Abstract
Over the past four decades, a substantial body of evidence has emerged
demonstrating the permeability of the placenta to thyroid hormones. Maternal thyroid
hormones cross the placental barrier, becoming present in embryonic tissues well
before the onset of thyroid gland function in both rodents and humans. This raises a
fundamental question regarding the extent to which certain early developmental
processes rely on maternal hormonal influence. While this concept is firmly supported
by robust experimental data in rodents, the situation in humans is more nuanced.
Numerous clinical observations suggest that a reduction in T4 levels in the blood of
otherwise euthyroid pregnant women, a condition known as hypothyroxinemia, may
have adverse effects on fetal development. However, clinical trials aimed at assessing
the impact of treating maternal hypothyroxinemia with T4 have yielded disappointing
results thus far, leaving the matter unresolved.
