Diagnostic Accuracy of S100B Urinary Testing at Birth in Full-Term Asphyxiated Newborns to Predict Neonatal Death

BACKGROUND: Neonatal death in full-term infants who suffer from perinatal asphyxia (PA) is a major subject of investigation, since few tools exist to predict patients at risk of ominous outcome. We studied the possibility that urine S100B measurement may identify which PA-affected infants are at risk of early postnatal death. METHODOLOGY/PRINCIPAL FINDINGS: In a cross-sectional study between January 1, 2001 and December 1, 2006 we measured S100B protein in urine collected from term infants (n = 132), 60 of whom suffered PA. According to their outcome at 7 days, infants with PA were subsequently classified either as asphyxiated infants complicated by hypoxic ischemic encephalopathy with no ominous outcome (HIE Group; n = 48), or as newborns who died within the first post-natal week (Ominous Outcome Group; n = 12). Routine laboratory variables, cerebral ultrasound, neurological patterns and urine concentrations of S100B protein were determined at first urination and after 24, 48 and 96 hours. The severity of illness in the first 24 hours after birth was measured using the Score for Neonatal Acute Physiology-Perinatal Extension (SNAP-PE). Urine S100B levels were higher from the first urination in the ominous outcome group than in healthy or HIE Groups (p<0.001 for all), and progressively increased. Multiple logistic regression analysis showed a significant correlation between S100B concentrations and the occurrence of neonatal death. At a cut-off >1.0 microg/L S100B had a sensitivity/specificity of 100% for predicting neonatal death. CONCLUSIONS/SIGNIFICANCE: Increased S100B protein urine levels in term newborns suffering PA seem to suggest a higher risk of neonatal death for these infants

High Urinary Concentrations of Activin A in Asphyxiated Full-Term Newborns with Moderate or Severe Hypoxic Ischemic Encephalopathy

AbstractBackground: Hypoxic ischemic encephalopathy (HIE) is a major cause of permanent neurological disabilities in full-term newborns. We measured activin A in urine collected immediately after birth in asphyxiated full-term newborns, and assessed the ability of the measurements to predict the occurrence of perinatal encephalopathy.Methods: We studied 30 infants with perinatal asphyxia and 30 healthy term neonates at the same gestational age. We recorded routine laboratory variables, cranial assessments by standard cerebral ultrasound, and the presence or absence of neurological abnormalities during the first 7 days after birth. Urinary activin A concentrations were measured at first urination and 12, 24, 48, and 72 h after birth.Results: Asphyxiated infants were subdivided as follows: group A (n = 18): no or mild HIE with good prognosis and group B (n = 12): moderate or severe HIE with a greater risk of neurological handicap. Activin A concentrations in urine collected at birth (median collection time at first urination &lt;2 h) and at 12, 24, 48, and 72 h from birth were significantly (P &lt;0.0001) higher in asphyxiated newborns with moderate or severe HIE (Group B) than in those with absent of mild HIE (group A) and controls. Concentrations did not differ between group A and controls. Activin A concentrations were &gt;0.08 μg/L at first urination in 10 of 12 patients with moderate or severe HIE but in none of 18 patients with no or mild HIE.Conclusions: Activin A measurements in urine soon after birth may be a promising tool to identify which asphyxiated infants are at risk of neurological sequelae

Urine S100B concentrations (µg/L) expressed as median [lower and upper 95% Confidence Interval (CI)] at first urination (0), and at 24 (1), 48 (2) and 96 (3) hours in healthy Group (n = 72), in newborns affected by PA without overt neurologic syndrome (n = 48, HIE Group) and with ominous outcome (n = 12, Ominous Outcome Group).

<p>Urinary S100B levels were significantly higher in the neonatal death group at all monitoring time-points (p<0.001, for all).</p>*<p>p<0.001 vs controls</p