Kaplan M, Hammerman C
Department of Neonatology, Shaare Zedek Medical Center, Jerusalem, Israel.
Clin Perinatol. 1998 Sep;25(3):575-90, viii.
G-6-PD deficiency is frequently associated with neonatal hyperbilirubinemia, which may be severe enough to cause kernicterus and death. Because of its association with acute trigger-induced hemolytic crises, G-6-PD deficiency-associated neonatal hyperbilirubinemia has been labelled as hemolytic in origin. In this article, the authors summarize recent evidence demonstrating that hemolysis cannot in and of itself be responsible for jaundice and that decreased bilirubin elimination plays a major role in its pathogenesis.
葡萄糖-6-磷酸脱氢酶（G-6-PD）缺乏症常与新生儿高胆红素血症相关，其严重程度可能足以导致核黄疸和死亡。由于它与急性触发因素诱发的溶血危象有关，G-6-PD缺乏症相关的新生儿高胆红素血症被认为起源于溶血。在本文中，作者总结了近期的证据，表明溶血本身并不能导致黄疸，胆红素清除减少在其发病机制中起主要作用。
