The contribution of postnatal steroid administration to early brain damage in preterm babies with bronchopulmonary dysplasia
The contribution of postnatal steroid administration to early brain damage in preterm babies with bronchopulmonary dysplasia
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.Key words: Bronchopulmonary dysplasia, neuron-specific enolase, microtubule-associated proteins, glial fibrillary acidic protein, S100 proteins
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- 1. Stoll BJ, Hansen NI, Bell EF, Shankaran S, Laptooket AR et al. Neonatal outcomes of extremely preterm infants from the NICHD Neonatal Research Network. Pediatrics 2010; 126 (3): 443-456. doi: 10.1542/peds.2009-2959
- 2. Doyle LW, Ehrenkranz RA, Halliday HL. Dexamethasone treatment in the first week of life for preventing bronchopulmonary dysplasia in preterm infants: a systematic review. Neonatology 2010; 98 (3): 217-224. doi: 10.1159/000286210
- 3. Onland W, De Jaegere AP, Offringa M, van Kaam A. Systemic corticosteroid regimens for prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Library: Cochrane Reviews 2017; 31; 1 (1): CD010941. doi: 10.1002/14651858. CD010941.pub2
- 4. Gray PH, O’Callaghan MJ, Rogers YM. Psychoeducational outcome at school age of preterm infants with bronchopulmonary dysplasia. Journal of Paediatrics and Child Health 2004; 40 (3): 114-120. doi: 10.1111/j.1440-1754.2004.00310.x
- 5. Qin G, Lo JW, Marlow N, Calvert SA, Greenough A et al. Postnatal dexamethasone, respiratory and neurodevelopmental outcomes at two years in babies born extremely preterm. PLoS One 2017; 19; 12 (7): e0181176. doi: 10.1371/journal. pone.0181176
- 6. Doyle LW, Halliday HL, Ehrenkranz RA, Davis PG, Sinclair JC. An update on the impact of postnatal systemic corticosteroids on mortality and cerebral palsy in preterm infants: effect modification by risk of bronchopulmonary dysplasia. The Journal of Pediatrics 2014; 165 (6): 1258-1260. doi: 10.1016/j. jpeds.2014.07.049
- 7. Lim G, Lee BS, Choi YS, Park HW, Chunget ML et al. Delayed dexamethasone therapy and neurodevelopmental outcomes in preterm infants with bronchopulmonary dysplasia. Pediatrics and Neonatology 2015; 56 (4): 261-267. doi: 10.1016/j. pedneo.2014.11.006
- 8. Doyle LW, Davis PG, Morley CJ, McPhee A, Carlin JB; DART Study Investigators. Outcome at 2 years of age of infants from the DART study: a multicenter, international, randomized, controlled trial of low-dose dexamethasone. Pediatrics 2007; 119 (4): 716-721. doi: 10.1542/peds.2006-2806
- 9. Bersani I, Pluchinotta F, Dotta A, Savarese I, Campi F et al. Early predictors of perinatal brain damage: the role of neurobiomarkers. Clinical Chemistry and Laboratory Medicine 2020; 26; 58 (4): 471-486. doi: 10.1515/cclm-2019- 0725
- 10. Jarjour IT. Neurodevelopmental outcome after extreme prematurity: a review of the literature. Pediatric Neurology 2015; 52 (2): 143-152. doi: 10.1016/j.pediatrneurol.2014.10.027
- 11. Jia W, Lei X, Dong W, Li Q. Benefits of starting hypothermia treatment within 6 h vs. 6-12 h in newborns with moderate neonatal hypoxic-ischemic encephalopathy. BMC Pediatrics 2018; 12; 18 (1): 50. doi: 10.1186/s12887-018-1013-2
