QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Résumé Extracto Full Text PDF Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Articles Ahead of Print [Order Reprint] Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Liang, Y.-L. Articles by Wu, T.-J. Search for Related Content PubMed PubMed Citation Articles by Liang, Y.-L. Articles by Wu, T.-J.

Amiodarone-Induced Thyrotoxicosis in a Patient with Autonomously Functioning Nodular Goiter

Fellow, Department of Internal Medicine, National Cheng Kung University Hospital, Taiwan, Republic of China

Shih-Ming Huang, MD

Professor of Surgery, College of Medicine, National Cheng Kung University

Shu-Ling Peng, MD

Consultant, Department of Pathology, National Cheng Kung University Hospital

Shu-Hwa Hsiao, BSc (Pharm)

Clinical Pharmacist, Department of Pharmacy, National Cheng Kung University Hospital

Hao-Chang Hung, MD

Consultant, Department of Internal Medicine, National Cheng Kung University Hospital

Horng-Yih Ou, MD

Assistant Professor, Department of Internal Medicine, College of Medicine, National Cheng Kung University

Ta-Jen Wu, MD

Associate Professor of Internal Medicine, College of Medicine, National Cheng Kung University

Reprints: Dr. Wu, College of Medicine, National Cheng Kung University, 138 Sheng-Li Road, Tainan 704, Taiwan, R.O.C., fax 886-6-276-6175, djwu{at}mail.ncku.edu.tw

OBJECTIVE: To report on adverse reactions associated with amiodarone and propylthiouracil.

CASE SUMMARY: A 64-year-old female with atrial fibrillation and nodular goiter progressed to overt thyrotoxicosis after receiving therapy with amiodarone 200 mg/day for less than 12 weeks. Thyroid scan revealed a hyperfunctioning nodule in the left lobe, while immunologic studies were negative for both thyroid peroxidase and thyroglobulin antibodies. The thyroid-stimulating hormone (TSH) receptor antibody level was transiently elevated. Propylthiouracil 100 mg 3 times/day was started after the withdrawal of amiodarone, but the patient developed severe generalized skin rash, fever, and leukocytosis after 4 weeks. Thyroidectomy was performed, and histopathology was compatible with type 1 amiodarone-induced thyrotoxicosis (AIT) associated with toxic nodular goiter. An objective causality assessment revealed that thyrotoxicosis was probably related to use of amiodarone.

DISCUSSION: Amiodarone is an antiarrhythmic agent that may cause thyroid dysfunction. Differentiating between the 2 types of AIT is important for implementation of the correct therapeutic strategy. The transient elevation of TSH receptor antibodies in AIT complicated the diagnosis. As a rare subtype, type 1 AIT by nodular goiter may be associated with early AIT. Initiating thyroid function monitoring within 3 months of amiodarone therapy should be considered.

CONCLUSIONS: Type 1 AIT caused by nodular goiter is rarely reported. Amiodarone should be avoided in such patients and subtotal thyroidectomy to remove the toxic nodule may be the treatment of choice.

Key Words: amiodarone, nodular goiter, thyrotoxicosis

Published Online, December 23, 2008. www.theannals.com, DOI 10.1345/aph.1L347