The effects of dexamethasone and anencephaly on newborn serum levels of apolipoprotein A-1

C. R. Parker, P. C. MacDonald, B. R. Carr, J. C. Morrison

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Abstract

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 lipoprotein (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.

Original languageEnglish (US)
Pages (from-to)1098-1101
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume65
Issue number6
StatePublished - 1987

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Anencephaly
Apolipoprotein A-I
Dexamethasone
Newborn Infant
HDL Lipoproteins
Serum
LDL Cholesterol
Hypercholesterolemia
Apoproteins
Umbilical Cord
Lipoproteins
Plasmas
Premature Infants

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

The effects of dexamethasone and anencephaly on newborn serum levels of apolipoprotein A-1. / Parker, C. R.; MacDonald, P. C.; Carr, B. R.; Morrison, J. C.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 65, No. 6, 1987, p. 1098-1101.

Research output: Contribution to journalArticle

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abstract = "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 lipoprotein (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.",
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