Some patients treated with amiodarone develop hyperthyroidism. Amiodarone-induced thyrotoxicosis (AIT) consists of 2 forms that differ in underlying cause and therapy.
|
Findings |
Type I |
Type II |
|
thyroid gland prior to amiodarone therapy |
nodular goiter or "latent" Graves disease |
normal thyroid |
|
process |
unmasks underlying abnormal thyroid gland |
destructive thyroiditis induced by amiodarone, with release thyroid hormone stores |
|
physical exam |
normal, nodular or diffuse goiter; thyroid bruit or ophthalmopathy in Graves |
normal or diffuse goiter |
|
thyroid autoantibodies present |
may be present in patients with underlying Graves disease |
usually absent |
|
serum interleukin- 6 (IL-6) |
normal to slightly increased |
markedly increased |
|
color flow Doppler sonography pattern |
I, II or III |
0 |
|
24 hour radioiodine uptake |
low, normal or high |
very low |
|
therapeutic response to thionamides |
yes |
no |
|
therapeutic response to perchlorate |
yes |
no |
|
therapeutic response to glucocorticoids (prednisone) |
usually not |
yes |
|
risk of hypothyroidism as sequelae |
no |
possible once thyroid hormone stores depleted |
where:
• Mixed patterns with an underlying thyroid disorder and concomitant thyroid destruction can occur).
• Radioiodine uptake in Type I disease tends to be low in areas with sufficient iodine.
• Classical symptoms of thyrotoxicosis may be absent, since amiodarone has an anti-adrenergic action and because it reduces conversion of T4 to T3.
Specialty: Endocrinology, Clinical Laboratory
ICD-10: ,
