Related Experiment Videos
Bilirubin binding and acid-base equilibrium in newborn infants with low birthweight
P Meisel1, D Jährig, E Beyersdorff
1Department of Paediatrics, Ernst Moritz Arndt University, Greifswald, GDR.
Insights
Acidosis in newborns may increase the risk of bilirubin encephalopathy by reducing bilirubin-albumin binding in serum, not just increasing tissue binding. This impacts the toxic potential of serum bilirubin.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pediatric Physiology
Background:
- Acidosis is a known risk factor for bilirubin encephalopathy in neonatal jaundice.
- The effect of acid-base status on bilirubin-albumin binding in newborns is not well understood.
Purpose of the Study:
- To investigate the relationship between acid-base state and bilirubin binding in newborn infants.
- To evaluate how acidosis influences the toxic potential of serum bilirubin.
Main Methods:
- Studied 171 appropriate and 83 small for gestational age newborns (birthweight < 2,500 g).
- Measured blood acid-base status and serum bilirubin (BR) binding at 3, 4, 5, and 8 days of age.
Main Results:
- A significant correlation was found between standard base deficit and the BR/reserve albumin ratio.
- Acidosis showed a correlation with the toxic potential of serum BR.
- Results indicate a weak but significant link between acidosis and altered bilirubin binding.
Conclusions:
- Acidosis in newborns may increase bilirubin encephalopathy risk partly due to decreased serum bilirubin binding.
- This finding suggests a dual mechanism involving both tissue and serum binding alterations in acidosis-related hyperbilirubinemia.
Abstract:
Acidosis is known as a risk factor for the development of bilirubin encephalopathy in neonatal jaundice. However, few attempts have been made to evaluate the influence of acid-base state on bilirubin-albumin binding state in blood of newborn infants. Therefore, in 171 appropriate and 83 small for gestational age newborns (birthweight less than 2,500 g) the acid-base state in blood and bilirubin (BR) binding state in serum was measured at the ages of 3, 4, 5, and 8 days. There is a weak but significant correlation between standard base deficit and the ratio BR/reserve albumin as well as the toxic potential of serum BR. The results suggest that the higher risk in acidosis is not only caused by increased tissue binding of BR but also--at least partially--attributable to decreased BR binding in serum.