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Titolo:
The effects of amiodarone on the thyroid
Autore:
Martino, E; Bartalena, L; Bogazzi, F; Braverman, LE;
Indirizzi:
Univ Insubria, Cattedra Endocrinol, Varese, Italy Univ Insubria Varese Italy Insubria, Cattedra Endocrinol, Varese, Italy Boston Med Ctr, Sect Endocrinol Diabet & Nutr, Boston, MA 02118 USA BostonMed Ctr Boston MA USA 02118 ol Diabet & Nutr, Boston, MA 02118 USA Univ Pisa, Dipartimento Endocrinol & Metab, I-56124 Pisa, Italy Univ PisaPisa Italy I-56124 nto Endocrinol & Metab, I-56124 Pisa, Italy
Titolo Testata:
ENDOCRINE REVIEWS
fascicolo: 2, volume: 22, anno: 2001,
pagine: 240 - 254
SICI:
0163-769X(200104)22:2<240:TEOAOT>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
IODINE-INDUCED THYROTOXICOSIS; CONGESTIVE-HEART-FAILURE; RECEPTOR MESSENGER-RNA; LOW-DOSE AMIODARONE; INDUCED HYPOTHYROIDISM; INDUCED HYPERTHYROIDISM; ANTITHYROID ANTIBODIES; POTASSIUM PERCHLORATE; FOLLOW-UP; IN-VITRO;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
152
Recensione:
Indirizzi per estratti:
Indirizzo: Braverman, LE Univ Pisa, Dipartimento Endocrinol & Metab, Osped Cisanello,Via Paradisa 2, I-56124 Pisa, Italy Univ Pisa Via Paradisa 2 Pisa Italy I-56124 124 Pisa, Italy
Citazione:
E. Martino et al., "The effects of amiodarone on the thyroid", ENDOCR REV, 22(2), 2001, pp. 240-254

Abstract

Amiodarone is a benzofuranic-derivative iodine-rich drug widely used for the treatment of tachyarrhythmias and, to a lesser extent, of ischemic heartdisease. It often causes changes in thyroid function tests (typically an increase 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 ina decrease in the generation of T-3 from T-4 and a decrease in the clearance of rT(3). in 14-18% of amiodarone-treated patients, there is overt thyroid dysfunction, either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH). Both AIT and AIH may develop either in apparently normal thyroid glands or in glands with preexisting, clinically silent abnormalities. Preexisting Hashimoto's thyroiditis is a definite risk factor for the occurrence of AIH. The pathogenesis of iodine-induced AW is related to a failure to escape from the acute Wolff-Chaikoff effect due to defects in thyroid hormonogenesis, and, in patients with positive thyroid autoantibody tests, to concomitant Hashimoto's thyroiditis. AIT is primarily related to excess iodine-induced thyroid hormone synthesis in an abnormal thyroid gland (type I AIT) or to amiodarone-related destructive thyroiditis (type II AIT), but mixed forms frequently exist. Treatment of AIH consists of L-T-4 replacement while continuing amiodarone therapy; alternatively, if feasible, amiodarone can be discontinued, especially in the absence of thyroid abnormalities, and the natural course toward euthyroidism can be accelerated by a short course of potassium perchlorate treatment. In type I AIT the main medical treatment consists of the simultaneous administration of thionamides and potassium perchlorate, while in type II AIT, glucocorticoids are the most useful therapeutic option. Mixed forms are best treated with acombination of thionamides, potassium perchlorate, and glucocorticoids. Radioiodine therapy is usually not feasible due to the low thyroidal radioiodine uptake, while thyroidectomy can be performed in cases resistant to medical therapy, with a slightly increased surgical risk.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 09:13:24