4 level spinal stroke, moderate LVSD, and recurrent ventricular tachycardia with an implantable cardioverter-defibrillator. Of note he had been on amiodarone for 18 years. He had undetectable thyroid receptor antibodies. He was commenced on prednisolone 40 mg once daily for presumed type two amiodarone induced thyrotoxicosis (AIT2). He was not initially commenced on carbimazole due to his acute liver dysfunction. A request for a thyroid uptake scan was rejected by radiology as he was COVID 19 positive. Amiodarone was stopped on discussion with cardiology and dronedarone was commenced. He received alendronic acid for bone protection and required three weeks of gliclazide for steroid induced hyperglycaemia. TFTs improved as below and prednisolone was gradually weaned. Amiodarone has large proportion of iodine and a long half life. It can cause both hypothyroidism and thyrotoxicosis. Amiodarone induced thyrotoxicosis (AIT) can be split into type 1 AIT and type 2 AIT. Type 1 AIT is more common in those with underlying thyroid disease, is due to increased synthesis of thyroid hormones and is usually treated with anti-thyroid drugs. Type 2 AIT is caused by a direct toxic effect of amiodarone on the thyroid cells leading to thyroiditis and release of preformed thyroid hormones. It can be treated with steroids. In practice it can be difficult to distinguish between the type of AIT and some patients have a mixed type.
Reference range | 13/02 | 16/02 | 23/02 | 01/03 | 15/03 | 19/04 | 07/05 | |
TSH | 0.2-4.5mU/l | <0.01 | <0.01 | <0.01 | <0.01 | 0.23 | 5.3 | 2.3 |
Free T4 | 9-21 pmol/l | 58 | 43 | 25 | 18 | 13 | 12 | 12 |
Free T3 | 2.4-6 pmol/l | 9.1 | 5.6 | _ | 3.3 | _ | _ | _ |