Amiodarone induced thyrotoxicosis

Amiodarone induced thyrotoxicosis (AIT) is a form of hyperthyroidism due to treatment with antiarrhythmic drug, amiodarone. Amiodarone notably has a large side effect profile, impacting numerous organ systems including the pulmonary, gastrointestinal, neurologic, dermatologic, ophthalmologic, and thyroid systems. Amiodarone induced thyroid dysfunction more commonly results in hypothyroidism, estimated to occur in 6-32% of patients, whereas hyperthyroidism from amiodarone use falls between 1-12%. However, the prevalence of AIT varies based on geographical region, and is more common in areas with low dietary iodine intake, occurring in around 10-12% of patients in those areas. In the United States, clinical manifestations of AIT occur in between 3-5% of patients. AIT may present clinically early after drug initiation or can be delayed up to a few years. Common symptoms associated with AIT closely resemble symptoms of hyperthyroidism, and they include new-onset or recurrence of arrhythmias, worsening of pre-existing heart conditions such as ischemic heart disease or heart failure, unattributed weight loss, and fever. Development of AIT is associated with an increased risk for major adverse cardiovascular events, and increased mortality specifically in patients with AIT and underlying heart failure. Amiodarone has both direct and indirect effects on thyroid function. The most notable indirect thyroid altering property is that the drug is approximately one-third iodine by weight. As a result, amiodarone therapy elevates free circulating iodine levels up to 40 times greater than the iodine intake from the average American diet. Iodine plays a role in thyroid production, and excess iodine levels within the body can result in overproduction of thyroid hormone. Initially, the thyroid reacts according to the auto-regulatory Wolff-Chaikoff effect to prevent an excess of thyroid hormone production. Usually, the thyroid normalizes within 24-48 hours.