- 12. Ennen CS, Huisman TA, Savage WJ, Northington FJ, Jennings JM et al. Glial fibrillary acidic protein as a biomarker for neonatal hypoxic-ischemic encephalopathy treated with wholebody cooling. American Journal of Obstetrics and Gynecology 2011; 205 (3): 251. e1-7. doi: 10.1016/j.ajog.2011.06.025
- 13. Florio P, Abella R, Marinoni E, Iorio RD, Volti GL et al. Biochemical markers of perinatal brain damage. Frontiers in Bioscience (Scholar Edition) 2010; 1; 2: 47-72. doi: 10.2741/s45
- 14. Lv HY, Wang QL, Chen HY, You YJ, Ren PS et al. Study on serum Tau protein level and neurodevelopmental outcome of placental abruption with neonatal hypoxic-ischemic encephalopathy. The Journal of Maternal-Fetal & Neonatal Medicine 2019; 28; 1-7. doi: 10.1080/14767058.2019.1588878
- 15. Carson R, Monaghan-Nichols AP, DeFranco DB, Rudine AC. Effects of antenatal glucocorticoids on the developing brain. Steroids 2016; 114: 25-32. doi: 10.1016/j.steroids.2016.05.012
- 16. Filippone M, Nardo D, Bonadies L, Salvadori S, Baraldi E. Update on postnatal corticosteroids to prevent or treat bronchopulmonary dysplasia. American Journal of Perinatology 2019; 36 (S 02): S58-S62. doi: 10.1055/s-0039- 1691802
- 17. Blennow M, Sävman K, Ilves P, Thoresen M, Rosengren L. Brain-specific proteins in the cerebrospinal fluid of severely asphyxiated newborn infants. Acta Paediatrica 2001; 90 (10): 1171-1175. doi: 10.1080/080352501317061594
- 18. Chaparro-Huerta V, Flores-Soto ME, Merin Sigala ME, de León JCB, Lemus-Varela ML et al. Hypoxic-ischemic encephalopathy following perinatal asphyxia in newborns. Pediatrics and Neonatology 2017; 58 (1): 70-76. doi: 10.1016/j. pedneo.2016.05.001
- 19. Lu H, Huang W, Chen X, Wang Q, Zhang Q et al. Relationship between premature brain injury and multiple biomarkers in cord blood and amniotic fluid. The Journal of MaternalFetal & Neonatal Medicine 2018; 31 (21): 2898-2904. doi: 10.1080/14767058.2017.1359532
- 20. Summanen M, Seikku L, Rahkonen P, Stefanovic V, Teramo K et al. Comparison of umbilical serum copeptin relative to erythropoietin and S100B as asphyxia biomarkers at birth. Neonatology 2017; 112 (1): 60-66. doi: 10.1159/000456063
- 21. León-Lozano MZ, Arnaez J, Valls A, Arca G, Agut T et al. Cerebrospinal fluid levels of neuron-specific enolase predict the severity of brain damage in newborns with neonatal hypoxic-ischemic encephalopathy treated with hypothermia. PLoS One 2020; 1; 15 (6): e0234082. doi: 10.1371/journal. pone.0234082
- 22. Garcia-Alix A, Cabañas F, Pellicer A, Hernanz A, Stiris TA et al. Neuron-specific enolase and myelin basic protein: relationship of cerebrospinal fluid concentrations to the neurologic condition of asphyxiated full-term infants. Pediatrics. 1994; 93 (2): 234-240
- 23. Sun J, Li J, Cheng G, Sha B, Zhou W. Effects of hypothermia on NSE and S-100 protein levels in CSF in neonates following hypoxic/ischaemic brain damage. Acta Paediatrica 2012; 101 (8): e316-320. doi: 10.1111/j.1651-2227.2012.02679.x
- 24. Catherine RC, Vishnu Bhat B, Adhisivam B, Bharadwaj SK, Vinayagamet V et al. Neuronal biomarkers in predicting neurodevelopmental outcome in term babies with perinatal asphyxia. The Indian Journal of Pediatrics 2020; 87 (10): 787- 792. doi: 10.1007/s12098-020-03283-2
- 25. Celtik C, Acunaş B, Oner N, Pala O. Neuron-specific enolase as a marker of the severity and outcome of hypoxic ischemic encephalopathy. Brain and Development 2004; 26 (6): 398-402. doi: 10.1016/j.braindev.2003.12.007