• Sabahattin Ertuğrul, Savaş Mert Darakci, İbrahim Kaplan, İlyas Yolbaş, İbrahim Deger, Sibel Tanrıverdi Yilmaz, and Şerafettin Aktaş.
• Department of Pediatrics, Division of Neonatology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey
• Turk J Med Sci. 2021 Aug 30; 51 (4): 1917-1923.

Background/AimPostnatal 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 MethodsIn 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.ResultsThere 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.ConclusionNSE levels, which indicate brain damage in the early period, increased in preterm babies with BPD who had been administered postnatal dexamethasone.This work is licensed under a Creative Commons Attribution 4.0 International License.

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