Hyaline membrane disease in black newborns: does fetal lung maturation occur earlier?

Abstract We measured the microviscosity of amniotic fluid between 28 and 40 weeks of gestation in 252 normal pregnancies and in 172 pregnancies complicated by factors known to influence fetal lung maturation, including chronic high blood pressure, pregnancy-induced hypertension, diabetes mellitus, and therapy with betamethasone. Comparison of the microviscosity value distributions and regression analysis indicated significantly lower microviscosity values in hypertensive disorders, in Class D and Classes F or R diabetes, and after 48 h of treatment with betamethasone. Few changes were observed in Classes A, B, or C diabetes. These observations are consistent with the accelerated maturation of surfactant observed in chronic intrauterine stress and the lower incidence of hyaline membrane disease reported after glucocorticoids.

Download Full-text

Racial and Environmental Influences on Fetal Lung Maturation

PEDIATRICS ◽

10.1542/peds.68.6.790 ◽

1981 ◽

Vol 68 (6) ◽

pp. 790-795

Author(s):

Samuel Ross ◽

Richard L. Naeye

Keyword(s):

South African ◽

Fetal Lung ◽

Hyaline Membrane Disease ◽

The United States ◽

African Women ◽

The South ◽

Lung Maturation ◽

The Us ◽

Hyaline Membrane ◽

Fetal Lung Maturation

Claims that fetal lung maturation is more rapid in blacks than in whites were investigated. Histologic measurements of lung maturation and the frequency of hyaline membrane disease were compared in four groups of neonates: 490 South African blacks, 841 Ethiopians, 767 US blacks, and 560 US whites. Lungs matured much more rapidly in the Ethiopian and more slowly in the South African than in the US fetuses. The rate of maturation was about the same in US blacks and whites. Hyaline membrane disease was more frequent in the South Africans and less frequent in the Ethiopians than in either US group. Environmental factors in the mother may explain some of these differences. Lungs matured more rapidly in the fetuses of cigarette smokers than in fetuses of nonsmokers. Half of the US mothers but almost none of the South African mothers smoked during pregnancy. The rate of lung maturation had an inverse correlation with maternal body weights. The South African women were heavier and the Ethiopians lighter than women in the United States.

Download Full-text

In Quest of the Prevention of Hyaline Membrane Disease

Annals of Otology Rhinology & Laryngology ◽

10.1177/000348947708600501 ◽

1977 ◽

Vol 86 (5) ◽

pp. 573-576 ◽

Cited By ~ 2

Author(s):

Mary Ellen Avery

Keyword(s):

Fetal Lung ◽

Hyaline Membrane Disease ◽

Maternal Diabetes ◽

Lung Maturation ◽

Familial Predisposition ◽

Surfactant Synthesis ◽

Elective Delivery ◽

Hyaline Membrane ◽

Specific Receptors ◽

Prematurely Born Infants

Hyaline membrane disease or respiratory distress syndrome of prematurely born infants is more common in males, in Caucasians, has a familial predisposition, and is associated with maternal diabetes and delivery by cesarean section before the onset of labor. Now known to be the sequel of surfactant deficiency, it can be predicted prenatally by assay of amniotic liquid for surface active materials produced by the fetal lung. Deficiency of adequate surfactant synthesis or secretion can result in low levels of lecithins and other phospholipids in amniotic liquid. Lung maturation can be accelerated if labor or elective delivery can be deferred at least 24 hours. Glucocorticoids given to the mother cross the placenta and enter fetal lung tissues; specific receptors exist in the lung which permit glucocorticoids to promote cell differentiation and surfactant synthesis precociously. Clinical trials support the efficacy and lack of short-term toxicity of glucocorticoids in human pregnancy after 28 weeks gestation in the event of premature onset of labor. Maternal toxemia, infection or illness which may be aggravated by glucocorticoids may contraindicate prenatal treatment. Postnatally endogenous glucocorticoids accelerate lung maturation, and further administration confers no additional benefit.

