Enio Martino,
Luigi Bartalena,
Fausto Bogazzi and
Lewis E. Braverman
Dipartimento di Endocrinologia e Metabolismo (E.M., F.B.),
University of Pisa, Pisa, Italy 56124; Cattedra di Endocrinologia
(L.B.), University of Insubria, Varese, Italy; Section of
Endocrinology, Diabetes and Nutrition (L.E.B.), Boston Medical Center,
Boston, Massachusetts 02118-2393
Amiodarone is a benzofuranic-derivative iodine-rich drug widelyused
for the treatment of tachyarrhythmias and, to a lesserextent, of
ischemic heart disease. It often causes changes inthyroid function
tests (typically an increase in serum T4 and
rT3,and a decrease in serum T3,
concentrations), mainly relatedto the inhibition of 5'-deiodinase
activity, resulting in adecrease in the generation of T3
from T4 and a decrease in theclearance of rT3.
In 14–18% of amiodarone-treated patients,there is overt thyroid
dysfunction, either amiodarone-inducedthyrotoxicosis (AIT) or
amiodarone-induced hypothyroidism (AIH).Both AIT and AIH may develop
either in apparently normal thyroidglands or in glands with
preexisting, clinically silent abnormalities.Preexisting Hashimoto’s
thyroiditis is a definite riskfactor for the occurrence of AIH. The
pathogenesis of iodine-inducedAIH is related to a failure to escape
from the acute Wolff-Chaikoffeffect due to defects in thyroid
hormonogenesis, and, in patientswith positive thyroid autoantibody
tests, to concomitant Hashimoto’sthyroiditis. AIT is primarily
related to excess iodine-inducedthyroid hormone synthesis in an
abnormal thyroid gland (typeI AIT) or to amiodarone-related
destructive thyroiditis (typeII AIT), but mixed forms frequently
exist. Treatment of AIHconsists of L-T4
replacement while continuing amiodarone therapy;alternatively, if
feasible, amiodarone can be discontinued,especially in the absence of
thyroid abnormalities, and thenatural course toward euthyroidism can
be accelerated by a shortcourse of potassium perchlorate treatment. In
type I AIT themain medical treatment consists of the simultaneous
administrationof thionamides and potassium perchlorate, while in type
II AIT,glucocorticoids are the most useful therapeutic option. Mixed
formsare best treated with a combination of thionamides, potassium
perchlorate,and glucocorticoids. Radioiodine therapy is usually not
feasibledue to the low thyroidal radioiodine uptake, while
thyroidectomycan be performed in cases resistant to medical therapy,
witha slightly increased surgical risk.
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