What will most likely enhance surfactant production by fetal type II alveolar cells in a woman at 28 weeks' gestation?

From the Guidelines

Corticosteroids, specifically betamethasone or dexamethasone, will most likely enhance surfactant production by fetal type II alveolar cells in a woman at 28 weeks' gestation. The recommended regimen is betamethasone 12 mg intramuscularly given twice, 24 hours apart, or dexamethasone 6 mg intramuscularly given four times, 12 hours apart. This treatment should be administered to pregnant women between 24 and 34 weeks' gestation who are at risk of preterm delivery within 7 days.

Benefits of Corticosteroids

• Reduce the risk of respiratory distress syndrome
• Reduce the risk of intraventricular hemorrhage
• Reduce the risk of necrotizing enterocolitis
• Reduce overall neonatal mortality in premature infants Corticosteroids work by accelerating fetal lung maturity through direct stimulation of type II pneumocytes to produce surfactant, which reduces surface tension in the alveoli and prevents alveolar collapse during expiration 1. The beneficial effects begin within 24 hours of the first dose and last for at least 7 days, with optimal benefit occurring when delivery occurs between 24 hours and 7 days after completing the course.

Key Considerations

• Antenatal steroids significantly reduce mortality, respiratory distress syndrome, and surfactant use in preterm infants, most consistently in those born between 28 and 34 weeks’ gestation 1.
• Results of observational studies and clinical trials have inferred that antenatal steroids may reduce the need for prophylactic and early rescue surfactant replacement in infants born after 27 to 28 weeks’ gestation 1.

From the Research

Surfactant Production Enhancement

The administration of corticosteroids, such as dexamethasone or betamethasone, will most likely enhance the production of surfactant by fetal type II alveolar cells in a woman at 28 weeks' gestation.

• Corticosteroids stimulate the production of surfactant phospholipids by alveolar type II cells, enhance the expression of surfactant-associated proteins, and accelerate overall structural maturation of the lungs 2.
• Betamethasone has been shown to increase surfactant phospholipids, phosphatidylinositol, and disaturated phosphatidylcholine in premature rabbits 3.
• Dexamethasone has been found to increase surfactant protein-B (SP-B) mRNA in alveolar and bronchiolar epithelium, indicating an increase in surfactant production 4.
• The combination of antenatal corticosteroids and postnatal surfactant treatment has been shown to have synergistic beneficial effects on neonatal lung function 2, 5.
• Steroid-mediated downregulation of natriuretic peptide receptor-C (NPR-C) in neonatal lungs may provide a novel mechanism for their effect on perinatal surfactant production 6.

Comparison of Treatment Options

• Beta-sympathomimetic drugs, such as ritodrine, may not have a significant effect on surfactant production and may even decrease it at high doses 3.
• Antenatal corticosteroids, such as dexamethasone, have been shown to have an additive effect with exogenous surfactant replacement therapy in reducing the incidence and severity of respiratory distress syndrome in preterm infants 5.