open access

Vol 66, No 2 (2015)
Postgraduate education
Published online: 2015-05-01
Submitted: 2014-11-15
Accepted: 2014-11-17
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Amiodarone and the thyroid

Agata Jabrocka-Hybel, Tomasz Bednarczuk, Luigi Bartalena, Dorota Pach, Marek Ruchała, Grzegorz Kamiński, Marta Kostecka-Matyja, Alicja Hubalewska-Dydejczyk
DOI: 10.5603/EP.2015.0025
·
Endokrynologia Polska 2015;66(2):176-196.

open access

Vol 66, No 2 (2015)
Postgraduate education
Published online: 2015-05-01
Submitted: 2014-11-15
Accepted: 2014-11-17

Abstract

Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15–20% of cases. Amiodarone can cause both hypothyroidism (AIH, amiodarone-induced hypothyroidism) and thyrotoxicosis (AIT, amiodarone-induced thyrotoxicosis). AIH is treated by L-thyroxin replacement and does not need amiodarone discontinuation. There are two main forms of AIT: type 1, a form of true iodineinduced hyperthyroidism; and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist, contributed to by both pathogenic mechanisms. Type 1 AIT usually occurs in diseased thyroid glands, whereas type 2 AIT develops in substantially normal thyroid glands. Thioamides represent the first-line treatment for type 1 AIT, but iodine-replete glands are poorly responsive; sodium/potassium perchlorate, by inhibiting thyroidal iodine uptake, may increase the response to thioamides. Type 2 AIT is best treated by oral glucocorticoids. Response depends on thyroid volume and severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thioamides, potassium perchlorate, and steroids. Radioiodine treatment is usually not feasible because amiodarone-related iodine load decreases thyroidal radioiodine uptake. Thyroidectomy represents an important and helpful option in cases resistant to medical therapy. Surgery performed by a skilled surgeon may represent an emergent treatment in patients who have severe cardiac dysfunction. (Endokrynol Pol 2015; 66 (2): 176–196)

Abstract

Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15–20% of cases. Amiodarone can cause both hypothyroidism (AIH, amiodarone-induced hypothyroidism) and thyrotoxicosis (AIT, amiodarone-induced thyrotoxicosis). AIH is treated by L-thyroxin replacement and does not need amiodarone discontinuation. There are two main forms of AIT: type 1, a form of true iodineinduced hyperthyroidism; and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist, contributed to by both pathogenic mechanisms. Type 1 AIT usually occurs in diseased thyroid glands, whereas type 2 AIT develops in substantially normal thyroid glands. Thioamides represent the first-line treatment for type 1 AIT, but iodine-replete glands are poorly responsive; sodium/potassium perchlorate, by inhibiting thyroidal iodine uptake, may increase the response to thioamides. Type 2 AIT is best treated by oral glucocorticoids. Response depends on thyroid volume and severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thioamides, potassium perchlorate, and steroids. Radioiodine treatment is usually not feasible because amiodarone-related iodine load decreases thyroidal radioiodine uptake. Thyroidectomy represents an important and helpful option in cases resistant to medical therapy. Surgery performed by a skilled surgeon may represent an emergent treatment in patients who have severe cardiac dysfunction. (Endokrynol Pol 2015; 66 (2): 176–196)

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Keywords

amiodarone; AIT; AIH; radioiodine therapy; thyroidectomy

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About this article
Title

Amiodarone and the thyroid

Journal

Endokrynologia Polska

Issue

Vol 66, No 2 (2015)

Pages

176-196

Published online

2015-05-01

DOI

10.5603/EP.2015.0025

Bibliographic record

Endokrynologia Polska 2015;66(2):176-196.

Keywords

amiodarone
AIT
AIH
radioiodine therapy
thyroidectomy

Authors

Agata Jabrocka-Hybel
Tomasz Bednarczuk
Luigi Bartalena
Dorota Pach
Marek Ruchała
Grzegorz Kamiński
Marta Kostecka-Matyja
Alicja Hubalewska-Dydejczyk

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