Click here for Frequently Asked Questions on Amiodarone.
Amiodarone is a medication commonly used to treat patients with irregular heart beats, or cardiac arrhythmias. Each amiodarone tablet contains considerable amounts of iodine, which is normally utilized by the thyroid gland for synthesis of thyroid hormone. In about 10% of patients taking thyroid hormone, abnormal thyroid function may develop, leading to either hyperthyroidism or hypothyroidism. An under active thyroid gland following amiodarone therapy is generally simple to treat, although small doses of thyroid hormone are generally initiated initially in most patients with heart disease. For an overview of amiodarone and thyroid function, see Effects of amiodarone therapy on thyroid function Nat Rev Endocrinol. 2010 Jan;6(1):34-41 and Determinants and outcome of amiodarone-associated thyroid dysfunction Clin Endocrinol (Oxf). 2011 Apr 30. doi: 10.1111/j.1365-2265.2011.04087. and J Clin Endocrinol Metab. 2021 Jan 1;106(1):226-236 Evaluation and Treatment of Amiodarone-Induced Thyroid Disorders
Hyperthyroidism in patients taking amiodarone is more problematic than hypothyroidism and can be quite severe. Due to the iodine content of the amiodarone, patients with amiodarone-associated hyperthyroidism may have accumulated considerable stores of thyroid hormone which may be liberated during the course of amiodarone-induced hyperthyroidism. Furthermore, amiodarone is fat soluble and stored in our fat cells for weeks to months even after the medication is discontinued. Although thyroid function may return to normal once amiodarone is discontinued in some patients, it must be recognized that for some patients amiodarone is the only medication that successfully controls their irregular heart arrhythmias, which at times can be life threatening. Accordingly, in these clinical situations, patients may need to continue on the amiodarone and the thyroid dysfunction can usually be treated successfully while the patient stays on the drug.
Due to the marked iodine content of the medication, patients with amiodarone-associated hyperthyroidism generally do not take up exogenously administered iodine, and hence radioactive iodine treatment of this condition will usually not be an option. Accordingly, medications or surgery are the two treatment regimens of choice for hyperthyroid patients on amiodarone.
Following the resolution of the hyperthyroidism, patients may develop hypothyroidism, similar to the clinical course that develops in patients with other forms of thyroiditis. For an overview of amiodarone and the thyroid, see The effects of amiodarone on the thyroid. Endocr Rev. 2001 Apr;22(2):240-54 or The various effects of amiodarone on thyroid function. Thyroid. 2001 May;11(5):511-9 and Effects of amiodarone therapy on thyroid function Nat Rev Endocrinol. 2010 Jan;6(1):34-41. Epub .
Amiodarone-associated hyperthyroidism, or amiodarone-induced thyrotoxicosis (AIT) is generally sub-divided into two types, an iodine-induced hyperthyroid condition (Type 1 AIT), and a destructive form of thyroiditis (Type 2 AIT). The latter form can be particularly severe and may require treatment with glucocorticoids (Steroids). A small pilot study has suggested that in some patients with severe hyperthyroidism from amiodarone, improvement may be obtained using an agent that blocks conversion of T4 top T3. See Lopanoic acid rapidly controls type I amiodarone-induced thyrotoxicosis prior to thyroidectomy. J Endocrinol Invest. 2002 Feb;25(2):176-80.
If amiodarone has so many potentially adverse side effects, why do the doctors still use it to treat heart disease?
Despite the numerous potential side effects that may arise in patients on long term amiodarone therapy, the drug remains remarkably effective for patients with cardiac rhythm disturbances. For example, amiodarone has proven to be more effective than agents such as sotalol or propafenone for the prevention of recurrent atrial fibrillation in a multicenter Canadian study.
I had hyperthyroidism, and now my thyroid is under active, with an elevated TSH. Will my thyroid function return to normal?
Many patients with amiodarone-associated hyperthyroidism will have an illness that resembles thyroiditis, with an initial hyperthyroid phase that resolves, and is followed by a hypothyroid phase. In some cases, the damaged thyroid will gradually repair itself and thyroid function will return to normal. In other instances, the hypothyroidism may be permanent, and treatment with thyroid hormone may be indicated.
I am taking amiodarone and my TSH is now elevated but I feel fine. Do I have to take thyroid hormone?
For most patients with heart disease, it is prudent to normalize thyroid function. As hypothyroidism may affect heart muscle function and drug metabolism (for such drugs as coumadin, the blood thinner), it seems reasonable to optimize thyroid status if it is safe to do so. If the patient has unstable angina and coronary artery disease, then the risks and benefits of gradual thyroid hormone replacement should be discussed with your physician.
I have thyroid disease from amiodarone and I am pregnant. Will the amiodarone affect my baby?
Amiodarone can cross the placenta, and the iodine released from amiodarone can affect thyroid function in the developing baby, as described in Transient fetal hypothyroidism due to direct fetal administration of amiodarone for drug resistant fetal tachycardia. Am J Perinatol. 2001;18(2):113-6.
Is it necessary to use steroids (prednisone) in the treatment of amiodarone-associated hyperthyroidism?
The answer to this question generally depends on the clinical and biochemical severity of the hyperthyroid condition. Many experts advocate an individualized approach, with medications other than steroids used first, followed by introduction of steroids if indicated by the clinical circumstances. See A stepwise approach to the treatment of amiodarone-induced thyrotoxicosis. Thyroid. 2003 Feb;13(2):205-9. and Treatment of Type II Amiodarone-Induced Thyrotoxicosis by Either Iopanoic Acid or Glucocorticoids: A Prospective, Randomized Study. J Clin Endocrinol Metab. 2003 May;88(5):1999-2002.