The transplacental passage of thyroid hormones (TH) from the maternal to fetal circulations is important for normal fetal development, particularly the fetal central nervous system. This is particularly so before the onset of endogenous fetal TH production from the second trimester of pregnancy. The human hemochorial placenta regulates the quantity of TH passing through and the complement of the different forms of TH to ensure requisite levels are present in the fetus for each stage of development. Transplacental TH supply to the fetus is modulated by several factors including plasma membrane TH transporters which regulate the passage of TH in and out of cells, the metabolism of TH by iodothyronine deiodinases, as well as TH binding to several different proteins within placental cells themselves. In pathological situations of either maternal or fetal TH deficiency during pregnancy, the placenta appears to lack the full compensatory mechanisms required to optimize maternal-fetal transfer of TH to achieve normal fetal TH levels, and this may contribute to the development of neurodevelopmental delay associated with such conditions. Thus, maintaining normal maternal TH status is likely to be the primary factor in ensuring adequate transplacental TH passage and iodide supply to the fetus.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology