Mechanism of Bilirubin Entry into the Brain in an Animal Model

Abstract

Hyperbilirubinemia is still one of the most common problems in the newborn, particularly in the premature infant. Kernicterus may occur when unconjugated bilirubin enters the brain and produces toxic effects on the nerve celes(1). Although the mechanism is not fully understood, it has been assumed that the toxicity is caused by the entry of the non-albumin bound fraction of the unconjugated bilirubin into the brain. As long as the molar concentration of serum bilirubin is less than that of serum albumin, the bilirubin molecule is usually firmly bound to the albumin molecule, and only insignificant levels of free or unbound bilirubin can be detected (2, 3). Several studies have, however, shown that multiple factors can affect the binding of bilirubin to albumin and thus increase the serum level of free bilirubin in the newborn and thereby probably also the risk for bilirubin toxicity (3, 4). A large number of tests have therefore been developed to measure the free bilirubin concentration in the blood of the newborn (5) as a way of assessing the potential risk of kernicterus.