Amiodarone-induced type 2 thyrotoxicosis

Abstract

The authors present a case of a 55-year-old gentleman with a medical history of atrial fibrillation on amiodarone who presented with weight loss, palpitations and exertional dyspnoea. Thyroid function tests revealed thyrotoxicosis with a free thyroxine (T4) of 117 pmol/L and a thyroid-stimulating hormone (TSH) of <0.008 mIU/L. Interleukin-6 level was low. The negative TSH-receptor antibody status, the presence of a small thyroid gland with heterogeneous echotexture and decreased internal vascularity on ultrasound together with the relatively quick drop in free T4 and free tri-iodothyronine (T3) levels once prednisolone therapy was added to carbimazole suggested that this was typical of amiodarone-induced thyrotoxicosis (AIT) type 2. Subsequently, carbimazole was discontinued and treatment with prednisolone was continued. This case highlights that AIT management may be challenging and it is of paramount importance to establish the type of AIT present as this will guide management and is key to improving prognosis.

How do I diagnose and treat my patient’s amiodarone-induced thyrotoxicosis?

“…Amiodarone is an iodine-rich antiarrhythmic drug 3 that can cause thyrotoxicity through several mechanisms. Iodine is required for thyroid hormone synthesis.…”

“…The Wolff-Chaikoff effect is a protective phenomenon wherein elevated plasma iodine concentrations temporarily halt the synthesis of thyroid hormones. 3 The escape from this protective effect leads to the Jod-Basedow effect, wherein thyroid gland hyperactivation or autonomous production by thyroid nodules…”

“…occurs in the absence of negative feedback to the pituitary gland. 3 Amiodarone-induced thyrotoxicosis can be confi rmed by low TSH, high T4, and high-normal or high T3. Additionally, patients may be asymptomatic or may exhibit signs of overt thyrotoxicosis, including palpitations, tremors, diaphoresis, and weight loss.…”