Download Full-text

Faculty of 1000 evaluation for Different corticosteroids and regimens for accelerating fetal lung maturation for women at risk of preterm birth.

F1000 - Post-publication peer review of the biomedical literature ◽

10.3410/f.718089952.793484597 ◽

2013 ◽

Author(s):

Monika Gappa

Keyword(s):

At Risk ◽

Preterm Birth ◽

Fetal Lung ◽

Lung Maturation ◽

Fetal Lung Maturation

Download Full-text

Faculty Opinions recommendation of Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.727428659.793572655 ◽

2020 ◽

Author(s):

Katie-Jane Wynne

Keyword(s):

At Risk ◽

Preterm Birth ◽

Fetal Lung ◽

Antenatal Corticosteroids ◽

Lung Maturation ◽

Fetal Lung Maturation

Download Full-text

The cellular mechanism of glucocorticoid acceleration of fetal lung maturation. Fibroblast-pneumonocyte factor stimulates choline-phosphate cytidylyltransferase activity.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)35914-8 ◽

1986 ◽

Vol 261 (5) ◽

pp. 2179-2184 ◽

Cited By ~ 2

Author(s):

M Post ◽

A Barsoumian ◽

B T Smith

Keyword(s):

Fetal Lung ◽

Cellular Mechanism ◽

Lung Maturation ◽

Choline Phosphate ◽

Fetal Lung Maturation

Download Full-text

Molecular regulation of lung maturation in near-term fetal sheep by maternal daily vitamin C treatment in late gestation

Pediatric Research ◽

10.1038/s41390-021-01489-4 ◽

2021 ◽

Author(s):

Erin V. McGillick ◽

Sandra Orgeig ◽

Beth J. Allison ◽

Kirsty L. Brain ◽

Youguo Niu ◽

...

Keyword(s):

Vitamin C ◽

Lung Development ◽

Fetal Lung ◽

Late Gestation ◽

Lung Maturation ◽

Maternal Vitamin ◽

Healthy Pregnancy ◽

Daily Vitamin ◽

Expression Of Genes ◽

Fetal Lung Maturation

Abstract Background In the fetus, the appropriate balance of prooxidants and antioxidants is essential to negate the detrimental effects of oxidative stress on lung maturation. Antioxidants improve respiratory function in postnatal life and adulthood. However, the outcomes and biological mechanisms of antioxidant action in the fetal lung are unknown. Methods We investigated the effect of maternal daily vitamin C treatment (200 mg/kg, intravenously) for a month in late gestation (105–138 days gestation, term ~145 days) on molecular regulation of fetal lung maturation in sheep. Expression of genes and proteins regulating lung development was quantified in fetal lung tissue. The number of surfactant-producing cells was determined by immunohistochemistry. Results Maternal vitamin C treatment increased fetal lung gene expression of the antioxidant enzyme SOD-1, hypoxia signaling genes (HIF-2α, HIF-3α, ADM, and EGLN-3), genes regulating sodium movement (SCNN1-A, SCNN1-B, ATP1-A1, and ATP1-B1), surfactant maturation (SFTP-B and ABCA3), and airway remodeling (ELN). There was no effect of maternal vitamin C treatment on the expression of protein markers evaluated or on the number of surfactant protein-producing cells in fetal lung tissue. Conclusions Maternal vitamin C treatment in the last third of pregnancy in sheep acts at the molecular level to increase the expression of genes that are important for fetal lung maturation in a healthy pregnancy. Impact Maternal daily vitamin C treatment for a month in late gestation in sheep increases the expression of gene-regulating pathways that are essential for normal fetal lung development. Following late gestation vitamin C exposure in a healthy pregnancy, an increase in lung gene but not protein expression may act as a mechanism to aid in the preparation for exposure to the air-breathing environment after birth. In the future, the availability/development of compounds with greater antioxidant properties than vitamin C or more specific targets at the site of oxidative stress in vivo may translate clinically to improve respiratory outcomes in complicated pregnancies at birth.

Download Full-text