Iodine-induced hyperthyroidism synthesis

The use of iodine has been held responsible for the increasing frequency of relapse of Graves disease in the USA. Treatment of more severe cases of iodine-induced hyperthyroidism can be difficult, as thyroid synthesis inhibitors are not immediately active and 131I cannot be used because of low thyroid uptake. The carefully supervised combination of perchlorate and methimazole is effective (40), but surgery has also occasionally been advocated. 

AIT can be categorized into two subtypes, which are termed type 1 and type 2 (Table 96.5). Type 1 AIT is primarily iodine-induced hyperthyroidism that develops in patients with underlying thyroid disease, such as nontoxic multinodular goiter or Graves disease. Synthesis and release of thyroid hormones are increased in type 1 AIT. In contrast, type 2 AIT is a destructive thyroiditis that occurs in persons with no apparent thyroid disease (Basaria and Cooper, 2005 Ursella et al, 2005). Type 1 AIT is more prevalent in iodine-deficient regions and type 2 AIT is more prevalent in iodine-sufficient regions (Daniels, 2001). Thus, type 1 AIT is rare in Japan where dietary iodine intake is high (Sato et al, 1999). 

Endocrine In patients receiving the minimum dose of amiodarone, thyroid abnormalities were observed at a rate between 14% and 18%. The effects on the thyroid gland are variable. Amiodarone may cause abnormal thyroid function detected only by laboratory test as well as clinically manifested thyroid dysfunction. The mechanism of this adverse effect is complex. Amiodarone inhibits the action of deiodinase and decreases peripheral conversion of thyroid hormones. Moreover, it decreases their renal elimination and inhibits their entry to peripheral tissues. The level of T4 increases by 40% within 1-4 months of amiodarone therapy. The deiodinase activity inhibition can be noticed after 3 months of treatment. It leads to an increase in the level of thyroid stimulating hormones. Amiodarone and its metabolite have a direct cytotoxic effect on thyroid follicular cells, which results in destructive thyroiditis. Amiodarone-induced thyroid damage can lead either to hypo- or hyperthyroidism. The latter can be of two types. Type 1 usually occurs in patients with prior thyroid damage. In this type, iodine excess causes excessive synthesis of thyroid hormones whereas in type 2 the inflammatory process is followed by destruction. A destructive thyroiditis leads to the release of hormones from damaged thyroid follicular cells. This mechanism occurs in patients with no history of thyroid disorders [15]. 

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