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The contribution of postnatal steroid administration to early brain damage in preterm babies with bronchopulmonary
Sabahattin Ertuğrul1, Savaş Mert Darakci2, İbrahim Kaplan3
1Department of Pediatrics, Division of Neonatology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey
Insights
Neuron-specific enolase (NSE) levels increased in preterm infants with bronchopulmonary dysplasia (BPD) treated with postnatal dexamethasone, indicating early brain damage. This suggests NSE may be a useful biomarker for neurological assessment in these vulnerable infants.
Area of Science:
- Neonatal Medicine
- Neuroscience
- Pediatric Pulmonology
Background:
- Bronchopulmonary dysplasia (BPD) is a common respiratory complication in preterm infants.
- Postnatal corticosteroids, such as dexamethasone, are frequently used to manage BPD.
- Concerns exist regarding potential neurodevelopmental effects of these treatments in premature infants.
Purpose of the Study:
- To investigate early neurological damage in preterm infants with BPD receiving low-dose dexamethasone.
- To assess the utility of specific biomarkers: S100 calcium-binding B (S100B), neuron-specific enolase (NSE), Tau protein (MAPT), and glial fibrillary acid protein (GFAP).
Main Methods:
- A cohort study involving 136 preterm infants with BPD and 64 controls (≤32 weeks gestation).
- Measurement of NSE, S100B, GFAP, and MAPT levels at day 28 and post-treatment in the BPD group.
- Comparison of biomarker levels between BPD and control groups, and within the BPD group before and after treatment.
Main Results:
- Significant differences in GFAP, MAPT, and NSE levels were observed between BPD and control groups at day 28.
- No significant difference in S100B levels was found between the groups at day 28.
- NSE levels showed a statistically significant increase within the BPD group after dexamethasone treatment.
Conclusions:
- Elevated NSE levels in preterm infants with BPD treated with postnatal dexamethasone suggest early brain damage.
- NSE may serve as a potential biomarker for monitoring neurological status in this population.
- Further research is warranted to fully understand the long-term neurological implications.
Background/Aim:
Postnatal corticosteroids are commonly used to treat bronchopulmonary dysplasia (BPD). We aimed to show whether S100 calcium-binding B (S100B), neuron-specific enolase (NSE), Tau protein or microtubule-associated protein tau (MAPT), and glial fibrillary acid protein (GFAP) levels would provide any evidence of early neurological damage in premature infants receiving postnatal low dose dexamethasone therapy for BPD treatment.
Materials And Methods:
In this cohort study, 136 preterm infants diagnosed with BPD at ≤32 weeks of gestation formed the study group, and 64 preterm infants formed the control group. NSE, S100B, GFAP, and MAPT levels were first measured before the postnatal corticosteroid treatment in both the patient and the control group on the 28th day and, for a second time, after treatment termination in the patient group.
Results:
There were significant differences between the measured GFAP, MAPT, and NSE values of the BPD and control groups on the 28th day, whereas there was no significant difference between the measured S100B values of the two groups. There were a statistically significant difference between the NSE values measured on the 28th day and after the treatment within the BPD group, whereas no significant difference existed between the GFAP, MAPT, and S100B values.
Conclusion:
NSE levels, which indicate brain damage in the early period, increased in preterm babies with BPD who had been administered postnatal dexamethasone.
