Abstract

Pediatricians are confronted daily with the problem of the jaundiced newborn infant. The newborn infant is unique because (a) some elevation of serum bilirubin concentration is found in virtually all babies in the first few days of life, (b) the serum bilirubin concentration frequently rises to levels that are almost never encountered outside of the neonatal period, and (c) the newborn period remains the only time in which an elevated plasma bilirubin concentration per se represents a threat to the well-being of the organism. FETAL AND NEONATAL BILIRUBIN METABOLISM Chemical Structure and Properties of Bilirubin Bilirubin IXα (so called because it is derived from cleavage at the α position of the heme ring of ferropro-toporphyrin IX) is the end product of the catabolism of heme, of which the major source is circulating hemoglobin. Recent observations on the stereochemistry and conformation of the bilirubin molecule are helpful in understanding the potential neurotoxicity of bilirubin as well as the mechanism of phototherapy.1 The isomer, bilirubin IXα(Z,Z), is the major form of bilirubin as it exists in the blood where it is tightly bound to albumin. When this form of bilirubin takes up two hydrogen ions, it forms bilirubin IXα(Z,Z) acid, which is an involuted structure containing intramolecular hydrogen bonds.

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