Related Experiment Video
Updated: Jun 12, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
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.
Background:
Maternal glucocorticoid (GC) treatment is widely used to prevent lung immaturity in preterm infants. There is growing evidence that GCs may be detrimental to the Central Nervous System (CNS). We investigated whether antenatal GC administration affects CNS function in a dose-dependent manner by measuring urine concentrations of a well-established brain damage marker, S100B.
Methods:
We conducted a case-control-study in 70 preterm infants (1 GC vs 1 control) whose mothers received a complete GC-course (GC2, n=16), half-course (GC1, n=19), and controls (n=35). At four predetermined time-points, in the first 72 h from birth, we assessed S100B urine concentrations, using a commercially available immunoluminometric assay (Lia-mat Sangtec 100, AB Sangtec Medical, Bromma, Sweden). Data were correlated with primary neonatal outcomes (incidence of respiratory distress syndrome, length of ventilatory support and hospital stay, incidence of intraventricular hemorrhage, adverse 7th day neurological follow-up and neonatal death).
Results:
S100B in GC2 group at all monitoring time-points was significantly lower (P<0.01) than controls and GC1 group, while no differences (P>0.05) were evident between controls and GC1 group. No significant differences (P>0.05) were shown in primary outcomes between half or complete GC-course treated groups.
Conclusion:
S100B levels of infants antenatally treated with GCs differed in a dose-dependent manner. Data on primary outcomes suggest that lowering antenatal GC-course may be less detrimental for brain without affecting lung maturation. Further clinical trials are needed to elucidate the low GC-course issue.
Related Concept Videos
Teratogenicity
Pharmacokinetics in Pediatric Patients: Drug Metabolism
Glucose Transporters
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:
