Possible platelet contribution to pathogenesis of transient neonatal hyperammonaemia syndrome.
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.
Van Geet
C
C
Center for Thrombosis and Vascular Research, University Hospital Gasthuisberg, Leuven, Belgium.
Vandenbossche
L
L
Eggermont
E
E
Devlieger
H
H
Vermylen
J
J
Jaeken
J
J
D000641:Ammonia / Q000097:blood*; D002404:Catheterization / Q000009:adverse effects; D005069:Evaluation Studies as Topic; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000097:blood* / Q000209:etiology* / Q000652:urine; D008297:Male; D008659:Metabolic Diseases / Q000097:blood* / Q000209:etiology* / Q000652:urine; D015539:Platelet Activation / Q000502:physiology*; D013577:Syndrome; D013929:