Amiodarone, a potent antiarrhythmic medication, can induce both hypothyroidism and hyperthyroidism due to its high iodine content and direct toxic effects on thyroid cells
Amiodarone-induced hypothyroidism (AIH)
- AIH occurs due to the Wolff-Chaikoff effect, where excess iodine inhibits thyroid hormone synthesis.
- The European Thyroid Association (ETA) 2018 guidelines recommend initiating levothyroxine treatment in all patients with overt AIH. In some subclinical cases, particularly in the elderly, treatment may be avoided but with frequent assessment of thyroid status to monitor possible progression to overt hypothyroidism
- Amiodarone should not be discontinued in patients with AIH
Amiodarone-induced thyrotoxicosis (AIT)
- AIT is classified into two types: Type 1 and Type 2.
- Type 1 AIT occurs in patients with preexisting thyroid disease, such as multinodular goiter or latent Graves disease, and is due to iodine-induced increased thyroid hormone synthesis.
- Type 2 AIT is a destructive thyroiditis resulting from direct toxic effects of amiodarone on thyroid follicular cells, leading to the release of preformed thyroid hormones.
- The ETA 2018 guidelines recommend initiating antithyroid drugs as the medical treatment of choice in most patients with Type 1 AIT
- For Type 2 AIT, the ETA 2018 guidelines recommend initiating oral corticosteroids as first-line therapy in patients with moderate-to-severe thyrotoxicosis
- In patients with life-threatening arrhythmias or with critical illness and poor prognosis, amiodarone may be continued
In conclusion, amiodarone can induce both hypothyroidism and thyrotoxicosis, and the management of these conditions depends on the type and severity of the thyroid disorder, as well as the patient's overall clinical status