Kaplan Michael, Bromiker Ruben, Hammerman Cathy
Department of Neonatology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem 91031, Israel; Faculty of Medicine, Hebrew University, Jerusalem, Israel.
Department of Neonatology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem 91031, Israel; Faculty of Medicine, Hebrew University, Jerusalem, Israel.
Semin Perinatol. 2014 Nov;38(7):429-37. doi: 10.1053/j.semperi.2014.08.006. Epub 2014 Oct 3.
Increased hemolysis in the presence of severe neonatal hyperbilirubinemia appears to augment the risk of bilirubin neurotoxicity. The mechanism of this intensifying effect is uncertain. In direct antiglobulin titer (DAT) positive, isoimmune hemolytic disease, the bilirubin threshold at which neurotoxicity occurs appears to be lower than in DAT-negative hyperbilirubinemia. In other hemolytic conditions, the hemolysis may simply facilitate the development of extremely high serum bilirubin levels. Whether the hemolytic process per se exerts an independent effect or whether a very rapid rise in serum bilirubin might lead to greater penetration of the blood-brain barrier is unclear. In this review, we survey the synergistic role of hemolysis associated with severe hyperbilirubinemia in the potentiation of bilirubin-induced neurotoxicity and suggest methods of identifying at-risk babies with increased hemolysis to allow for their increased surveillance.
在严重新生儿高胆红素血症情况下,溶血增加似乎会加大胆红素神经毒性的风险。这种强化作用的机制尚不清楚。在直接抗球蛋白试验(DAT)阳性的同族免疫性溶血病中,发生神经毒性的胆红素阈值似乎低于DAT阴性的高胆红素血症。在其他溶血情况下,溶血可能只是促使血清胆红素水平极高。溶血过程本身是否发挥独立作用,或者血清胆红素的快速升高是否可能导致血脑屏障的更大穿透尚不清楚。在本综述中,我们探讨了与严重高胆红素血症相关的溶血在增强胆红素诱导的神经毒性中的协同作用,并提出识别溶血增加的高危婴儿的方法,以便对其加强监测。