The effects of amiodarone on the thyroid

Citation
E. Martino et al., The effects of amiodarone on the thyroid, ENDOCR REV, 22(2), 2001, pp. 240-254
Citations number
152
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINE REVIEWS
ISSN journal
0163769X → ACNP
Volume
22
Issue
2
Year of publication
2001
Pages
240 - 254
Database
ISI
SICI code
0163-769X(200104)22:2<240:TEOAOT>2.0.ZU;2-G
Abstract
Amiodarone is a benzofuranic-derivative iodine-rich drug widely used for th e treatment of tachyarrhythmias and, to a lesser extent, of ischemic heart disease. It often causes changes in thyroid function tests (typically an in crease in serum T-4 and rT(3), and a decrease in serum T-3, concentrations) , mainly related to the inhibition of 5'-deiodinase activity, resulting in a decrease in the generation of T-3 from T-4 and a decrease in the clearanc e of rT(3). in 14-18% of amiodarone-treated patients, there is overt thyroi d dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone -induced hypothyroidism (AIH). Both AIT and AIH may develop either in appar ently normal thyroid glands or in glands with preexisting, clinically silen t abnormalities. Preexisting Hashimoto's thyroiditis is a definite risk fac tor for the occurrence of AIH. The pathogenesis of iodine-induced AW is rel ated to a failure to escape from the acute Wolff-Chaikoff effect due to def ects in thyroid hormonogenesis, and, in patients with positive thyroid auto antibody tests, to concomitant Hashimoto's thyroiditis. AIT is primarily re lated to excess iodine-induced thyroid hormone synthesis in an abnormal thy roid gland (type I AIT) or to amiodarone-related destructive thyroiditis (t ype II AIT), but mixed forms frequently exist. Treatment of AIH consists of L-T-4 replacement while continuing amiodarone therapy; alternatively, if f easible, amiodarone can be discontinued, especially in the absence of thyro id abnormalities, and the natural course toward euthyroidism can be acceler ated by a short course of potassium perchlorate treatment. In type I AIT th e main medical treatment consists of the simultaneous administration of thi onamides and potassium perchlorate, while in type II AIT, glucocorticoids a re the most useful therapeutic option. Mixed forms are best treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. Rad ioiodine therapy is usually not feasible due to the low thyroidal radioiodi ne uptake, while thyroidectomy can be performed in cases resistant to medic al therapy, with a slightly increased surgical risk.