Thyroid dysfunction in fetuses and newborns

There is an increased demand for thyroid hormones during pregnancy. This is due to an increase in thyroxine-binding globulin, placental type 3 deiodinase, and placental transfer of maternal thyroxine to the fetus. Thyroxine is essential for fetal neurodevelopment. Therefore it is critical that maternal delivery of thyroxine to the fetus is ensured early in gestation. Cretinism occurs from severe iodine deficiency because the mother’s body is unable to manufacture thyroxine for transport to the fetus, especially in the first trimester. Persistently low levels of thyroxine at 12 weeks of gestation are associated with an 8–10-point deficit in mental and motor function scores in infants, compared to children of mothers with normal thyroid function. Other thyroid conditions in fetuses and newborns include congenital goiter, thyroid agenesis or dysplasia, transient hypothyroidism, and consumptive hypothyroidism.