Background: Hypoxic-ischemic encephalopathy (HIE) has deleterious neurological consequences. To identify patients at risk of neuronal damage deserving implementation of neuroprotective strategies clinicians have relied on prenatal sentinel events, postnatal clinical assessment (Apgar score), and blood gas analysis. This feasibility study aimed to assess if lipid peroxidation byproducts associated with neuronal damage correlated with cord blood metabolic acidemia in patients with HIE.
Population and methods: This is a case/control study in which cases were newborn infants with severe acidemia (pH<7.00; base excess ≥12mmol/L) while control babies exhibited normal gases (pH=7.20-7.40; base excess=-4 to +4mmol/L) in the first cord blood analysis performed immediately after birth. Concomitantly, lipid peroxidation byproducts were determined using ultra performance liquid chromatography coupled to mass spectrometry in the same cord blood sample.
Results: A total of 19 controls and 20 cases were recruited. No differences in gestational characteristics were present. However, cases exhibited profound metabolic alterations as compared to controls (Cases vs.
Control: pH=6.90±0.1 vs. 7.33±0.03; base excess=-15±3 vs. -1±2mmol/L), 85% were admitted to the NICU, and 50% developed symptoms of HIE. 8-iso-15(R)-PGF2α (P=0.01) and total isoprostanes (P=0.045) presented statistically significant differences between cases and control groups and correlated with level of HIE.
Conclusions: The 8-iso-15(R)-PGF2α and isoprostanes reflecting oxidative damage are significantly increased in severe postnatal acidemia. Follow up studies with adequate power are necessary to confirm if these biomarkers measured in cord blood serum could be predictive of neonatal encephalopathy.
Keywords: Biomarker; Birth asphyxia; Delivery; Hypoxia; Isoprostanes; Lactic acid; Metabolic acidosis; Oxidative stress.
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