The relationship of melatonin concentration in preterm infants and adverse outcomes in the late neonatal period

Abstract

Introduction:The aim of research was to assess the melatonin concentrations in the early neonatal period as a predictor of adverse outcomes of late neonatal period in preterm infants and to estimate its optimal predictive cut-off values. Materials and methods: A total of 115 preterm infants admitted to the neonatal intensive care unit were screened for eligibility, five did not meet the criteria, six parents declined the participation. So, a total of 104 preterm infants with gestational age 25-34 weeks were included in research. The concentration of melatonin in urine was determined by the Enzyme Immunoassay method (Human Melatonin Sulfate ELISA kit, Elabscience, China). The Mann-Whitney U-test and analysis of the receiver operating characteristic (ROC) curve were used in statistical analysis. Results: Analysis of the ROC curves has revealed optimal cut-off values for urinary melatonin concentration to predict late outcomes. Melatonin concentration below 3.58 ng/ml with sensitivity of 72% can predict development of retinopathy of prematurity (ROP) (AUC = 0.73; 95% confidence intervals (CI) 0.61-0.86). Good diagnostic accuracy (AUC = 0.80; 95% CI 0.67-0.93) has been shown for bronchopulmonary dysplasia (BPD). The optimal cut-off value for melatonin concentration in BPD prediction is 3.71 ng/ml (sensitivity 80%, specificity 64%). Urinary melatonin concentration below 3.79 ng/ml can be associated with late-onset sepsis (AUC = 0.76; 95% CI 0.64-0.87; sensitivity 72%; specificity 62%). There were no significant associations between melatonin concentration and necrotizing enterocolitis (P = 0.912). Conclusion: Urinary melatonin concentration below the certain cut-off values in the early neonatal period may serve as one of the predictors of adverse outcomes such as BPD, ROP, and late-onset sepsis in the late neonatal period in preterm infants.

Fate of melatonin orally administered in preterm newborns: Antioxidant performance and basis for neuroprotection

“…Since ME is an active bio component of human milk with concentrations higher at night, the newborn can take advantage of breastfeeding 19 . Although the use of ME as a neuroprotector appears to be a promising strategy in preterm infants, few recent studies tested the effect of ME administration on the clinical outcome in preterm populations 21,22 . By contrast, several trials reported the effectiveness of ME administration in term newborns suffering from hypoxic‐ischemic encephalopathy 23–25 …”

“…19 Although the use of ME as a neuroprotector appears to be a promising strategy in preterm infants, few recent studies tested the effect of ME administration on the clinical outcome in preterm populations. 21,22 By contrast, several trials reported the effectiveness of ME administration in term newborns suffering from hypoxic-ischemic encephalopathy. [23][24][25] Our study aimed to assess: (i) the endogenous ME production in very preterm infants (gestational age, GA ≤ 29 + 6 WE) measuring plasma concentration within 96 h from birth; (ii) plasma ME availability and its metabolization to the main metabolite 6-OH-ME after 15 days of oral ME treatment (3 mg/kg/day or equivalent placebo); (iii) MDA plasma concentrations in the ME and the placebo groups.…”