早产儿：因葡萄糖-6-磷酸脱氢酶缺乏导致新生儿高胆红素血症的高危情况。
The Preterm Infant: A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency.
作者信息
Kaplan Michael, Hammerman Cathy, Bhutani Vinod K
机构信息
Faculty of Medicine, The Hebrew University of Jerusalem, Ein Kerem, P.O. Box 12271, Jerusalem, 9112102 Israel; Department of Neonatology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem 91031, Israel.
Faculty of Medicine, The Hebrew University of Jerusalem, Ein Kerem, P.O. Box 12271, Jerusalem, 9112102 Israel; Department of Neonatology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem 91031, Israel.
出版信息
Clin Perinatol. 2016 Jun;43(2):325-40. doi: 10.1016/j.clp.2016.01.008. Epub 2016 Feb 28.
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.
早产和葡萄糖-6-磷酸脱氢酶（G6PD）缺乏是新生儿高胆红素血症的危险因素。这两种情况可能会相加或协同作用，导致极重度高胆红素血症，并有可能引发胆红素神经毒性。这种高胆红素血症是由于突然、不可预测的急性溶血发作，以及胆红素清除（主要是结合）不成熟所致。避免G6PD缺乏个体接触已知的溶血触发因素可预防部分但并非全部溶血发作。所有G6PD缺乏的早产儿在住院期间和出院回家后都应密切观察黄疸的发生情况。
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