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  Vol. 263 No. 11, March 16, 1990 TABLE OF CONTENTS
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Thyroidectomy for Amiodarone-Induced Thyrotoxicosis

Alan P. Farwell, MD; Susan L. Abend, MD; S. K. Stephen Huang, MD; Nilima A. Patwardhan, MD; Lewis E. Braverman, MD

JAMA. 1990;263(11):1526-1528.


Abstract

Amiodarone hydrochloride, an iodine-rich drug used in the treatment of tachyarrhythmias, is responsible for the development of thyrotoxicosis in approximately 10% of patients who reside in areas of moderate iodine deficiency. Treatment of amiodarone-induced thyrotoxicosis is difficult since the drug has a prolonged half-life, cardiac decompensation due to underlying heart disease occurs often, and discontinuation of amiodarone therapy may not be possible. We report a patient with severe thyrotoxicosis who received amiodarone for 34 months. Prolonged treatment with methimazole, potassium perchlorate, iopanoic acid, and dexamethasone was unsuccessful in controlling the hyperthyroid state. A near-total thyroidectomy resulted in rapid amelioration of thyrotoxicosis. Since surgery results in rapid control of thyrotoxicosis and permits continued therapy with amiodarone, we suggest that near-total thyroidectomy warrants consideration as definitive treatment for resistant amiodarone-induced thyrotoxicosis.

(JAMA. 1990;263:1526-1528)



Author Affiliations

From the Divisions of Endocrinology and Metabolism (Drs Farwell, Abend, and Braverman) and Cardiology (Dr Huang) and the Department of Surgery (Dr Patwardhan), University of Massachusetts Medical School, Worcester.


Footnotes

Reprint requests to Division of Endocrinology and Metabolism, Department of Medicine, University of Massachusetts Medical School, 55 Lake Ave N, Worcester, MA 01655 (Dr Farwell).



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