• Kavitha Ganesan, Bobby Bradley, David W Jones, and Dr Solomon Solomon.
• Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, TN, USA.
• Am. J. Med. Sci. 2021 Sep 1; 362 (3): 308-313.

AbstractAmiodarone, the most commonly used antiarrhythmic drug, can cause either hypothyroidism by inhibiting iodide transport into the thyroid gland or hyperthyroidism. We present a rare case of type 2 amiodarone-induced thyrotoxicosis with hypercalcemia. A 64-year-old man with systolic heart failure, hypertension, and hyperthyroidism presented with complaints of dyspnea on exertion, orthopnea, and vomiting for several days. Laboratory tests showed low thyroid stimulating hormone <0.01 mIU/L, high free triiodothyronine (FT3) of 24.8 ng/dL, free thyroxine (FT4) of >5.0 ng/dL, and hypercalcemia of 12.9 mg/dL. Hypercalcemia, a rare presentation of AIT, was treated with calcitonin and intravenous fluids. The patient was taken off methimazole and started on propylthiouracil for the persistent elevation of thyroid hormones, especially FT3, and to reduce the conversion of T4 to T3. The patient was not completely responding to treatment with propylthiouracil alone, so prednisone was added to the regimen on day 12, effectively returning the patient to the euthyroid state.Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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