» Articles » PMID: 33819976

The Contribution of Postnatal Steroid Administration to Early Brain Damage in Preterm Babies with Bronchopulmonary Dysplasia

Overview
Journal Turk J Med Sci
Specialty General Medicine
Date 2021 Apr 5
PMID 33819976
Citations 3
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Prediction of serum neuritin and neuron-specific enolase for prognosis in patients with traumatic brain injury combined with spinal cord injury.

Pu B, Chen Y, Bi Q, Shen J, Wang L, Han Y J Med Biochem. 2025; 43(6):870-878.

PMID: 39876915 PMC: 11771968. DOI: 10.5937/jomb0-45469.


Risk factors and nomogram for the prediction of intracranial hemorrhage in very preterm infants.

Wang Y, Yang Y, Wen L, Li M BMC Pediatr. 2024; 24(1):793.

PMID: 39633312 PMC: 11616105. DOI: 10.1186/s12887-024-05274-0.


Systemic postnatal corticosteroid use for the prevention of bronchopulmonary dysplasia and its relationship to early neurodevelopment in extremely preterm infants.

Esterman E, Goyen T, Jani P, Lowe G, Baird J, Maheshwari R World J Pediatr. 2023; 19(6):586-594.

PMID: 36967444 PMC: 10198830. DOI: 10.1007/s12519-023-00708-8.


No increase in GFAP and S-100B in very preterm infants with mild periventricular leukomalacia or intraventricular hemorrhage: a pilot study.

Koce M, Jerin A, Plut D, Erculj V, Kornhauser Cerar L, Grosek S Croat Med J. 2023; 63(6):564-569.

PMID: 36597568 PMC: 9837718.

References
1.
Catherine R, Vishnu Bhat B, Adhisivam B, Bharadwaj S, Vinayagam V, Chinnakali P . Neuronal Biomarkers in Predicting Neurodevelopmental Outcome in Term Babies with Perinatal Asphyxia. Indian J Pediatr. 2020; 87(10):787-792. DOI: 10.1007/s12098-020-03283-2. View

2.
Celtik C, Acunas B, Oner N, Pala O . Neuron-specific enolase as a marker of the severity and outcome of hypoxic ischemic encephalopathy. Brain Dev. 2004; 26(6):398-402. DOI: 10.1016/j.braindev.2003.12.007. View

3.
Onland W, De Jaegere A, Offringa M, van Kaam A . Systemic corticosteroid regimens for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database Syst Rev. 2017; 1:CD010941. PMC: 6464844. DOI: 10.1002/14651858.CD010941.pub2. View

4.
Doyle L, Ehrenkranz R, Halliday H . Dexamethasone treatment in the first week of life for preventing bronchopulmonary dysplasia in preterm infants: a systematic review. Neonatology. 2010; 98(3):217-24. DOI: 10.1159/000286210. View

5.
Doyle L, Halliday H, Ehrenkranz R, Davis P, Sinclair J . An update on the impact of postnatal systemic corticosteroids on mortality and cerebral palsy in preterm infants: effect modification by risk of bronchopulmonary dysplasia. J Pediatr. 2014; 165(6):1258-60. DOI: 10.1016/j.jpeds.2014.07.049. View