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Ascorbic acid combined with ibuprofen in hypoxic ischemic encephalopathy: a randomized controlled trial.
H Aly1, L Abd-Rabboh, M El-Dib
1Department of Neonatology, George Washington University and Children's National Medical Center, Washington, District of Columbia, USA. haly@mfa.gwu.edu
This study found that combining ascorbic acid and ibuprofen did not improve outcomes for newborns with hypoxic ischemic encephalopathy (HIE). Further research is needed to understand why this treatment for HIE was ineffective.
Area of Science:
- Neonatal neurology
- Perinatal medicine
- Biochemistry
Background:
- Hypoxic ischemic encephalopathy (HIE) in neonates is linked to free oxygen radicals and inflammatory cytokines.
- Effective treatments are crucial to mitigate brain injury and improve neurodevelopmental outcomes in affected infants.
Purpose of the Study:
- To investigate if a combination of antioxidants (ascorbic acid) and anti-inflammatory agents (ibuprofen) could reduce brain injury in HIE.
- To determine if this combined therapy improves neurodevelopmental outcomes in term infants treated immediately after birth.
Main Methods:
- A prospective, randomized, double-blinded controlled trial involving 60 asphyxiated term infants.
- Infants received either intravenous ascorbic acid and oral ibuprofen or a placebo for 3 days.
- Cytokine levels were measured, and neurological/developmental assessments were conducted at 6 months.
Main Results:
- No significant differences were observed between the intervention and control groups in HIE severity, mortality, neurological abnormalities, or developmental delay.
- Serum IL-1 beta and IL-6 concentrations correlated with HIE severity, and IL-6 correlated with 6-month neurodevelopmental outcomes.
- No complications were attributed to the ascorbic acid and ibuprofen intervention.
Conclusions:
- Early administration of ascorbic acid and ibuprofen did not alter outcomes for infants experiencing perinatal asphyxia.
- The ineffectiveness may be due to inadequate dosing, route of administration, or the involvement of other potent mediators in HIE brain injury.
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