Out of 1,119 term infants, 435 cases presented with
jaundice. For the etiology analysis,
infection was responsible for 16.09% (70/435),
G6PD deficiency accounted for 9.66% (42/435), of which 3 were complicated with acute
bilirubin encephalopathy),
bleeding accounted for 8.05% (35/435), hemolytic diseases accounted for 3.45% (15/435), and breast milk
jaundice accounted for 2.53% (11/435). One case (0.23%) was attributed to
congenital hypothyroidism, multiple etiologies accounted for 22.3% (97/435), and 35.63% (155/435) were of unknown etiology. Of the jaundiced infants, 19.54% (85/435) had
G6PD deficiency, while only 10.23% (70/684) of non-jaundiced infants had
G6PD deficiency; this difference was found to be statistically significant (P < 0.001). Furthermore, the
hemoglobin levels in the jaundiced infants with
G6PD deficiency (146.85 ± 24.88 g/L) were lower than those without
G6PD deficiency (156.30 ± 22.07 g/L) (P = 0.001). 65 jaundiced infants with
G6PD deficiency underwent G6PD mutation testing, and six different genotypes were identified, including c.95A > G, c.392G > T, c.1024C > T, c.1311C > T, c.1376G > T, c.1388G > A, c.871G > A/c.1311C > T, c.392G > T/c.1388G > A, and c.1376G > T/c.1311C > T.65iciency.
Conclusion: