Thyroid and Brain: Understanding the Actions of Thyroid Hormones in Brain Development and Function

Endemic Goiter and Cretinism: Pathophysiology of Iodine Deficiency

Author(s): Juan Bernal * .

Pp: 83-98 (16)

DOI: 10.2174/9789815274226124010009

* (Excluding Mailing and Handling)

Abstract

Iodine is an essential component of thyroid hormones, and its deficiency causes endemic goiter, cretinism, and a constellation of syndromes known as iodine deficiency disorders. Although iodine deficiency still affects most of the world, national or regional salt iodization programs have increased the number of countries with adequate intake. Endemic cretins were classified as either predominantly neurological or myxedematous (hypothyroid). Severe maternal iodine deficiency causes fetal neurological damage during the first half of gestation, which is prevented by administering iodine to mothers before or early in pregnancy. Myxedematous cretins present thyroid atrophy, hypothyroidism, and growth arrest, and no neurological involvement. Physiological adaptations to iodine deficiency include thyroid growth (goiter) and thyroidal autoregulatory mechanisms leading to decreased serum T4 and preserved serum T3. This situation is known as hypothyroxinemia, as described in Chapter 4. The brain, which depends on the T3 generated locally, shows an increased type 2 deiodinase activity and T3 formation from T4. When iodine intake is severe, these mechanisms cannot maintain T3 concentrations in the brain, leading to brain damage.


Keywords: Cretinism, Dehalogenase, Deiodinases, Goiter, Hypothyroidism, Hypothyroxinemia, Micronutrients, Pregnancy, Selenium.

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