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Effects of Amiodarone on Thyroid Function

Kishore J. Harjai, MD; and Angelo A. Licata, MD, PhD
[+] Article, Author, and Disclosure Information

From Alton Ochsner Medical Foundation, New Orleans, Louisiana; and the Cleveland Clinic Foundation, Cleveland, Ohio. Requests for Reprints: Kishore J. Harjai, MD, 113 Betz Avenue, Jefferson, LA 70121. Current Author Addresses: Dr. Harjai: 113 Betz Avenue, Jefferson, LA 70121.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1997;126(1):63-73. doi:10.7326/0003-4819-126-1-199701010-00009
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Purpose: To review the literature on the effects of amiodarone on thyroid physiology and management of amiodarone-induced thyroid disease.

Data Sources: English-language articles identified through a MEDLINE search (for 1975 to 1995, using the terms amiodarone and thyroid) and selected cross-referenced articles.

Study Selection: Articles on the effects of amiodarone on thyroid physiology and function tests and occurrence, recognition, and management of amiodarone-induced thyroid disease.

Data Extraction: Data were manually extracted from selected studies and reports; emphasis was placed on information relevant to the practicing clinician.

Data Synthesis: Amiodarone can have many effects on thyroid function test results, even in the absence of hyperthyroidism or hypothyroidism. It may cause an increase in serum levels of thyroxine, reverse triiodothyronine, and thyroid-stimulating hormone and a decrease in serum triiodothyronine levels. Thyrotoxicosis occurs in some patients and is related to several pathogenetic mechanisms. It often presents dramatically with obvious clinical manifestations and further changes in thyroid function test results. Medical options include therapy with thionamides, perchlorate, and prednisone. Radioactive iodine is of little use. Thyroidectomy is effective and is the only measure that consistently allows continued use of amiodarone. Unlike thyrotoxicosis, hypothyroidism is related to a persistent Wolff-Chaikoff effect and often has a vague presentation. The goal of treatment of amiodarone-induced hypothyroidism is to bring serum thyroxine levels to the upper end of the normal range, as often seen in euthyroid patients who are receiving amiodarone.

Conclusions: Thyroid dysfunction commonly occurs with amiodarone therapy. It may be difficult to recognize the dysfunction because of the many changes in thyroid function test results that occur in euthyroid patients who are receiving amiodarone. Effective strategies exist for the management of hyperthyroidism and hypothyroidism; these should be tailored to the needs of the individual patient.


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Figure 1.
Chemical structures of thyroxine, triiodothyronine, and amiodarone.
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Figure 2.
Changes in thyroid hormone physiology and thyroid function test results in euthyroid patients who received amiodarone.43334

The following changes in thyroid function test results occur: 1) increase in serum levels of thyroxine (T ) and reverse triiodothyronine [rT ], 2) initial increase followed by normalization of serum levels of thyroid-stimulating hormone [TSH], and 3) decrease in serum levels of triiodothyronine (T ). Asterisks indicate steps in thyroid hormone dynamics inhibited by amiodarone. Daggers indicate physiologic feedback inhibition. Bold arrow indicates that most feedback inhibition of TSH production is mediated by T rather than T .

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Figure 3.
Suggested algorithm for evaluation and management of thyroid dysfunction in patients treated with amiodarone.43

*Test should be done to serve as a reference for comparison with future test results. † Goal is to increase serum levels of thyroxine (T ) to high normal or slightly above normal (normalization of levels of thyroid-stimulating hormone [TSH] should not be attempted). ‡ Combination of thionamides (methimazole, 40 mg/d, or propylthiouracil, 400 to 800 mg/d) with potassium perchlorate (800 to 1000 mg/d for 15 to 45 days) or prednisone (0.5 to 1.25 mg/kg of body weight per day for 40 days) is beneficial; β-blockers may be added. AIH = amiodarone-induced hypothyroidism; AIT = amiodarone-induced thyrotoxicosis; T = triiodothyronine.

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