Since the control of production and clearance of plasma
lipoproteins in utero is largely unknown, we sought to evaluate the effects of glucocorticosteroid (
dexamethasone) treatment of developing fetuses and of chronic intrauterine
hypercholesterolemia, due to fetal
anencephaly, on newborn serum levels of
apolipoprotein A-1 (Apo A-1), the major
apoprotein of
high density lipoproteins (HDL). Among preterm newborn infants (26-32 weeks gestation), the total, HDL, and
low density lipoprotein cholesterol levels in umbilical cord serum of 11 newborns exposed to 4 doses of
dexamethasone (5 mg each) within 1 week of delivery [mean, 3.05 +/- 1.01 (+/- SD), 0.83 +/- 0.18, and 1.84 +/- 0.69 mmol/L, respectively] and of 3 anencephalic newborns (2.84 +/- 0.57, 0.83 +/- 0.36, and 1.89 +/- 0.54 mmol/L) were increased to a similar extent over those in 17 normal newborns (1.76 +/- 0.16, 0.62 +/- 0.16, and 1.14 +/- 0.13 mmol/L). On the other hand, umbilical cord serum
Apo A-1 levels were markedly increased only in the
dexamethasone-treated preterm newborns (1.35 +/- 0.55 g/L; anencephalic, 0.78 +/- 0.15 g/L; normal, 0.68 +/- 0.06 g/L). Also, whereas serum total, HDL, and
low density lipoprotein cholesterol levels in 5 term anencephalic newborns (3.85 +/- 1.37, 1.06 +/- 0.08, and 2.64 +/- 0.91 mmol/L) were substantially higher than those in 41 normal term newborns (1.42 +/- 0.28, 0.57 +/- 0.12, and 0.74 +/- 0.05 mmol/L), serum
Apo A-1 levels were similar at term in anencephalic (1.01 +/- 0.30 g/L) and normal newborns (0.99 +/- 0.08 g/L). Normal
Apo A-1 and
lipoprotein cholesterol levels were found in an additional newborn who was delivered 30 days after exposure to
dexamethasone. We conclude that intrauterine glucocorticosteroid treatment leads to transiently increased serum
Apo A-1 levels in the newborn. This increase, however, is not likely to be secondary consequence of the
hypercholesterolemia that also occurs in such newborns, since
hypercholesterolemia of a similar extent in anencephalic newborns, who have atrophic adrenals, was not associated with marked changes in serum
Apo A-1 levels.