Neonatal Jaundice Review Article Text

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To review best practices for early recognition and treatment of conditions resulting in neonatal cholestasis, in order to improve long term outcomes for affected infants. Studies, review articles, and meta analyses pertaining to neonatal onset cholestasis were sought via electronic databases. Reference lists of studies and review articles supplemented the electronic search. Studies were included if they examined the importance of early diagnosis and intervention for cholestatic jaundice of any cause, and mainly comprised level ii and level i evidence. Revoir les meilleures m x0e9 thodes pour d x0e9 tecter et traiter pr x0e9 cocement les conditions r x0e9 sultant de la cholestase n x0e9 onatale afin d x02019 am x0e9 liorer les issues x0e0 long terme chez les nourrissons affect x0e9 s.

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Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin. In most infants, unconjugated hyperbilirubinemia reflects a normal transitional phenomenon. However, in some infants, serum bilirubin levels may rise excessively, which can be cause for concern because unconjugated bilirubin is neurotoxic and can cause death in newborns and lifelong neurologic sequelae in infants who survive kernicterus . For these reasons, the presence of neonatal jaundice frequently results in diagnostic evaluation. Bilirubin production is elevated because of increased breakdown of fetal erythrocytes. This is the result of the shortened lifespan of fetal erythrocytes and the higher erythrocyte mass in neonates.

2, 3 hepatic excretory capacity is low both because of low concentrations of the binding protein ligandin in the hepatocytes and because of low activity of glucuronyl transferase, the enzyme responsible for binding bilirubin to glucuronic acid, thus making bilirubin water soluble conjugation. Bilirubin is produced in the reticuloendothelial system as the end product of heme catabolism and is formed through oxidation reduction reactions. Approximately 75% of bilirubin is derived from hemoglobin, but degradation of myoglobin, cytochromes, and catalase also contributes. In the first oxidation step, biliverdin is formed from heme through the action of heme oxygenase, the rate limiting step in the process, releasing iron and carbon monoxide. The iron is conserved for reuse, whereas carbon monoxide is excreted through the lungs and can be measured in the patient's breath to quantify bilirubin production. Next, water soluble biliverdin is reduced to bilirubin, which, because of the intramolecular hydrogen bonds, is almost insoluble in water in its most common isomeric form bilirubin ixα z,z.

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Because of its hydrophobic nature, unconjugated bilirubin is transported in the plasma tightly bound to albumin. Binding to other proteins and erythrocytes also occurs, but the physiologic role is probably limited. Binding of bilirubin to albumin increases postnatally with age and is reduced in infants who are ill. The presence of endogenous and exogenous binding competitors, such as certain drugs, also decreases the binding affinity of albumin for bilirubin.

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This free bilirubin is able to cross lipid containing membranes, including the blood brain barrier, leading to neurotoxicity. In fetal life, free bilirubin crosses the placenta, apparently by passive diffusion, and excretion of bilirubin from the fetus occurs primarily through the maternal organism. When it reaches the liver, bilirubin is transported into liver cells, where it binds to ligandin.

Uptake of bilirubin into hepatocytes increases with increasing ligandin concentrations. Ligandin concentrations are low at birth but rapidly increase over the first few weeks of life. Ligandin concentrations may be increased by the administration of pharmacologic agents such as phenobarbital. Bilirubin is bound to glucuronic acid conjugated in the hepatocyte endoplasmic reticulum in a reaction catalyzed by uridine diphosphoglucuronyltransferase udpgt. Diconjugates appear to be formed at the cell membrane and may require the presence of the udpgt tetramer.

Bilirubin conjugation is biologically critical because it transforms a water insoluble bilirubin molecule into a water soluble molecule. In addition, certain drugs phenobarbital, dexamethasone, clofibrate can be administered to increase udpgt activity. Infants who have gilbert syndrome or who are compound heterozygotes for the gilbert promoter and structural mutations of the udpgt1a1 coding region are at an increased risk of significant hyperbilirubinemia. Interactions between the gilbert genotype and hemolytic anemias such as glucose 6 phosphatase dehydrogenase g 6 pd deficiency. Hereditary spherocytosis, or abo hemolytic disease also appear to increase the risk of severe neonatal jaundice.

Further, the observation of jaundice in some infants with hypertrophic pyloric stenosis may also be related to a gilbert type variant. Genetic polymorphism for the organic anion transporter protein oatp 2 correlates with a 3 fold increased risk for developing marked neonatal jaundice. Combination of the oatp 2 gene polymorphism with a variant udpgt1a1 gene further increases this risk to 22 fold. 4 studies also suggest that polymorphisms in the gene for glutathione s transferase ligandin may contribute to higher levels of total serum bilirubin. Thus, some interindividual variations in the course and severity of neonatal jaundice may be explained genetically. As the impact of these genetic variants is more fully understood, development of a genetic test panel for risk of severe and/or prolonged neonatal jaundice may become feasible.

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