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Free bilirubin concentrations and bilirubin-binding affinity in term and preterm infants
Insights
Serious neonatal illness in preterm infants significantly reduces bilirubin binding capacity and affinity, increasing the risk of kernicterus. This study measured free bilirubin, binding capacity, and affinity in newborns.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pediatrics
Background:
- Neonatal jaundice is common, with unconjugated bilirubin posing a risk for brain damage (kernicterus).
- Bilirubin binding to albumin influences its toxicity, but the impact of neonatal illness on binding parameters is not fully understood.
Purpose of the Study:
- To investigate the relationship between neonatal illness, bilirubin-binding capacity, bilirubin-binding affinity, and free bilirubin concentration.
- To determine if reduced binding parameters are associated with an increased risk of kernicterus in preterm infants.
Main Methods:
- Determined free bilirubin concentration, bilirubin-binding capacity, and bilirubin-binding affinity using peroxidase oxidation.
- Studied 66 newborn infants, categorized into healthy term infants, term infants with complications, and preterm infants with and without complications.
Main Results:
- Sick preterm infants with complications showed significantly higher free bilirubin levels (19 +/- 11 nmol/l) compared to other groups.
- These infants also had markedly reduced bilirubin-binding capacity and affinity (P < 0.01).
- Five sick preterm infants with kernicterus had higher free bilirubin and lower binding capacity/affinity than other sick preterm infants.
Conclusions:
- Serious neonatal illness is linked to a significant decrease in bilirubin-binding capacity and affinity in preterm infants.
- This reduction in binding capacity and affinity appears to increase the risk of kernicterus in sick preterm infants.
- The underlying mechanisms by which neonatal morbidity affects bilirubin binding require further investigation.
Abstract:
Free bilirubin concentration, bilirubin-binding capacity, and bilirubin-binding affinity were determined by peroxidase oxidation in 66 newborn infants. Twelve healthy term infants whose unconjugated bilirubin concentration was 15.8 +/- 3.7 mg/dl (mean +/- SD) had a binding capacity of 31.9 +/- 3.7 mg/dl (bilirubin: albumin molar ratio = 0.89 +/- 0.07) and Ka = 28 +/- 11 x 10(7)/M. Twelve term infants with clinical complications of asphyxia, acidosis, respiratory distress, or sepsis, and 17 preterm infants with no complications had lower serum albumin concentrations and slightly reduced binding capacity and affinity compared to the healthy term infants. Free bilirubin concentrations were similar in these three groups, averaging 8 to 9 nmol/l in each group. Twenty-five preterm infants with complications had significantly higher free bilirubin (19 +/- 11 nmol/l), lower binding capacity, and lower binding affinity than any of the other three groups (P less than 0.01 for all comparisons). Five of the 25 sick preterm infants had kernicterus at autopsy. These five infants were similar to the other 20 in birth weight, gestational age, serum bilirubin, and serum albumin level, but had significantly higher free bilirubin and significantly lower binding capacity and affinity. The data suggest that serious neonatal illness is associated with a marked reduction in bilirubin-binding capacity and affinity and an increased risk of kernicterus in preterm infants. The mechanism by which neonatal morbidity decreases bilirubin binding is not known.