The Preterm Infant A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency

被引：7
作者：
Kaplan, Michael [1 ,2 ]
Hammerman, Cathy [1 ,2 ]
Bhutani, Vinod K. [3 ]
机构：
[1] Hebrew Univ Jerusalem, Fac Med, POB 12271, IL-9112102 Jerusalem, Israel
[2] Shaare Zedek Med Ctr, Dept Neonatol, POB 3235, IL-91031 Jerusalem, Israel
[3] Stanford Univ, Sch Med, Dept Pediat, 750 Welch Rd,Suite 315, Palo Alto, CA 94305 USA
来源：
CLINICS IN PERINATOLOGY | 2016年 / 43卷 / 02期
关键词：
Glucose-6-phosphate dehydrogenase deficiency; Prematurity; Hyperbilirubinemia; Kernicterus; Bilirubin encephalopathy; Hemolysis; Bilirubin conjugation; DEHYDROGENASE-DEFICIENT; EXCHANGE-TRANSFUSION; ACUTE HEMOLYSIS; DONOR BLOOD; BILIRUBIN; PREMATURE; KERNICTERUS; JAUNDICE; BIRTH; TERM;
D O I：
10.1016/j.clp.2016.01.008
中图分类号：
R71 [妇产科学];
学科分类号：
100211 ;
摘要：
Prematurity and glucose-6-phosphate dehydrogenase (G6PD) deficiency are risk factors for neonatal hyperbilirubinemia. The 2 conditions may interact additively or synergistically, contributing to extreme hyperbilirubinemia, with the potential for bilirubin neurotoxicity. This hyperbilirubinemia is the result of sudden, unpredictable, and acute episodes of hemolysis in combination with immaturity of bilirubin elimination, primarily of conjugation. Avoidance of contact with known triggers of hemolysis in G6PD-deficient individuals will prevent some, but not all, episodes of hemolysis. All preterm infants with G6PD deficiency should be vigilantly observed for the development of jaundice both in hospital and after discharge home.
引用
收藏
页码：325 / +
页数：17
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