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Journal of Clinical Endocrinology & Metabolism, Vol 47, 1073-1077, Copyright © 1978 by Endocrine Society

ARTICLES

Perinatal vitamin D metabolism. IV. Maternal and cord serum 24,25- dihydroxyvitamin D concentrations

LS Hillman, E Slatopolsky and JG Haddad

Fetal and maternal compartments differ in factors shown to regulate 24.25 dihydroxyvitamin D [24,25(OH)2D] metabolism [calcium, phosphorus, and parathyroid hormone (PTH)] such that one might predict that maternal serum 24,25(OH)2D levels are decreased and fetal 24,25(OH)2D concentrations are increased. To evaluate this, 25-hydroxyvitamin D (25OHD), 24,25(OH)2D, calcium, magnesium, calcitonin, and PTH were measured in 24 paired maternal and cord sera. The mean maternal serum 24,25(OH)2D concentration (2.9 +/- 0.26 ng/ml) was significantly lower than that of nonpregnant females (3.9 +/- 0.37 ng/ml). Mean serum PTH and calcitonin levels were, however, normal in maternal sera. The normal elevations of PRL, estrogen, and placental lactogen in serum of pregnant women could possibly decrease 24,25(OH)2D production, as seen in animal experimental systems. There was no correlation (R = -0.25) between 24,25(OH)2D levels in maternal and cord sera, as predicted; however, mean (+/-SE) fetal 24,25(OH)2D (2.5 +/- 0.26 ng/ml) was similar to the mean maternal concentration and significantly below the mean level in normal adults. The low fetal 24,25(OH)2D concentration may be due to 1) decreased 24-hydroxylase capacity of the fetus; 2) regulation by fetal factors other than calcium, phosphorus, and PTH; or 3) increased utilization of 24,25(OH)2D possibly for fetal bone mineralization.


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