Abstract
80% of healthy neonates present with some degree of hyperbilirubinemia after birth, however, only 5-10% would require therapy to prevent damage or treat the cause of jaundice. Neonatal jaundice can be classified as physiological and pathological and can have several causes such as breast milk feeding, blood group incompatibility, hemolysis, or genetic defects of enzymes in the bilirubin metabolism pathway. We tried to understand the various types of neonatal jaundice, and also focus on its management. We conducted this review using a comprehensive search of MEDLINE, PubMed and EMBASE from January 2001 to March 2017. The following search terms were used: neonatal jaundice, hyperbilirubinemia, ABO incompatibility, neonatal hemolysis, kernicterus, phototherapy, exchange transfusion. Hyperbilirubinemia and jaundice are common issues encountered neonates and infants. Most cases of neonatal hyperbilirubinemia and jaundice are physiological and benign. However, some severe cases may progress to develop severe and permanent long-term complications. Therefore, early diagnosis and management is essential. Neonatal jaundice can be treated using phototherapy, pharmacological agents, intravenous immunoglobulins and exchange transfusion in severe cases.
Highlights
It has been reported that up to 80% of healthy neonates can present with idiopathic jaundice at birth
Many previous studies have suggested the strong association between neonatal hyperbilirubinemia, and certain genetic variations that alter the activity of enzymes
Examples of these include a variation in the gene encoding for the the uridine 5′-diphosphate glucuronosyltransferase 1A1 enzyme, which will lead to a significant reduction in the activity of the gene in both children and adults, leading to the accumulation of unconjugated bilirubin. Another example is the variation in the gene encoding for the organic anion transporter 2 (OATP2) which leads in severe neonatal hyperbilirubinemia.[3]
Summary
It has been reported that up to 80% of healthy neonates can present with idiopathic jaundice at birth. When bilirubin levels increase in a neonate, the first thing to notice is yellowish discoloration of the dermal icterus, which will later continue to include the extremities and the body. Significant increases in bilirubin levels are usually toxic and cause significant damage to the development of the central nervous system They may be associated with neurological and behavioral impairments on both preterm and full-term neonates. Many previous studies have suggested the strong association between neonatal hyperbilirubinemia, and certain genetic variations that alter the activity of enzymes Examples of these include a variation in the gene encoding for the the uridine 5′-diphosphate glucuronosyltransferase 1A1 enzyme, which will lead to a significant reduction in the activity of the gene in both children and adults, leading to the accumulation of unconjugated bilirubin. Another example is the variation in the gene encoding for the organic anion transporter 2 (OATP2) which leads in severe neonatal hyperbilirubinemia.[3]
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