الفهرس 
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Abstract
Jaundice is one of the most common and annoying problem affect the newborn, it affect about 60% of full term infants and 80% of preterm infants in the first 3 days of life .
Hyperbilirubinemia is the most common reason for re-hospitalization during the first month after birth.
In pathological hyperbilirubinemia, increased production of bilirubin, deficiency in hepatic uptake, impaired conjugation of bilirubin, and/or increased enterohepatic circulation of bilirubin are observed.
However, there is no identifiable factor in almost half of cases.
It has been suggested that genetic variation could enhance the risk of neonatal hyperbilirubinemia when coexpressed with other icterogenic conditions.
Among these, uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) was identified to be associated with neonatal hyperbilirubinemia.
UGT1A1 is the key rate-limiting enzyme in the liver for bilirubin
glucuronidation, which is a clearance mechanism for numerous dietary and environmental chemicals, including bilirubin.
The polymorphisms of the UGT1A1 coding region or the promoter may produce structural or functional enzymatic deficiencies, leading to intermittent elevation of unconjugated serum bilirubin, resulting in hyperbilirubinemias known as Gilbert’s syndrome (GS) and Crigler-Najjar syndrome(CNS).