UGT1A1 mutation association with increased bilirubin levels and severity of unconjugated hyperbilirubinemia in ABO incompatible newborns of China

Table 4 The associations between risk of severe neonatal hyperbilirubinemia and UGT1A1 coding sequence variants and different type of UGT1A1 haplotype in neonates with ABO hemolysis disease: multivariate logistic regression analysis (N = 59^a)

Genotype	Total	TBIL > 342 umol/L			TBIL > 427umol/L
Genotype	N(%)	N(%)	OR_adj^b (95%CI)	P	N(%)	OR_adj^b (95%CI)	P
Model 1(n = 59)
Wild type	38(64.4%)	16(57.1%)	1.00		4(30.8%)	1.00
Heterozygous mutation	19(32.2%)	10(35.7%)	2.25(0.66–7.61)	0.076	8(61.5%)	8.74(1.86–41.09)	0.008
Homozygous mutation	2(3.4%)	2(7.1%)	NA(0.00-NA)		1(7.7%)	15.09(0.61–375.49)
Model 2(n = 59)
Wild type	38(64.4%)	16(57.1%)	1.00		4(30.8%)	1.00
Heterozygous + Homozygous mutation	21(35.6%)	12(42.9%)	2.72(0.82–9.03)	0.093	9(69.2%)	9.16(1.99–42.08)	0.002
Halplotype (Frequency)
TA6GC(75.89%)			1.00			1.00
TA6AC(16.58%)			3.46(0.97–12.39)	0.062		9.41(1.80–49.26)	0.011
TA7GC(5.08%)			2.57(0.37–17.89)	0.35		8.18(0.80–83.65)	0.083
TA6GT(2.17%)			2.38(0.12–48.13)	0.57		10.64(0.44–254.56)	0.15
Other^c			–	–		–	–

^a Ten cases with the feeding practice unknown were not taken into the regression analysis
^bAdjusted for age, gender, and feeding practice
^c Other haplotypes had frequencies less than 1%

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