Endocrine Abstracts

Case presentation: A 66 year old male presented to the clinical physiology department for a routine ECHO. He was found to be hemodynamically unstable with fast Atrial fibrillation and was referred to ED for immediate management. He was subsequently admitted in CCU under Cardiology. He presented with a 3 month history of shortness of breath, palpitations, persistent tremors, unintentional weight loss and generalised fatigue. No previous thyroid problems. He had a longstanding history of dilated cardiomyopathy and uncontrolled atrial fibrillation and was awaiting ablation. He had underwent 3 unsuccessful cardioversions previously. He was on Amiodarone which was stopped 8 months ago. His LVEF on admission to CCU was < 20%. On examination, he had a small firm goitre, fine tremors and mild ankle oedema.

Investigations: Serum TSH – 0.01 mu/l [0.3–4.2]

Serum free T3 – 25.4 pmol/l [3.1 – 6.8]

Serum free T4 – >100 pmol/l [12 – 22]

Thyroid stimulating Immunoglobulins and Thyroid Peroxidase Antibodies – negative

Ultrasound thyroid: The thyroid gland appeared diffusely enlarged and hypoechogenic in keeping with chronic thyroiditis. Tiny colloid cyst in the right lobe of the thyroid. No solid nodules identified

Treatment: While the patient was in CCU, an endocrine referral was sought. He was started on Carbimazole 60 mg OD and PTU 100 mg TDS. As it was unclear if this was Amiodarone induced type 1 or 2 thyrotoxicosis, the case was discussed with tertiary care centre and it was decided to start Dexamethasone 0.5 mg BD with a subsequent thyroidectomy when thyroid levels settled. In the following weeks the patient was reviewed in the endocrine clinic and had a marked improvement in his symptoms and TFT's. Furthermore, the LVEF significantly improved to >40%. The Dexamethasone and Carbimazole were gradually tapered and stopped completely. An outpatient cardioversion is planned by cardiologists. Due to his marked improvement it was decided not to proceed with thyroidectomy.

Conclusion and points for discussion: AIT is a condition which when diagnosed correctly responds rapidly to treatment. Despite this it still presents as a challenge to clinicians for proper diagnosis and differentiation between type 1 and type 2 AIT. Thionamides represent the first-line treatment for type 1 AIT. Type 2 AIT is best treated by oral glucocorticoids. The response very much depends on the thyroid volume and the severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thionamides, potassium perchlorate, and steroids.