Direct evidence of sudden rise in fetal corticoids late in human gestation.
Glucocorticoids accelerate fetal lung maturation in all mammals studied, 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 parturition. 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 origin and its concentration, if sampled at delivery, is affected by maternal stress. 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 glands and is present in greater concentrations in human fetal plasma than in maternal plasma. It is hydrolysed by the placental sulphatases and is a poor substrate for for placental 11 beta- hydroxysteroid dehydrogenase. We report here confirmation that the bulk of maternal BS originates from the fetus, and that its concentration increases suddenly at term.
D000311:Adrenal Glands / Q000196:embryology*; D000757:Anencephaly / Q000196:embryology; D003345:Corticosterone / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism*; D005260:Female; D005865:Gestational Age; D006801:Humans; D007743:Labor, Obstetric; D008431:Maternal-Fetal Exchange; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy
C024200:corticosterone sulfate; D003345:Corticosterone