What are the racial predilections of unconjugated hyperbilirubinemia?

Updated: May 21, 2019
  • Author: Hisham Nazer, MBBCh, FRCP, DTM&H; Chief Editor: BS Anand, MD  more...
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In Gilbert syndrome, differences exist in the mutation of the UGT1A1 gene in certain ethnic groups; the TATAA element in the promoter region is the most common mutation site in the white population. For example, a strong correlation has been found between the UGT1A1*28 polymorphism and hyperbilirubinemia in Romanian patients with Gilbert syndrome. [6] In a study of 292 Romanian patients with Gilbert syndrome and 605 healthy counterparts, investigators used PCR gene amplification and found that the highest frequency polymorphism was UGT1A1*28 (7TA), occurring in nearly 62% of the entire study group, followed by nearly 37% with the UGT1A1*1 (6TA) allele, and 0.61% and 0.72%, respectively, with the 5TA and 8TA variants. [6] Nearly 58% of the study cohort had the (TA)6/7 heterozygous genotype, followed by 32% with the homozygous (TA)7/7 genotype.

A racial variation exists in the development of neonatal jaundice. A common mutation in the UGT gene (Gly71Arg) leads to an increased incidence of severe neonatal hyperbilirubinemia (approximately 20%) in Asians.

Obstetric obesity appears to correspond with both maternal and neonatal hyperbilirubinemia, potentially via the inhibition of hepatic UGT1A1 enzyme, with the highest prevalence in Native Hawaiian and Pacific Island women. [47] Investigators found that increasing obesity and maternal obesity correlated with elevated maternal unconjugated bilirubin; maternal obesity was also associated with neonatal hyperbilirubinemia, particularly in Native Hawaiian and Pacific Island women. [47]

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