**Conflict of interest**

*Goiter - Causes and Treatment*

case of thioamide allergy, lithium is used to control the hyperthyroidism temporarily [91, 92], but it has a narrow therapeutic range, produces nephrotoxicity, and its efficacy is not well documented. Therefore, it is not recommended by ETA for the type 1 AIT treatment [40]. However, it was reported that lithium-associated rhTSH

Type 2 AIT generally is self-limited and amiodarone is not necessary to discontinue. When the efficacy of non-thioamide type antithyroid drugs to restore euthyroid state was compared, the best results were obtained with 30 mg oral prednisone therapy. The rate of achievement of euthyroid state was 100% when glucocorticoids were used versus 71% obtained after perchlorate administration [94]. ETA recommendation, for this reason, is oral glucocorticoids as the first-line treatment for type 2 AIT. In patients in whom a mixed form of AIT is suspected, thioamides together with glucocorticoids should be given initially, or glucocorticoids should be added after a period of 4–6 weeks of inadequate response [40]. In addition, it must be noted that i.v. administration of glucocorticoids (hydrocortisone, dexamethasone) has crucial benefits (inhibiting T4 transformation to T3) in thyroid storm and preoperative management of any type of thyrotoxicosis [91]. It was reported that glucocorticoid therapy (oral prednisone) restored the normal thyroid function and shrink goiter, preventing surgery, in a patient diagnosed with iodine containing

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.

administration increases RAI sensibility of the thyroid follicles in AIT [93]. After resolution of the acute episode of iodine-induced hyperthyroidism, treatment of the underlying thyroid disease should be addressed. For patients with underlying Graves' disease, treatment options include continuing thiamazole, radioiodine ablation, or surgery. Patients with underlying autonomous adenoma or multinodular goiter who return to euthyroidism after discontinuation of iodine do not necessarily require definitive treatment. However, these patients are at risk for

recurrent hyperthyroidism if given iodine again.

supplement-induced hyperthyroidism [95].

**5. Conclusions**

**70**

The authors declare no conflict of interest.
