Amiodarone: Dysrhythmic Drug with Thyroid Effects

Clinicians are most likely to prescribe amiodarone when they see patients who have recurrent ventricular dysrhythmias; paroxysmal supraventricular dysrhythmias including atrial fibrillation and flutter; and or need sinus rhythm maintenance after electrical cardioversion for atrial fibrillation.

Clinicians are most likely to prescribe amiodarone when they see patients who have recurrent ventricular dysrhythmias; paroxysmal supraventricular dysrhythmias including atrial fibrillation and flutter; and or need sinus rhythm maintenance after electrical cardioversion for atrial fibrillation. Patients tolerate amiodarone well even if they have comorbid impaired left ventricular systolic function. However, like most drugs, it is less than an ideal intervention and can cause some adverse effects on various organs.

The October 2014 issue of the journal Internal and Emergency Medicine contains a review article that covers amiodarone’s effects on the thyroid gland.

The authors structure the article to look at amiodarone’s complex effects on thyroid physiology. They note that patients treated chronically with this drug often experience substantial changes in thyroid function tests, although most remain clinically euthyroid. Up to 20% of patients, however, develop amiodarone-induced hypothyroidism (AIH) or thyrotoxicosis (AIT).

Amiodarone’s thyroid effects result from two major mechanisms:

  • Intrinsic amiodarone-associated effects include inhibition of I 50-deiodinase which decreases monodeiodination of T4 to triiodothyronine (T3), creating noteworthy changes in thyroid-stimulating hormone (TSH) concentrations as early as the first days of therapy. This effect may be sustained for several months after patients stop taking amiodarone.
  • Its iodine-associated effects are generally seen in people with impaired autoregulation; exposure to supraphysiological levels of iodine may lead to AIT (Jod-Basedow phenomenon). Amiodarone may aggravate pre-existing thyroid autoimmune conditions in susceptible individuals.

Distinguishing the mechanisms underlying a specific patient’s amiodarone-induced thyroid issue is challenging, and the authors describe the clinical, laboratory, and imaging features that inform a correct diagnosis. They also address management techniques.

Although dronedarone is a new antiarrhythmic and alternative to amiodarone, it has been shown to be a poor choice for patients with heart failure and left ventricular dysfunction because of the risk of hepatic injury and increased mortality. Thus, amiodarone and its effects on various organ systems will remain a concern for endocrinologists. The authors urge clinicians to discuss therapeutic approaches with patients and their general practitioners, cardiologists, and endocrinologists.