Hypothyroidism Pathophysiology - Maternal Hypothyroxinemia

The notion of hypothyroxinemia of the mother wasestablished a comparable association among first
established as as the amount in the blood of thyroxine,trimester thyroxine and the early neurodevelopment of
under the standard value for women in the identicalbabies born from treated mothers with hypothyroidism.
trimester of pregnancy, regardless if hypothyroidismThese investigations did not discover important
was clinically apparent or not. Pertinent information isassociations when the neurodevelopmental result was
available from research performed in regions withoutlinked to maternal TSH, or to thyroxine later in
severe iodine deficiency, which have suggested apregnancy. The result that thyroxine amount after
significant function of maternal thyroxine in themidgestation are not interconnected with the
conclusion of the pregnancy and in thedevelopmental effect does not indicate that after
neuropsychological development of the offspring,midgestation the defensive outcome of maternal
offering growing proof that is the decisive cause inthyroxine has been vanished, or that the fetal brain no
maternal hypothyroxinemia early in development.longer have need of thyroid hormone.
There are a lot of information concerning thePunctual postnatal management of children without
augmented amount of failed or difficult pregnancies inthyroid gland function avoids the cruel mental
maternal hypothyroxinemia including congenitalretardation that was connected with this disease when
malformations, complications at delivery, perinatalstart of management was postponed. This very
deaths, births before term, spontaneous abortions, etcoptimistic result has been quoted as argument that the
and their association to first trimester low thyroxine, buthuman fetal brain does not require thyroid hormone for
not to thyroxine near term; treatment near thenormal development before birth. It has been argued
beginning to avoid such complications has beenan optional reason about that the fetal encephalon is
proposed. Such original investigations not just illustratescommonly protected by the regular thyroid condition of
the level of interest to the reduced cerebral maturity oftheir mothers. In other words, when thyroid hormone
the children of hypothyroxinemic women but alsovalues of the mother are not regular during pregnancy
described that this negative outcome was blocked byand thyroid function in the fetus is injured as well,
sufficient and early improvement of the maternalneurological break and mental retardation of the infant
hypothyroxinemia with thyroid supplementation.would be as brutal as in neurological cretinism, even
Some studies have confirmed data contrastingthough instantaneous postnatal management of the
indicators during prenatal growth, calculated at differentnewborn with thyroxine.
ages, with maternal thyroxine. Such studies have