The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the progeny

The adequate functioning of both the maternal and fetal thyroid glands play an important role to ensure that the fetal neuropsycho-intellectual develo pment progresses normally. Three sets of clinical disorders are considered, that may eventually lead to impaired brain development. Firstly, in infant s with a defect of glandular ontogenesis (congenital hypothyroidism), the p articipation of maternal thyroid hormones to the fetal circulating thyroxin e environment is normal and, therefore, risk of brain damage results exclus ively from the insufficient hormone production by the abnormal fetal thyroi d gland. Secondly, when it is only the maternal thyroid gland that is funct ionally deficient (autoimmune hypothyroidism), the severity and temporal oc currence of maternal underfunction will both drive the resulting consequenc es for impaired fetal neuronal development. Clinical situations of this typ e may obviously take place already during early gestation (in women with kn own but untreated hypothyroidism) or appear only during later gestational s tages (in women who have AITD and remain euthyroid during the first half of gestation). Lastly, in conditions with iodine deficiency, both maternal an d fetal thyroid functions are affected and, therfore, it is primarily the d egree and precocity of the maternal hypothyroxinemia due to iodine deficien cy during pregnancy that will drive the potential repercussions for fetal n eurological development. In the present review, we summarize available data and develop our present concepts concerning the complex feto-maternal thyroid relationships and the potential impacts of thyroid function abnormalities on the ideal developme nt of the offspring.