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. 1998 Feb;79(2):121–127. doi: 10.1136/hrt.79.2.121

Amiodarone and the thyroid: a practical guide to the management of thyroid dysfunction induced by amiodarone therapy

C Newman 1, A Price 1, D Davies 1, T Gray 1, A Weetman 1
PMCID: PMC1728611  PMID: 9538302

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Figure 1  .

Figure 1  

Structure of amiodarone and thyroid hormones.

Figure 2  .

Figure 2  

Synthetic pathway of thyroid hormones. The organification of oxidised iodine takes place at the apical membrane of the thyrocyte and involves iodination of tyrosine residues on thyroglobulin (TG) molecules stored in the thyroid follicular colloid. Monoiodotyrosine (MIT) residues and diiodotyrosine (DIT) residues within the same and adjacent thyroglobulin molecules then combine to form triiodothyronine (T3, the major biologically active hormone), thyroxine (T4), and, to a limited extent, the inactive compound reverse triiodothyronine (rT3). Thyroid hormones are cleaved from thyroglobulin after pinocytosis of colloid into the thyrocyte, and are then released into the circulation. The thyroid gland is the only source of circulating T4, whereas 80% of circulating T3 is generated by deiodination of T4 in peripheral tissues, especially the liver. The sites of action of antithyroid drugs are highlighted. TPO, thyroid peroxidase; I*, oxidised form of iodide.

Figure 3  .

Figure 3  

Suggested protocol for screening thyroid function in patients treated with amiodarone. TPO, thyroid peroxidase; * amiodarone withdrawal considered an alternative option in some cases.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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