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 Vol. 8 No. 7, July 2007
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NeoReviews Vol.8 No.7 2007 e282
© 2007 American Academy of Pediatrics

Neonatal Jaundice and Breastfeeding

Maria Fernanda B. de Almeida, MD, FAAP*
Cecilia Maria Draque, MD{dagger}

* Associate Professor, Pediatrics, Division of Neonatal Medicine, São Paulo Federal University, São Paulo, Brazil
{dagger} Medical Assistant, Pediatrics, Division of Neonatal Medicine, São Paulo Federal University, São Paulo, Brazil

Neonatal jaundice is related to breastfeeding in three primary clinical situations: exclusively breastfed healthy term newborns during the first postnatal week, newborns who receive inadequate breastfeeding and have high concentrations of indirect bilirubin during the first postnatal week ("nonfeeding" jaundice), and breastfed infants who experience prolonged unconjugated hyperbilirubinemia (breast milk jaundice). Nonfeeding jaundice has been suggested to be related to a significantly greater weight loss on the third postnatal day compared with the birthweight following delayed initiation of or inadequate breastfeeding. This can be a particular problem among neonates discharged from the hospital within 48 hours, often requiring readmission for treatment of hyperbilirubinemia. Several hypotheses have been proposed for the source of breast milk jaundice, including the presence of a UDP-glucuronosyltransferase inhibitor, beta-glucuronidase, or a yet-unidentified factor in human milk that could inhibit bilirubin excretion and result in hyperbilirubinemia. Careful education about breastfeeding and monitoring of mothers as well as assessment of newborns for the risk of developing severe hyperbilirubinemia can aid in preventing neonatal jaundice. Treatment of hyperbilirubinemia is based on total serum bilirubin concentrations and can range from administration of intravenous fluids and supplementation with milk formula to intensive phototherapy and exchange transfusion. Experimental treatments include the use of stannsoporfin and beta-glucuronidase inhibitors as chemoprevention therapies and minimal aliquots of L-aspartic acid and enzymatically hydrolyzed casein to inhibit beta-glucuronidase.


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