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Reduced iron-associated antioxidants in premature newborns suffering intracerebral hemorrhage
G M Lackmann1, L Hesse, U Töllner
1Department of Pediatrics, Städtisches Klinikum, Fulda, Germany.
Insights
Neonatal iron overload contributes to free radical damage, increasing the risk of periventricular-intraventricular hemorrhage (PIVH) in premature infants. Lower iron-binding proteins and higher iron saturation in blood plasma indicate this risk.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pathophysiology
Background:
- Oxygen radical injury is implicated in neonatal diseases.
- Premature infants face higher risks of conditions like intracerebral hemorrhage.
- Periventricular-intraventricular hemorrhage (PIVH) is a significant concern in premature neonates.
Purpose of the Study:
- To investigate if ionic iron overload, due to reduced iron-binding proteins, causes free radical damage in premature newborns with PIVH.
- To test the hypothesis linking iron metabolism alterations to PIVH pathogenesis.
Main Methods:
- Blood plasma analysis of newborns with PIVH (n=7) and controls (n=10) within 12 hours of birth.
- Quantification of transferrin and ceruloplasmin levels.
- Measurement of transferrin saturation.
Main Results:
- Newborns who developed PIVH showed reduced transferrin (2.05 vs. 2.24 g/l) and ceruloplasmin (89.9 vs. 126.3 mg/l) levels.
- Increased transferrin saturation (54.2 vs. 38.4%) was observed in the PIVH group.
- These findings suggest altered iron metabolism in infants who develop PIVH.
Conclusions:
- Reduced iron-binding proteins and increased iron saturation in plasma are associated with PIVH in premature newborns.
- Iron-catalyzed lipid peroxidation during reoxygenation after perinatal asphyxia may contribute to PIVH.
- These results support the role of iron dysregulation in the pathogenesis of PIVH.
Abstract:
Oxygen radical injury may be a common pathogenic mechanism in several neonatal diseases. The term "oxygen radical disease of prematurity" has been proposed in the face of the greater incidence of intracerebral hemorrhage, bronchopulmonary dysplasia, and retinopathy in premature neonates. To test the hypothesis that overload with ionic iron due to decreased concentrations of iron-oxidizing and iron-binding proteins induces free radical damage in premature asphyxiated newborns suffering periventricular-intraventricular hemorrhage (PIVH), blood plasma of newborns with PIVH (n = 7) was compared with that of controls (n = 10) within the first 12 h of life. We found reduced transferrin (2.05 vs. 2.24 g/l; p < 0.05) and ceruloplasmin (89.9 vs. 126.3 mg/l; p < 0.01) levels and an increased transferrin saturation (54.2 vs. 38.4%; p < 0.05) in those newborns who later developed PIVH. These findings support the theory that iron-catalyzed lipid peroxidation of the brain during reoxygenation after perinatal asphyxia may be involved in the pathogenesis of PIVH.