Only in human pregnancy is the fetus exposed to high concentrations of estrogens throughout gestation, owing to the unique interplay of steroidogenesis between fetus, placenta, and mother. It is well recognized that both the fetal and maternal adrenal glands contribute to placental estrogen synthesis by secretion of steroidal precursor androgens.1 The principal estrogen of human pregnancy, estriol, is produced in disproportionately large quantities because of the extensive 16α-hydroxylation of fetal dehydroepiandrosterone sulfate (DHEAS) in fetal liver and other tissues. 16α-Hydroxy DHEAS is directly converted to estriol within the placenta by the abundant sulfatase, 3β-hydroxysteroid dehydrogenase-isomerase, and aromatase enzymes contained therein. Thus, the fetus is the source of most of the estriol precursor during pregnancy. Fetal and maternal DHEAS secretion contribute roughly one half of the precursor for placental estradiol synthesis late in pregnancy. Although most of the placental estrogen is secreted into the maternal circulation, a large quantity is delivered to the fetus via the umbilical vein. Table I lists the approximate concentrations of free estrone, estradiol, and estriol, as well as progesterone, in umbilical venous and arterial plasma as compared with the concentrations found in the maternal circulation at term of normal pregnancy. It can be seen that the concentration of estriol is approximately ten times that of estradiol and five times greater than that of estrone entering the fetus. The level of estradiol in the fetal circulation (5 to 6 ng/ml at term) is 10 to 20 times higher than that found in the normal adult female just prior to the midcycle gonadotropin surge.
- Copyright © 1978 by the American Academy of Pediatrics