Since amiodarone was introduced in Japan in 1992, the incidence of the drug
-induced thyroid dysfunction has been increasing. We studied the thyroid fu
nction of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 p
atients with amiodarone-associated hypothyroidism (AAH) who had been referr
ed to our Institute in the last 6 years. AIT and AAH developed after 39+/-2
1 and 20+/-16 months of amiodarone treatment, respectively. One patient dev
eloped AAH followed by AIT. The AIT ranged from subclinical to overt thyrot
oxicosis. Four patients with moderate to marked AIT were treated with methi
mazole. Their thyrotoxicosis persisted for 3 to 9 months, despite administr
ation of antithyroid agents. One patient with mild thyrotoxicosis was treat
ed with prednisolone, resulting in a euthyroid state in a few months. Eight
patients with asymptomatic to moderate thyrotoxicosis resolved spontaneous
ly without any treatment. In four asymptomatic patients with AIT, serum lev
els of T-3 and T-4 were in the upper normal range or slightly high (<12 mu
g/dl), accompanied by suppressed TSH (<0.1 mu U/ml) and high thyroglobulin
levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical t
hyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies
revealed no nodular lesion in the thyroid, and color flow Doppler sonograp
hy demonstrated no hypervascularity in the thyroid gland in any AIT patient
. Although it is postulated in Europe that there are two types of AIT, name
ly type I, which develops in patients with latent Graves' disease or toxic
multinodular goiter, and type II, which develops in an apparently normal th
yroid as destructive thyroiditis, all AIT patients we have seen so far had
developed destructive type AIT. Sufficient intake of iodide and a very low
incidence of toxic multinodular goiter may account for the rare incidence o
f type I AIT in our country. Mild to moderate AIT resolved spontaneously wi
thout discontinuing amiodarone, but it was discontinued in two of 13 AIT pa
tients because of extrathyroidal adverse reactions.