Direct evidence of sudden rise in fetal corticoids late in human gestation

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Abstract
Glucocorticoids accelerate fetal lung maturation in all mammals studied1, and in some species, such as goat and sheep, concentrations of fetal cortisol increase sharply before term, bringing about a train of events leading to parturition2. Studies of cortisol in the umbilical cord blood have revealed no such increase at the end of human pregnancy. But information obtained in that way is difficult to interpret because much of the fetal cortisol is of maternal origin3,4 and its concentration, if sampled at delivery, is affected by maternal stress5. These problems can be avoided to some extent by studying other fetal corticoids. Corticosterone sulphate (Once called compound B, and abbreviated to BS) is produced by fetal adrenal glands6 and is present in greater concentrations in human fetal plasma than in maternal plasma7. It is not hydrolysed by the placental sulphatases and is a poor substrate for placental 11 β-hydroxysteroid dehydrogenase8. We report here confirmation that the bulk of maternal BS originates from the fetus, and that its concentration increases suddenly at term.