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[仅葡萄糖-6-磷酸脱氢酶缺乏能否解释新生儿黄疸]

[Can glucose-6-phosphate dehydrogenase deficiency alone explain neonatal jaundice].

作者信息

Verdy E, Herve J, Boisson C, Combrisson A

出版信息

Rev Fr Transfus Immunohematol. 1978 Dec;21(5):1081-91. doi: 10.1016/s0338-4535(78)80005-1.

Abstract

Several authors have insisted on the role of a glucose 6-phosphate deshydrogenase (G6PD) deficiency in the occurrence of neonatal jaundice which can be severe, leading to exchange transfusion. Considering the fact that haemolysis, occuring in deficient patients, is most of the time induced, our aim was to search if a neonatal hyperbilirubinemia could be explained by the sole G6PD deficiency or by extra "oxidant stress". Red blood cell G6PD activity of 289 newborn babies of African or Antillian origin was tested by a Tetrazolium linked method. 21 newborns were deficient. 8 female babies were heterozygous for G6PD deficiency. No neonatal jaundice was observed. With Bienzle and all., we can suppose that the "environment" takes an important part in the incidence of neonatal jaundice among G6PD deficient newborn of African or Antillian origin. However as triggering factors could be ignored, we think compulsary to search a G6PD deficiency in every neonatal jaundice necessitating an exchange-transfusion.

摘要

几位作者坚持认为葡萄糖-6-磷酸脱氢酶(G6PD)缺乏在新生儿黄疸的发生中起作用,这种黄疸可能很严重,导致换血治疗。考虑到在缺乏该酶的患者中发生的溶血大多数情况下是由诱发因素引起的,我们的目的是探究新生儿高胆红素血症是否仅由G6PD缺乏或额外的“氧化应激”所导致。通过一种偶氮四唑法检测了289名非洲或安的列斯群岛血统新生儿的红细胞G6PD活性。21名新生儿缺乏该酶。8名女婴为G6PD缺乏杂合子。未观察到新生儿黄疸。与比恩泽尔等人的观点一致,我们可以认为“环境”在非洲或安的列斯群岛血统的G6PD缺乏新生儿的新生儿黄疸发病率中起重要作用。然而,由于触发因素可能被忽视,我们认为在每例需要换血治疗的新生儿黄疸病例中都必须检查是否存在G6PD缺乏。

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