Fetal thyroid hormone plays a role in the normal development of virtually all fetal tissues, especially the brain (Forhead, 2014; Rovet, 2014). Its inluence is illustrated by congenital hyperthyroidism, which develops when maternal thyroidstimulating antibody crosses the placenta to stimulate the fetal gland to secrete thyroxine (Donnelley, 2015). These fetuses develop large goiters as shown in Figure 58-3 (p. 1121). They also display tachycardia, hepatosplenomegaly, hematological abnormalities, craniosynostosis, and growth restriction. As children, they have perceptual motor diiculties, hyperactivity, and reduced growth (Wenstrom, 1990). Fetal thyroid disease and its treatment are discussed in Chapter 16 (p. 318) . Neonatal efects of fetal thyroid deficiency are discussed in Chapter 58 (p. 1126).
The placenta prevents substantial passage of maternal thyroid hormones to the fetus by rapidly deiodinating maternal T 4 and T 3 to form reverse T 3' a relatively inactive thyroid hormone (Vulsma, 1989). Several antithyroid antibodies cross the placenta when present in high concentrations (Pelag, 2002). Those include the long-acting thyroid stimulators (LATS), LATSprotector (LATS-P), and thyroid-stimulating immunoglobulin (TSI). It was previously believed that normal fetal growth and development, which occurred despite fetal hypothyroidism, provided evidence that T 4 was not essential for fetal growth. It is now known, however, that growth proceeds normally because small quantities of maternal T4 prevent antenatal cretinism in fetuses with thyroid agenesis (Forhead, 2014; Vulsma, 1989).
The fetus with congenital hypothyroidism typically does not develop stigmata of cretinism until after birth (Abduljabbar, 2012). Because administration of thyroid hormone will prevent this, by state law, all newborns are tested for high serum levels ofTSH (Chap. 32, p. 614).
Immediately after birth, thyroid function and metabolism undergo major change. Cooling to room temperature evokes sudden and marked increase in TSH secretion. his in turn causes a progressive increase in serum T 4 levels that are maximal 24 to 36 hours after birth. here are nearly simultaneous eleva tions of serum T levels.
These glands develop from two separate tissues. The medulla derives from neural crest ectoderm, whereas the fetal and adult cortex arise from intermediate mesoderm. The gland grows rapidly through cell proliferation and angiogenesis, cellular migration, hypertrophy, and apoptosis (Ishimoto, 2011). Fetal glands are much larger in relation to total body size than in adults. he bulk is made up of the inner or fetal zone of the adrenal cortex and involutes rapidly after birth. his zone is scant to absent in rare instances in which the fetal pituitary gland is congenitally absent. he function of the fetal adrenal glands is discussed in detail in Chapter 5 (p. 104).
Infections in utero have provided an opportunity to examine mechanisms of the fetal immune response. Evidence of immunological competence has been reported as early as 13 weeks (Kohler, 1973; Stabile, 1988). In cord blood at or near term, the average level for most components is approximately half that of the adult values (Adinolfi, 1977).