Pediatrics & Neonatology
Volume 51, Issue 3 , Pages 143-148, June 2010

Understanding Neonatal Jaundice: A Perspective on Causation

Department of Pediatrics, Stanford University School of Medicine, Stanford, California, USA

Received 19 November 2009; received in revised form 23 December 2009; accepted 15 January 2010.

Article Outline

Neonatal jaundice can be best understood as a balance between the production and elimination of bilirubin, with a multitude of factors and conditions affecting each of these processes. When an imbalance results because of an increase in circulating bilirubin (or the bilirubin load) to significantly high levels (severe hyperbilirubinemia), it may cause permanent neurologic sequelae (kernicterus). In most infants, an increase in bilirubin production (e.g., due to hemolysis) is the primary cause of severe hyperbilirubinemia, and thus reducing bilirubin production is a rational approach for its management. The situation can become critical in infants with an associated impaired bilirubin elimination mechanism as a result of a genetic deficiency and/or polymorphism. Combining information about bilirubin production and genetic information about bilirubin elimination with the tracking of bilirubin levels means that a relative assessment of jaundice risk might be feasible. Information on the level of bilirubin production and its rate of elimination may help to guide the clinical management of neonatal jaundice.

Key Words:  carbon monoxide , heme oxygenase , hyperbilirubinemia , jaundice , metalloporphyrin

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PII: S1875-9572(10)60027-7

doi:10.1016/S1875-9572(10)60027-7

Pediatrics & Neonatology
Volume 51, Issue 3 , Pages 143-148, June 2010