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Dosing and formulation of antenatal corticosteroids for fetal lung maturation and gene expression in rhesus macaques

Augusto F Schmidt1,2,3, Paranthaman S Kannan4, James P Bridges4,5

  • 1Division of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. aschmidt@med.miami.edu.

Scientific Reports
|June 23, 2019
PubMed

Insights

Low-dose antenatal corticosteroids (ANS) using betamethasone-acetate (Beta-Ac) alone effectively mature fetal lungs and reduce exposure to corticosteroids compared to the standard clinical drug.

Area of Science:

  • Perinatal Medicine
  • Developmental Biology
  • Pharmacology

Background:

  • Antenatal corticosteroids (ANS) are crucial for preventing respiratory distress syndrome in premature infants.
  • Current ANS dosing regimens require optimization for efficacy and reduced fetal exposure.
  • The standard clinical drug is a mixture of betamethasone-phosphate and betamethasone-acetate (Beta-Ac).

Purpose of the Study:

  • To evaluate the efficacy of slow-release betamethasone-acetate (Beta-Ac) alone in promoting fetal lung maturation.
  • To assess the impact of Beta-Ac on fetal corticosteroid exposure and potential toxic effects.
  • To compare the effects of Beta-Ac alone versus the clinical drug on fetal gene expression.

Main Methods:

  • A primate model (pregnant rhesus macaques) was used at 127 days of gestation.
  • Animals were treated with either the clinical drug (0.25 mg/kg) or Beta-Ac (0.125 mg/kg).
  • Lung function (compliance, surfactant concentration) and transcriptome analyses were performed.

Main Results:

  • Beta-Ac alone enhanced fetal lung compliance and surfactant concentration similarly to the clinical drug.
  • Transcriptome analysis showed less suppression of immune and developmental genes with Beta-Ac compared to the clinical drug.
  • The clinical drug suppressed neuronal development genes in the fetal hippocampus, while Beta-Ac did not.

Conclusions:

  • Low-dose antenatal corticosteroids with Beta-Ac alone is a potential alternative to the current standard treatment.
  • This approach may offer equivalent lung maturation benefits with reduced fetal corticosteroid exposure and toxicity.
  • Further human trials are warranted to assess the efficacy of Beta-Ac in low-dose ANS treatment.

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