Endocrine Abstracts

Case History: A 71-year old male, who had been on amiodarone therapy for many years, was receiving Levothyroxine therapy due to amiodarone-induced hypothyroidism. He was subsequently found to have thyrotoxicosis, which remained after levothyroxine discontinuation. He had type 2 diabetes and ischaemic cardiomyopathy and had an implanted cardiac defibrillator due to multiple VT arrests. Amiodarone therapy had contributed to stabilisation of his cardiac arrhythmias and had continued beyond his diagnosis of amiodarone-induced hypothyroidism for that reason.

Investigations: The patient complained of 10 kg unintentional weight loss and agitation and examination revealed a regular heart rate of 58 bpm, blood pressure 127/73 mmHg, euvolaemia and resting tremor. Neck examination was unremarkable. Thyroid function confirmed thyrotoxicosis with TSH <0.01 milliunit/l, FT4 31.8 pmol/l, FT3 5.9 pmol/l. TSH receptor and TPO antibodies were negative. HbA1c was 50 mmol/l. An urgent technetium uptake scan showed type 2 amiodarone-induced thyroiditis, with absent gland uptake.

Results and treatment: After consultation with the Cardiologist, amiodarone was discontinued and bisoprolol was uptitrated. He was commenced on prednisolone 40mg daily for one month, along with Gliclazide for glycaemic control, and repeat blood tests showed marked improvement (TSH 0.17 milliunit/l, FT3 3.2 pmol/l, FT4 15.7 pmol/l). Thereafter he was successfully weaned off the prednisolone and the Gliclazide within a total period of less than 3 months. At the end of that period his thyroid function has normalised, HbAc1c has remained stable at 43 mmol/mol and he is being monitored for the development of hypothyroidism once again. A short synachthen test was also performed to ensure his adrenal axis has not been affected and that was normal. He has not had any cardiac complications since stopping the amiodarone.

Conclusion and points for discussion: Amiodarone is a potent antiarrhythmic drug that is used to treat arrhythmias, but can precipitate thyroid dysfunction due to its iodine-rich chemical structure and long half-life. It remains unclear whether amiodarone should be continued after diagnosis of thyrotoxicosis. There have been instances of amiodarone-induced coronary vasospasm and ischaemic ventricular fibrillation related to hyperthyroidism and some studies have shown that continuation of amiodarone delays restoration of euthyroid status, and increases risk of recurrence. Risk of recurrence has been documented in the literature as being as high as 10%. However, in other cases euthyroid states are still achieved with continuation of amiodarone and treatment with steroids.