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Hypothyroidism Pathophysiology – Thyroid Hormone Deficit in Pregnancy


A gradual interest has been raised in medical community to the thyroid deficits in pregnant woman and the upcoming neuropsychological development of her baby.


Such topic represents a very significant problem that has, unluckily, been rather understood in a wrong way many times. Even discontinuing thyroid hormone treatment by women discovering they were pregnant, a number of them following a recommendation from their doctors, and others as a consequence of fear for the possible dangerous result of thyroid medicines on the fetus.

Scarcity in thyroid hormones, plus the birth of children with congenital hypothyroidism, are permanent cost of the iodine deficiency and can simply be blocked within the earliest months of development with a sufficient provision of iodine. Such discovery is in conformity with the extremely early growth of nervous system formation that is typically injured in neurological cretinism.

It is very important to elucidate whether the main issue producing inferior neurodevelopment of the infant is: 1) maternal hypothyroidism; or 2) maternal hypothyroxinemia.

Significant knowledge acquired from basic science, clinical and epidemiological studies robustly propose that thyroid status of the mother, particularly in near the beginning of pregnancy, is directly associated to the survival and neuropsychological development of the progeny.

Subsequent to extended annotations about children with congenital hypothyroidism born in regions with prevalent goiter, an essential task of maternal thyroid function was assumed; therefore it is of the most significance to find out relevant data about the prenatal record of all backward children and to study the mother for thyroid deficiency.

At present is currently argued the likelihood of keeping away from potentially avoidable changes of neuropsychological development by testing pregnant women for maternal thyroid hormone insufficiencies.

Approximately 40 years ago information was accessible that suggested the incapacity of the pregnant women to augment their little circulating thyroxine and this fact was causally associated to the birth of children with congenital hypothyroidism. Subsequently, several teams of medical researchers offered persuasive proof that hypothyroxinemia in the mother early in pregnancy is not only the origin of reproductive malfunction and the birth of neurological cretins, but too of mild cerebral insufficiencies that involve a great quantity of the actually healthy people of the identical region.

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