Case Presentation: A 73 year old woman with known ischemic cardiomyopathy with reduced ejection fraction and atrial fibrillation on Amiodarone presented with decompensated heart failure. Work up revealed Thyroid Stimulating Hormone (TSH) 0.0008 UIU/ML, Free Thyroxine (T4) >8 NG/DL, Total Triiodothyronine (T3) 144 NG/DL and Free T3 7.4 PG/ML. She had minimal symptoms consistent with hyperthyroidism reporting only heat intolerance and tachycardia. Thyroid ultrasound revealed normal appearance and size of her thyroid without nodule. Serum evaluation for antibodies against thyroglobulin, thyroid peroxidase and TSH receptor were all negative.
Given these results, it was thought that the patient had Amiodarone induced hyperthyroidism and the offending agent was discontinued. As the team was unable to differentiate between Type I or Type II, both were treated empirically with Propylthiouracil to cover Type I and Prednisone to cover Type II. Follow up lab work after initiation of treatment revealed persistently elevated Free T4. A 10 times dilution of Free T4 was performed on days 2 and 3 of treatment resulting in 21.7 NG/DL and 22 NG/DL, respectively. Thyroid removal was not pursued given high risk due to underlying cardiac disease and as it would not be curative if due to Type II hyperthyroidism. With diuresis and titration of her beta blocker, the patient’s presenting symptoms resolved and she was discharged on the above regimen with close follow up with Endocrinology for continued management.
Discussion: Amiodarone causes both hyperthyroidism and hypothyroidism. Hypothyroidism is due to inhibition of production of T3 or by blocking T3-receptor binding. Alternatively, hyperthyroidism occurs by the drug providing increased substrate in the form of iodine resulting in increased production of T4 and T3 (Type I) or by destroying thyroid tissue resulting in release of the hormones (Type II). Type I is typically seen in patients with underlying goiter or Graves’ disease and occurs within the first few months of Amiodarone use while Type II occurs in patients without preexisting thyroid disease and occurs later in their treatment course.
Conclusions: This case demonstrates simultaneous Amiodarone induced hyperthyroidism and hypothyroidism. Given her lack of goiter and presentation of disease later in her course of Amiodarone treatment (approximately 3 years after initiation), we suspect her hyperthyroidism was Type II; however, a thyroid uptake scan was not performed as they are often uninterpretable due to iodine load associated with Amiodarone administration. While it is likely she had Type II hyperthyroidism, her Free T4 out of proportion to her T3 and her relative lack of hyperthyroid symptoms were likely due to Amiodarone blocking the conversion of T4 to the active hormone, T3. Her concomitant thyroid abnormalities resulted in a largely euthyroid presentation and an interesting study on the drug’s thyroid injury modalities.