Key result
Prednisolone therapy successfully treated amiodarone-induced type 2 thyrotoxicosis, leading to a rapid decrease in free T4 and free T3 levels and restoration of a euthyroid state.
Case Report (n=1)
This case highlights that amiodarone-induced type 2 thyrotoxicosis can present with low interleukin-6 levels and is effectively managed with oral glucocorticoids and amiodarone cessation.
May aid type 2 AIT recognition via low IL-6 and imaging; leaves open management guidance from case-level data alone.
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.
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Portelli et al. (2021) conducted a case report in Amiodarone-induced type 2 thyrotoxicosis (n=1). Prednisolone was evaluated on Thyroid function (Free T4, Free T3, TSH). Prednisolone therapy successfully treated amiodarone-induced type 2 thyrotoxicosis, leading to a rapid decrease in free T4 and free T3 levels and restoration of a euthyroid state.
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