Abstract

Bilirubin is the end product of heme breakdown. Unconjugated bilirubin (UB) is formed in reticuloendothelial cells, transported to the liver where it is conjugated to glucuronides, and then secreted into the canaliculi. UB is solubilized in serum via very tight linkage to albumin. Bilirubin-albumin binding is a function of the concentration of bilirubin and albumin and the binding affinity for bilirubin. The fraction of unbound bilirubin or plasma free bilirubin (Bf) increases significantly as the total serum bilirubin (TSB) level approaches the binding capacity of albumin. Bf is thought to be better indicator of neurotoxicity than TSB, because only plasma free bilirubin can cross the blood-brain barrier. In medical practice bilirubin is a marker of liver dysfunction, cholestasis or hemolytic disease. A variety of factors limit both the sensitivity and the specificity of bilirubin measurement to detect the abnormalities: lipemia, hemolysis, exposure of visible light and fasting state. Hyperbilirubinemia can be categorised as prehepatic, hepatic or poshepatic, and this provides a useful framework for identifying the underlying cause. In addition, there are conjugated and unconjugated bilirubin. Neonatal hyperbilirubinemia and jaundice occur in almost all newborns and may be benign if its progression to extreme hyperbilirubinemia is recognized, monitored and prevented or managed in a timely manner.

Key words: Bilirubin; hyperbilirubinemia; jaundice; conjugation