Antenatal glucocorticoid treatment affects preterm infants' S100B urine concentration in a dose-dependent manner

Andrea Sannia1, Francesco M Risso, Laura D Serpero

  • 1Dept. of Neonatology Obstetrics and Neuroscience, G Gaslini Children's University Hospital, Genoa, Italy.

Insights

Maternal antenatal glucocorticoid (GC) treatment impacts infant S100B brain damage marker levels dose-dependently. Lower GC courses may reduce brain impact without compromising lung maturation in preterm infants.

Area of Science:

  • Neonatal Medicine
  • Neuroscience
  • Pharmacology

Background:

  • Maternal glucocorticoid (GC) therapy is standard for preterm infant lung immaturity.
  • Emerging evidence suggests potential adverse effects of GCs on the developing Central Nervous System (CNS).

Purpose of the Study:

  • To investigate the dose-dependent effects of antenatal GC administration on CNS function in preterm infants.
  • To assess S100B urine concentrations as a marker of brain damage following varying GC treatment regimens.

Main Methods:

  • A case-control study involving 70 preterm infants (GC vs. control) with mothers receiving complete (GC2), half (GC1), or no GC course.
  • Urine S100B concentrations were measured at four time-points within 72 hours of birth.
  • Neonatal outcomes including respiratory distress syndrome, ventilation duration, intraventricular hemorrhage, and mortality were correlated with S100B levels.

Main Results:

  • Infants exposed to a complete GC course (GC2) showed significantly lower S100B levels compared to controls and the half-course group (GC1) (P<0.01).
  • No significant difference in S100B levels was observed between the control and GC1 groups (P>0.05).
  • Primary neonatal outcomes did not differ significantly between infants receiving half or complete GC courses.

Conclusions:

  • Antenatal GC exposure influences S100B levels in a dose-dependent manner, indicating differential effects on the CNS.
  • Reducing antenatal GC dosage may mitigate potential neurodevelopmental risks without negatively impacting lung maturation.
  • Further research is warranted to confirm the benefits of reduced GC-course regimens.
Abstract

Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Pharmacokinetics in Pediatric Patients: Drug Metabolism01:24

Pharmacokinetics in Pediatric Patients: Drug Metabolism

In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses a challenge in...
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes: