Roux P, Karabus C D, Hartley P S
S Afr Med J. 1982 May 22;61(21):781-2.
A study was made of 3718 newborn infants with jaundice in excess of physiological levels. Prematurity, haemolytic disease, haematomas or infections were present in 1278 patients. Of the remaining 2440 neonates, 137 were deficient in glucose-6-phosphate dehydrogenase (G-6-PD) and 2303 had idiopathic hyperbilirubinaemia. Exchange transfusion was necessary in 59 (42,7%) of the patients with G-6-PD deficiency and in 426 (18,5%) of those with idiopathic hyperbilirubinaemia. Kernicterus occurred in 3 infants (2,2%) with G-6-PD deficiency and in 3 (0,13%) with idiopathic hyperbilirubinaemia. These findings indicate that G-6-PD deficiency contributes significantly to the severity of neonatal jaundice in the population group studied and should be regarded as a potentially dangerous condition.
对3718例黄疸超过生理水平的新生儿进行了研究。1278例患者存在早产、溶血病、血肿或感染。在其余2440例新生儿中,137例葡萄糖-6-磷酸脱氢酶(G-6-PD)缺乏,2303例患有特发性高胆红素血症。G-6-PD缺乏患者中有59例(42.7%)需要换血治疗,特发性高胆红素血症患者中有426例(18.5%)需要换血治疗。G-6-PD缺乏的3例婴儿(2.2%)和特发性高胆红素血症的3例婴儿(0.13%)发生了核黄疸。这些发现表明,在所研究的人群组中,G-6-PD缺乏显著加重了新生儿黄疸的严重程度,应被视为一种潜在的危险状况。