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Trummer, C; Theiler-Schwetz, V; Pilz, S.
Amiodarone-induced thyroid disorders.
AUST J CLIN ENDOCR M. 2020; 13(3): 119-123. Doi: 10.1007/s41969-020-00109-6 [OPEN ACCESS]
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Leading authors Med Uni Graz: Pilz Stefan; Trummer Christian
Co-authors Med Uni Graz: Theiler-Schwetz Verena
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Abstract:: Amiodarone, a class III antiarrhythmic drug, has several adverse effects on the thyroid that may lead to both hypothyroidism and hyperthyroidism. On one hand, this can be attributed to its high content of iodine, and on the other hand, amiodarone may cause destructive thyroiditis. Amiodarone-induced hypothyroidism (AIH) is treated with levothyroxine replacement therapy and does not necessitate the discontinuation of amiodarone. Amiodarone-induced thyrotoxicosis (AIT) can be categorized into two subtypes: AIT 1 is the consequence of iodine overload in underlying Graves' disease or thyroid autonomy, while AIT 2 represents a form of destructive thyroiditis. Since the first line therapy differs significantly between the two subtypes, a thorough diagnostic workup is paramount. AIT 1 is primarily treated with thionamides (+/- sodium perchlorate), whereas the initial therapy of choice for AIT 2 is glucocorticoids. In cases where a definitive distinction between the subtypes cannot be made (mixed types/indeterminate types) it is recommended to primarily initiate a therapeutic trial with thionamides or to start a combination therapy with glucocorticoids. While amiodarone does not need to be discontinued in most, especially mild cases of AIT 2, termination of treatment should be considered in AIT 1. In emergency situations and in patients with high cardiovascular risk, thyroidectomy is a possible alternative if immediate treatment is deemed necessary.
Find related publications in this database (Keywords): Amiodarone; Hyperthyroidism; Hypothyroidism; Glucocorticoids; Thionamides