Hypothyroxinemia is a condition characterized by normal thyroid-stimulating hormone (TSH) concentrations, but maternal free-thyroxine concentrations that are below the normal range for the stage of pregnancy. It occurs in very specific environmental and/or physiological circumstances, namely iodine deficiency and pregnancy. The coexistence of both of these conditions results in the highest risk of gestational hypothyroxinemia in the mothers, because the maternal thyroid gland cannot adapt to the increased hormonal requirements due to inadequate iodine availability. The epidemiological and experimental findings of the last few decades have demonstrated the critical need for adequate fetal thyroid hormone concentrations from the earliest stages of pregnancy, in order to achieve normal neurodevelopment. Whether or not minor degrees of maternal thyroid underfunction can be harmful to the fetal brain has been extensively debated. There is now evidence that maternal hypothyroxinemia during early gestation may lead to irreversible brain damage in the progeny, covering a broad spectrum of neurological phenotypes (endemic cognitive deficiency, minor neurological disorders, ADHD, intelligence deficit and autism). This being the case, early screening programs for maternal thyroid failure in mild-to-moderate ID areas need to be urgently implemented in western countries. The mass screening of pregnant women during the first trimester should consist of either serum FT4 or TSH assay as diagnostic criteria, and monitoring of maternal thyroid function should be encouraged in order to correct maternal hypothyroxinemia promptly and consequently prevent irreversible neurological damage in the progeny.

A Novel Iodine Deficiency Disorder: Gestational Hypothyroxinemia – How Safe is it for Progeny?

MOLETI, MARIACARLA;TRIMARCHI, Francesco;VERMIGLIO, Francesco
2009

Abstract

Hypothyroxinemia is a condition characterized by normal thyroid-stimulating hormone (TSH) concentrations, but maternal free-thyroxine concentrations that are below the normal range for the stage of pregnancy. It occurs in very specific environmental and/or physiological circumstances, namely iodine deficiency and pregnancy. The coexistence of both of these conditions results in the highest risk of gestational hypothyroxinemia in the mothers, because the maternal thyroid gland cannot adapt to the increased hormonal requirements due to inadequate iodine availability. The epidemiological and experimental findings of the last few decades have demonstrated the critical need for adequate fetal thyroid hormone concentrations from the earliest stages of pregnancy, in order to achieve normal neurodevelopment. Whether or not minor degrees of maternal thyroid underfunction can be harmful to the fetal brain has been extensively debated. There is now evidence that maternal hypothyroxinemia during early gestation may lead to irreversible brain damage in the progeny, covering a broad spectrum of neurological phenotypes (endemic cognitive deficiency, minor neurological disorders, ADHD, intelligence deficit and autism). This being the case, early screening programs for maternal thyroid failure in mild-to-moderate ID areas need to be urgently implemented in western countries. The mass screening of pregnant women during the first trimester should consist of either serum FT4 or TSH assay as diagnostic criteria, and monitoring of maternal thyroid function should be encouraged in order to correct maternal hypothyroxinemia promptly and consequently prevent irreversible neurological damage in the progeny.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11570/8404
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