ISO exposure can induce HO-1 expression in the liver and may explain the development of severe hyperbilirubinemia in postsurgical infants, especially in those undergoing hemolysis.
The objectives of this study were to compare the distribution of (GT)n repeat lengths in the HO-1 promoter region in a cohort of AA infants to those found in other ethnicities and to evaluate the contribution of this polymorphism to the degree of hyperbilirubinemia and the level of COHbc in this cohort.
The present study was undertaken to investigate the genotype and allele frequencies of the variants in the four bilirubin metabolism genes (UGT1A1, OATP2, HMOX1, and BLVRA) and their association with hyperbilirubinemia.
Additionally participants were genotyped for those polymorphisms that are known (UGT1A1*28) or likely (HMOX-1 microsatellites) to impact bilirubinemia.
The log-binomial analysis demonstrated greater risks of hyperbilirubinemia in infants with GA at nt211 in UGT1A1 (RR = 1.548; 95 % CI = 1.096-2.187), short HO-1 promoter GT-repeat (RR = 2.185; 95 % CI = 1.527-3.125), and G6PD deficiency (RR = 1.985; 95 % CI = 1.010-3.901).
To elucidate the genetic factors causing severe hyperbilirubinemia in these patients, we studied two notable factors associated with bilirubin production: heme oxygenase-1, a key enzyme of heme metabolism, and fetal Hb composition, a factor possibly associated with heme load in neonates.