Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P306

ECE2007 Poster Presentations (1) (659 abstracts)

Radioactive iodine in the treatment of type 2 amiodarone-induced thyrotoxicosis

Alptekin Gursoy 1 , Neslihan Bascil Tutuncu 1 , Arzu Gencoglu 2 , Hamiyet Yilmaz 1 , Asli Nar Demirer 1 & Nilgun Guvener Demirag 1


1Baskent University Faculty of Medicine, Department of Endocrinology and Metabolism, Ankara, Turkey; 2Baskent University Faculty of Medicine, Department of Nuclear Medicine, Ankara, Turkey.

Objective: Amiodarone-induced thyrotoxicosis (AIT) is usually classified into 2 types (type 1, in which a high iodine content triggers the autonomous production of thyroid hormone; and type 2, in which destructive thyroiditis causes the release of preformed thyroid hormone). A mixed form of AIT has also been also described. AIT is a difficult management problem that sometimes requires ablative thyroid therapy. The use of radioactive iodine (RAI) therapy in patients with type 1 AIT who had a 24-hour radioactive iodine uptake (RAIU) value of more than 10% has been previously reported. Despite its documented efficacy at usual doses (10–30 mCi) in patients with type 1 AIT, the efficacy of RAI in those with type 2 AIT has never been questioned, because type 2 patients usually have low RAIU. We thought that high adjusted-dose RAI (an adjustment made in accordance with the patient’s 24-hour RAIU value and thyroid weight) might be an attractive alternative to thyroid gland ablation in patients with type 2 AIT.

Patients and methods: Four patients with type 2 AIT who required thyroid ablation were included in the study. These individuals were either poor candidates for surgery or had refused surgery. The size of the thyroid gland in all subjects was within normal limits, and each thyroid was characterized by a homogenous echotexture on ultrasonography, the absence of vascularity on Doppler sonography, a low (< 4%) 24-hour RAIU value, and the absence of thyroid autoantibodies, all of which are characteristic of type 2 AIT.

Results: The patients were initially treated with thionamides and glucocorticoids. All patients except 1 were euthyroid before RAI therapy. All 4 patients received 1 dose of RAI (range, 29–80 mCi), and followed-up for 12 months. No exacerbation of thyrotoxicosis was noted after RAI therapy. Hypothyroidism (in 3 patients) or euthyroidism (in 1 patient) was achieved in first 6 months.

Conclusions: In patients with type 2 AIT, RAI treatment may be the therapy of choice for thyroid gland ablation.

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