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Non-protein-bound iron is elevated in cerebrospinal fluid from preterm infants with posthemorrhagic ventricular

K Savman1, U A Nilsson, M Blennow

  • 1Department of Pediatrics, Göteborg University, The Queen Silvia Children's Hospital, S-416 85 Göteborg, Sweden.

Pediatric Research
|February 7, 2001
PubMed

Insights

Non-protein-bound iron (NPBI) was elevated in cerebrospinal fluid (CSF) of preterm infants with posthemorrhagic ventricular dilatation (PHVD). This finding suggests free iron contributes to white matter damage in these vulnerable infants.

Area of Science:

  • Neonatal Neurology
  • Neurocritical Care
  • Biochemistry

Background:

  • Posthemorrhagic ventricular dilatation (PHVD) in preterm infants is linked to white matter injury and neurological deficits.
  • Immature oligodendroglia, rich in iron, are particularly susceptible to oxidative stress from reactive oxygen species.
  • Non-protein-bound iron (NPBI) significantly catalyzes hydroxyl radical generation via the Fenton reaction.

Purpose of the Study:

  • To investigate if NPBI levels are elevated in the cerebrospinal fluid (CSF) of preterm infants diagnosed with PHVD compared to healthy preterm controls.
  • To explore the potential role of NPBI in the pathogenesis of white matter damage associated with intraventricular hemorrhage in neonates.

Main Methods:

  • CSF samples were collected from 20 preterm infants with PHVD and 10 preterm control infants.
  • A novel spectrophotometric method utilizing bathophenanthroline was employed to quantify NPBI levels.
  • In vitro experiments assessed the impact of hemolysis on NPBI levels by mixing CSF and blood samples.

Main Results:

  • NPBI was detected in 75% of infants with PHVD, versus 0% in the control group (p = 0.0002).
  • Induced hemolysis in vitro did not significantly elevate NPBI levels.
  • In PHVD infants, CSF NPBI concentrations did not correlate with clinical outcomes like disability, brain lesions, or need for shunting.

Conclusions:

  • Preterm infants with PHVD exhibit increased NPBI in their CSF.
  • The elevated NPBI is not solely attributable to hemolysis, suggesting a distinct pathophysiological role.
  • Free iron accumulation may be a key factor mediating white matter damage following intraventricular hemorrhage in preterm neonates.

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