**5. Conclusions**

Iodine, as an essential microelement of the human body, plays a very important role in thyroid physiology. Adequate intake is necessary to keep thyroid hormone synthesis at normal rate. Dietary intake and urinary excretion should be equivalent, but a remarkable adaptive capacity of the thyroid gland can compensate for excess intake on short term. However, existing thyroid disease (subclinical or overt) or specific risk factors may impair the patient's response to high iodine exposure, which can result in hypothyroidism or hyperthyroidism. On the other hand, iodine excess may also be hardly recognizable because various sources (e.g. seafood, kelp, dairy products, iodized salt, iodized water, nutritional supplements, iodine containing contrast media, and drugs) can all contribute to iodine intake. Of these, iodine containing contrast media and drugs are administered only under controlled conditions but represent the most frequent cause of iodine-induced thyrotoxicosis. In general, preventive actions are not recommended, but screening for risk factors, such as elderly patients, persons with multinodular goiter, subclinical hyperthyroidism, or manifest hyperthyroidism should take place prior to iodine administration. Consequently, high-risk patients should benefit preventive treatment with thioamide or perchlorate. Amiodarone-induced thyrotoxicosis has remained a difficult task requiring a close collaboration between cardiology and endocrinology to overcome complications, but individualization of the therapy should be undertaken. Based on the specific features of thyrotoxicosis, thioamides, perchlorate, or high-dose glucocorticoids may be considered for an optimal therapeutic intervention. If contraindicated, radioiodine therapy may also be useful to treat amiodarone-induced thyrotoxicosis.

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**Author details**

Romania

Melinda Kolcsár and Zsolt Gáll\*

\*Address all correspondence to: zsolt.gall@umfst.ro

provided the original work is properly cited.

*Prevention and Treatment of Iodine-Induced Thyrotoxicosis*

The authors declare no conflict of interest.

AIT amiodarone-induced thyrotoxicosis ATA American Thyroid Association

ETA European Thyroid Association ICM iodinated contrast media MUIC median urinary iodine content

RDA recommended daily allowances

rT3 reverse 3,3′,5′-triiodothyronine

TSH thyroid stimulating hormone WHO World Health Organization

rhTSH recombinant human thyroid stimulating hormone

University of Medicine, Pharmacy, Sciences and Technology of Târgu Mureș,

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*DOI: http://dx.doi.org/10.5772/intechopen.89615*

CT computed tomography DEA N-desethylamiodarone

RAI radioactive iodine

T4 thyroxine

T3 3,5,3′-triiodothyronine

**Conflict of interest**

**Abbreviations**

*Prevention and Treatment of Iodine-Induced Thyrotoxicosis DOI: http://dx.doi.org/10.5772/intechopen.89615*
