Review article

https://doi.org/10.20471/acc.2022.61.02.20

Amiodarone and Thyroid Dysfunction

Filip Medić ; Department of Obstetrics and Gynecology, Sveti Duh University Hospital, Zagreb, Croatia
Miro Bakula ; Division of Endocrinology, Diabetes and Metabolic Diseases, Department of Internal Medicine, Sveti Duh University Hospital, Zagreb, Croatia; School of Medicine, University of Zagreb, Zagreb, Croatia
Maša Alfirević ; Department of Urology, Sveti Duh University Hospital, Zagreb, Croatia;
Maja Bakula ; Merkur University Hospital, Vuk Vrhovac University Clinic for Diabetes and Metabolism, Zagreb, Croatia
Katarina Mucić ; School of Medicine, University of Zagreb, Zagreb, Croatia
Nikolina Marić ; Intensive Care Unit, Department of Internal Medicine, Sveti Duh University Hospital, Zagreb, Croatia

Abstract

Thyroid gland has a key role in maintaining the body homeostasis. Thyroxine is the
main hormone secreted from the thyroid gland, its effect being predominantly achieved after the intracellular
conversion of thyroxine to triiodothyronine, which exhibits a higher affinity for the receptor
complex, thus modifying gene expression of the target cells. Amiodarone is one of the most commonly
used antiarrhythmics in the treatment of a broad spectrum of arrhythmias, usually tachyarrhythmias.
Amiodarone contains a large proportion of iodine, which is, in addition to the intrinsic effect of the
medication, the basis of the impact on thyroid function. It is believed that 15%-20% of patients treated
with amiodarone develop some form of thyroid dysfunction. Amiodarone may cause amiodarone-induced
hypothyroidism (AIH) or amiodarone-induced thyrotoxicosis (AIT). AIT is usually developed
in the areas with too low uptake of iodine, while AIH is developed in the areas where there is a sufficient
iodine uptake. Type 1 AIT is more common among patients with an underlying thyroid pathology,
such as nodular goiter or Graves’ (Basedow’s) disease, while type 2 mostly develops in a previously
healthy thyroid. AIH is more common in patients with previously diagnosed Hashimoto’s thyroiditis.
Combined types of the diseases have also been described. Patients treated with amiodarone should
be monitored regularly, including laboratory testing and clinical examinations, to early detect any
deviations in the functioning of the thyroid gland. Supplementary levothyroxine therapy is the basis
of AIH treatment. In such cases, amiodarone therapy quite often need not be discontinued. Type 1
AIT is treated with thyrostatic agents, like any other type of thyrotoxicosis. If possible, the underlying
amiodarone therapy should be discontinued. In contrast to type 1 AIT, the basic pathophysiological
substrate of which is the increased synthesis and release of thyroid hormones, the basis of type 2 AIT
is destructive thyroiditis caused by amiodarone, desethylamiodarone as its main metabolite, and an
increased iodine uptake. Glucocorticoid therapy is the basis of treatment for this type of disease.

Keywords

Amiodarone; Thyroid dysfunction; Amiodarone-induced hypothyroidism; Amiodarone-induced thyrotoxicosis

Hrčak ID:

285013

URI

https://hrcak.srce.hr/285013

Publication date:

1.8.2022.

Article data in other languages: croatian

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