Etiology analysis for term newborns with severe hyperbilirubinemia in eastern Guangdong of China

Table 1 Demographic and clinical characteristics of severe hyperbilirubinemia, n (%)

Basic data	Cases
Sex
Male	346 (59.66)
Female	234 (40.34)
Delivery pattern
Caesarean section	265 (45.69)
Vaginal delivery	315 (54.31)
Feeding pattern
Breast feeding	174 (29.90)
Mixed feeding	195 (33.62)
Formula feeding	165 (28.45)
Unknown	46 (7.93)
Proportion of exchange transfusion level	213 (36.72)
Prolonged jaundice	52 (8.97)
Bilirubin encephalopathy	20 (3.45)

Table 2 UGT1A1*6 variant combination with glucose-6-phosphate dehydrogenase deficiency in 94 cases of severe neonatal hyperbilirubinemia

	G6PD deficiency	G6PD normal	Total	P value
G211A variation
Wild type	16	32	48	0.787
c.211 hetereozygote	14	23	37
c.211 homozygote	4	5	9
Total	34	60	94

G6PD: Glucose-6-phosphate dehydrogenase.

Table 3 Comparison of UGT1A1*6 variant between neonates with severe hyperbilirubinemia and the control group

	Case	Control1	P value
G211A variation
Wild type	48	51	< 0.001
c.211 hetereozygote	37	13
c.211 homozygote	9	1
Total	94	65

¹Term newborns without major abnormality or illness, and with a total serum bilirubin not requiring phototherapy according to the updated clinical guidelines by the China Neonatal Association[11].