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Updated: Feb 5, 2026
08:47
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
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Changes in bilirubin in infants with hypoxic-ischemic encephalopathy
Carlo Dani1,2, Chiara Poggi3, Claudia Fancelli3
1Division of Neonatology, Careggi University Hospital of Florence, 3 Largo Brambilla, 50141, Florence, Italy. cdani@unifi.it.
European Journal of Pediatrics
|September 21, 2018
Summary
Total serum bilirubin (TSB) levels were lower in infants with hypoxic-ischemic encephalopathy (HIE) than in controls. Both HIE and therapeutic hypothermia independently decreased TSB, suggesting bilirubin does not offer neuroprotection in HIE.
Area of Science:
- Neonatal Medicine
- Neuroscience
- Biochemistry
Background:
- Oxidative stress is key in hypoxic-ischemic encephalopathy (HIE) pathophysiology.
- Bilirubin possesses antioxidant properties.
- The neuroprotective role of bilirubin in HIE remains unevaluated.
Purpose of the Study:
- To investigate the involvement of bilirubin in neuroprotection against oxidative stress in infants with HIE.
- To determine if total serum bilirubin (TSB) levels increase in infants with HIE.
Main Methods:
- Retrospective study of infants with moderate-to-severe HIE (gestational age ≥35 weeks, birth weight ≥1800 g).
- Comparison of peak and mean TSB values between HIE infants (with or without therapeutic hypothermia) and a control group.
- Regression analysis to identify factors influencing TSB levels.
Main Results:
- Infants with HIE had lower peak and mean TSB values compared to controls.
- Therapeutic hypothermia did not significantly alter TSB levels within the HIE group.
- HIE and hypothermia independently reduced the likelihood of elevated TSB.
Conclusions:
- Lower TSB levels in HIE infants suggest bilirubin is not a neuroprotective factor via TSB increase.
- HIE and hypothermia decrease TSB, potentially due to hypoxic repression of heme oxygenase (HO) expression.
- This decrease may represent a protective mechanism limiting brain injury in HIE.
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