Thyrotoxicosis is a challenging endocrine complication associated with amiodarone treatment in cardiac patients. We present a case of a 51-year-old man with type 2 amiodarone-induced thyrotoxicosis (AIT) occurring five months after cardiac transplantation. His medical background was significant for hypertrophic cardiomyopathy requiring left ventricular assist device prior to transplant and paroxysmal atrial fibrillation requiring amiodarone for greater than 12 months.
He presented to hospital acutely with deterioration in cardiac graft function. On examination, he was tachycardic (heart rate ~110 bpm) and hyperthermic. Laboratory evaluation on admission demonstrated thyrotoxicosis with fully suppressed TSH (< 0.02 mIU/L) and elevated FT4 (46.2 pmol/L) and FT3 (6.1 pmol/L). TRAB was not elevated. Thyroid ultrasound demonstrated diffuse heterogeneous echotexture with reduced vascularity, suggesting destructive type 2 amiodarone-induced thyrotoxicosis. Treatment with anti-thyroid medication and glucocorticoids was commenced empirically to cover both type 1 and type 2 AIT. Concurrently, he was admitted to hospital and treated with plasmapheresis for presumed antibody-mediated cardiac graft rejection.
Within days, there was marked biochemical resolution of thyrotoxicosis as well as improvement in cardiac ejection fraction from 15% to 50%. However, thyrotoxicosis rapidly recurred after plasmapheresis was ceased requiring re-initiation of high dose thionamide and glucocorticoid treatment with a slow wean over the ensuing 3 months. He remains euthyroid at follow up.
Our case highlights plasmapheresis as a highly effective therapy to rapidly remove circulating free thyroxine in emergent cases of AIT, however the effect is short term and transient.