Endocrine Abstracts

Thyroid hormone is required for normal brain development from early fetal life onwards. Maternal transfer of thyroxine (T4) constitutes a major fraction of fetal serum T4 in the first half of pregnancy. Early in gestation thyroid hormone receptors with T3 bound to it have been found in different human tissues, while type II deiodinase activity is present in human cortex.

In case of fetal and maternal hypothyroidism, severe mental retardation, combined with hearing deficit and muscle rigidity is the resulting clinical picture.

A more subtle picture has been described in association with increased maternal TSH and/or decreased maternal FT4 values in the first half of pregnancy. In 7-9 year old offspring of women with elevated TSH the full scale IQ was 4 points lower compared with those born from women with normal TSH; if FT4 was decreased in addition, this difference was 7 points. In another study a maternal FT4 value in the 12the week of pregnancy in the lowest 10 percentile range was associated with 8–10 points lower score of the offspring at 1 and 2 years both on the mental and motor domain. Also decreased visual contrast sensitivity was found in 3–6 month old offspring of women with hypothyroidism during pregnancy, as well as increased incidence of attention deficit hyperactivity disorder at the age of 10. These development impairments may be comparable with those of very preterm infants with transient hypothyroxinemia.

In the rat, a mild and transient period of maternal hypothyroxinemia has been found to affect radial distribution of certain neurons in the somatosensory cortex and hippocampus, with alterations of inhibitory circuits.

Although these papers all point towards deleterious consequences for cognitive and behavioural development of low maternal FT4 early in pregnancy, the lower normal limit for FT4 in pregnancy is not known presently.