Search

Objectives The early detection and stratification of asphyxiated infants at higher risk for impaired neurodevelopment is challenging. S100B protein is a well-established biomarker of brain damage, but lacks conclusive validation according to the "gold standard" methodology for hypoxic-ischemic encephalopathy (HIE) prognostication, i.e. brain MRI. The aim of the present study was to investigate the predictive role of urinary S100B concentrations, assessed in a cohort of HIE infants receiving therapeutic hypothermia (TH), compared to brain MRI. Methods Assessment of urine S100B concentrations was performed by immunoluminometric assay at first void and at 4, 8, 12, 16, 20, 24, 48, 72, 96, 108 and 120-h after birth. Neurologic evaluation, routine laboratory parameters, amplitude-integrated electroencephalography, and cerebral ultrasound were performed according to standard protocols. Brain MRI was performed at 7-10 days of life. Results Overall, 74 HIE neonates receiving TH were included in the study. S100B correlated, already at first void, with the MRI patterns with higher concentrations in infants with the most severe MRI lesions. Conclusions High S100B urine levels soon after birth constitute trustable predictors of brain injury as confirmed by MRI. Results support the reliability of S100B in clinical daily practice and open the way to its inclusion in the panel of parameters used for the selection of cases suitable for TH treatment.

Histologic chorioamnionitis (HCA) may lead to the fetal inflammatory response syndrome (FIRS). The aim of this pilot study was to evaluate S100A12, a marker of innate immune activation, in mothers with or without HCA and in their infants. Concentrations of S100A12, interleukin 6 (IL-6), and C-reactive protein (CRP) were evaluated in maternal, cord, and neonatal blood of very preterm infants. Histologic examinations of the placenta and umbilical cords were performed. The 48 mother-neonate pairs enrolled were subdivided into two groups: HCA group (N = 15) and control group without HCA (N = 33). Maternal S100A12 levels were similar between HCA and control group. Similarly, S100A12 concentrations in cord and neonatal blood did not differ between the groups. However, high S100A12 concentrations were detected in cord and neonatal blood of two out of three neonates exposed to HCA associated with advanced funisitis. Concentrations of IL-6 and CRP were higher in maternal blood of the HCA group compared with controls (p < 0.05, p < 0.001; respectively), but no differences in cord or neonatal blood was found. Conclusion:S100A12 did neither identify mothers with HCA nor very preterm infants exposed to HCA. It is currently unknown if S100A12 may identify neonates with FIRS.What is known:• Histologic chorioamnionitis (HCA) may lead to the fetal inflammatory response syndrome (FIRS).• S100A12 represents an early, sensitive, and specific diagnostic marker of inflammatory processes.What is new:• S100A12 did neither identify mothers with HCA nor very preterm infants exposed to HCA.• It is currently still unclear if S100A12 has a potential in identifying preterm infants with FIRS.

BACKGROUND: Term neonates (TN) are not routinely submitted to cranial ultrasound scan (CUS), since they are not considered at high risk for developing cerebral lesions. AIMS: To investigate the prevalence of cerebral abnormal findings in term neonates (TN), to identify the associated clinical features and to better target neonatal CUS investigations. STUDY DESIGN: Prospective observational study. SUBJECTS: A total number of 1805 healthy TN underwent CUS. 1181 neonates had clinical features supposed to increase the risk for cerebral abnormal findings (study cohort), 624 were controls. OUTCOME MEASURES: Prevalence of minimal, minor, and major cerebral abnormal findings was analyzed in six different categories of low-risk TN and compared to controls. RESULTS: Variations from normality at the neonatal CUS were observed in 402 TN (22.27%). In half of the cases the ultrasound findings were minimal abnormal findings, while minor abnormal findings were found in 179 TN (9.92%). About 1% of the studied neonates showed major cerebral abnormal findings potentially compromising neurodevelopmental outcome. The prevalence of the observed abnormal findings varied significantly in the different low-risk categories. CONCLUSIONS: The clinical features significantly increasing the risk for cerebral anomalies in healthy TN were microcrania, macrocrania, mild neurologic signs, and the detection of mild variations from normal cerebral aspect at the antenatal ultrasound evaluation