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Amiodarone-Induced Elevation of Thyroid Stimulating Hormone in Patients Receiving Levothyroxine for Primary Hypothyroidism

James Figge, MD; and Robert G. Dluhy, MD
[+] Article and Author Information

Grant Support: Dr. Figge was supported by a grant from the Lucille P. Markey Charitable Trust. The study was supported by Clinical Research Center and CLINFO facility grant RR-02635 from the National Institutes of Health.

Requests for Reprints: James Figge, MD, Division of Endocrinology and Metabolism, Albany Medical College, A44, 47 New Scotland Avenue, Albany, NY 12208.

Current Author Addresses: Dr. Figge: Division of Endocrinology and Metabolism, Albany Medical College, A44, 47 New Scotland Avenue, Albany, NY 12208.

Dr. Dluhy: Department of Medicine, Endocrine-Hypertension Unit, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115.


©1990 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1990;113(7):553-555. doi:10.7326/0003-4819-113-7-553
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This excerpt has been provided in the absence of an abstract.

Amiodarone, an iodinated antiarrhythmic agent, has complex effects on thyroid hormone physiology. As a potent hepatic 5′-deiodinase inhibitor, the drug decreases thyroxine (T4) conversion to 3,5,3′-triiodothyronine (T3), and slows 3,3′,5′-triiodothyronine (rT3) clearance (1-3). Amiodarone may inhibit both the cellular uptake of T3 and T4 (4, 5), and the binding of T3 to its receptor (5, 6). These effects modulate T3-mediated responses in vitro (5-7) and in animals (8). Finally, iodide released from metabolism of the drug may occasionally cause overt hypothyroidism or hyperthyroidism (9). Given the antagonistic effects of amiodarone on T3 action, we studied whether the drug could elevate

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