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Ju, Kim, Chung, Park, Kim, Jung, Choi, Kang, and Shim: Amiodarone Induced Thyrotoxicosis (Type II)
Case Report
Journal of Korean Endocrine Society

Journal of Korean Endocrine Society 2007; 22(3): 229-234.

Published online: 20 June 2007

DOI: https://doi.org/10.3803/jkes.2007.22.3.229

Amiodarone Induced Thyrotoxicosis (Type II)

Cho Young Ju, Hearn Kook Kim, Hyoung Jung Chung, Yong Jin Park, Jin Yeob Kim, Seung Mun Jung1, Su Jung Choi1, Gil Hyun Kang2, Myoung Sook Shim

Department of Internal Medicine, University of Ulsan, Gangneung Asan Hospital, Korea.

1Department of Diagnostic Radiology, University of Ulsan, Gangneung Asan Hospital, Korea.

2Department of Pathology, University of Ulsan, Gangneung Asan Hospital, Korea.

Received 16 January 2007       Accepted 15 March 2007

Copyright © 2007 Korean Endocrine Society

Abstract

Amiodarone is an iodinated benzofuran derivative, that is highly effective as an agent for the treatment of various cardiac arrhythmias; these arrthymias, range from paroxysmal atrial fibrillation to life-threatening ventricular tachyarrhythmias. Yet amiodarone is associated with several side effects that include dysfunction of liver, thyroid or various other organs. Two main forms of amiodarone induced thyrotoxicosis (AIT) have been described; type I AIT develops in an abnormal thyroid gland (nodular goiter, latent Graves' disease) and it is due to amiodarone-induced true hyperthyroidism; type II AIT occurs in an apparently normal thyroid gland and it is due to amiodarone-induced destructive thyroiditis. We recently experienced a case of type II thyrotoxicosis that was induced by amiodarone treatment for ventricular tachycardia after acute myocardial infarction. The symptoms of thyrotoxicosis were relieved after withdrawal of amiodarone and administering steroid. Type I AIT has often been reported on but type II AIT is relatively rare. We report here on a case of type II amiodarone induced thyrotoxicosis along with a literature review.

Keywords: Amiodarone, Amiodarone induced thyrotoxicosis, Hyperthyroidism

Figures and Tables

Fig. 1
Thyroid scan (99mTcO4). Non-visualization of both lobes (decreased 99mTcO4 uptake).
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Fig. 2
Color doppler ultrasound. It shows diffusely diminished vascularity in the parenchyma of the thyroid gland.
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Fig. 3
Cytologic finding of the thyroid gland. There are multinucleated giant cells phagocytising colloid, mononuclear macrophages and a few lymphocytes in the smear slide of aspiration. (Pap stain, ×100)
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Fig. 4
Abdominal CT scan without contrast enhancement. It shows increased density of the liver parenchyma compared to that of the spleen due to amiodarone toxicity.
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Fig. 5
Serial measurement of thyroid stimulating hormone and free thyroxine.
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Table 1
Change of laboratory profile during management of type 2 AIT
jkes-22-229-i001

free T4; free thyroxine, HD; hospital day, OPD; out patient department, TSH; thyroid stimulating hormone.

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