Van Geet C, Vandenbossche L, Eggermont E, Devlieger H, Vermylen J, Jaeken J
Center for Thrombosis and Vascular Research, University Hospital Gasthuisberg, Leuven, Belgium.
Lancet. 1991 Jan 12;337(8733):73-5. doi: 10.1016/0140-6736(91)90736-9.
The pathogenesis of the transient neonatal hyperammonaemia syndrome is largely unknown. The role of platelet activation was investigated in three preterm infants with this syndrome by non-invasive methods. In all three infants, urinary concentrations of beta-thromboglobulin and 11-dehydrothromboxane B2 levels were much higher during the hyperammonaemia than those in ten control preterm infants. It is possible that transient platelet activation occurs in the portal system of these infants, thereby causing the hyperammonaemia.
短暂性新生儿高氨血症综合征的发病机制在很大程度上尚不清楚。通过非侵入性方法对三名患有该综合征的早产儿的血小板活化作用进行了研究。在所有三名婴儿中，高氨血症期间尿中β-血小板球蛋白浓度和11-脱氢血栓素B2水平比十名对照早产儿中的水平高得多。这些婴儿的门静脉系统可能发生了短暂性血小板活化，从而导致高氨血症。
