Pathogenesis and etiology of unconjugated hyperbilirubinemia in the newborn
- Ronald J Wong, BA
Ronald J Wong, BA
- Senior Research Scientist
- Stanford University School of Medicine
- Vinod K Bhutani, MD, FAAP
Vinod K Bhutani, MD, FAAP
- Professor of Pediatrics
- Stanford University School of Medicine
- Section Editors
- Steven A Abrams, MD
Steven A Abrams, MD
- Section Editor — Neonatology
- Professor, Department of Pediatrics
- Dell Medical School at the University of Texas at Austin
- Elizabeth B Rand, MD
Elizabeth B Rand, MD
- Section Editor — Pediatric Hepatology
- Professor of Pediatrics
- University of Pennsylvania School of Medicine
Almost all newborn infants develop a total serum or plasma bilirubin (TB) level greater than 1 mg/dL (17 micromol/L), which is the upper limit of normal for adults. As the TB increases, it produces neonatal jaundice, the yellowish discoloration of the skin and/or conjunctiva caused by bilirubin deposition . Neonates with severe hyperbilirubinemia (defined as a TB >25 mg/dL [428 micromol/L]) are at risk for bilirubin-induced neurologic dysfunction (BIND), which occurs when bilirubin crosses the blood-brain barrier and binds to brain tissue
The pathogenesis and etiology of neonatal unconjugated hyperbilirubinemia is reviewed here. The clinical features, evaluation, prevention, and treatment of this disorder are discussed separately. (See "Clinical manifestations of unconjugated hyperbilirubinemia in term and late preterm infants" and "Evaluation of unconjugated hyperbilirubinemia in term and late preterm infants" and "Treatment of unconjugated hyperbilirubinemia in term and late preterm infants".)
●Severe neonatal hyperbilirubinemia is defined as a TB >25 mg/dL (428 micromol/L). It is associated with an increased risk for bilirubin-induced neurologic dysfunction (BIND), which occurs when bilirubin crosses the blood-brain barrier and binds to brain tissue. (See "Clinical manifestations of unconjugated hyperbilirubinemia in term and late preterm infants", section on 'Clinical manifestations'.)
●Acute bilirubin encephalopathy (ABE) is used to describe the acute manifestations of BIND. (See "Clinical manifestations of unconjugated hyperbilirubinemia in term and late preterm infants", section on 'Acute bilirubin encephalopathy'.)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- BILIRUBIN METABOLISM
- Bilirubin production
- Bilirubin clearance and excretion
- NEONATAL JAUNDICE
- Ethnic variation in conjugation ability
- CAUSES OF HYPERBILIRUBINEMIA
- Increased production
- Decreased clearance
- - Crigler-Najjar syndrome
- - Gilbert syndrome
- - OATP-2 polymorphism
- - Other causes
- Increased enterohepatic circulation
- - Breast milk jaundice
- - Intestinal obstruction
- Breastfeeding failure jaundice
- - Prevention
- Severe hyperbilirubinemia
- INFORMATION FOR PATIENTS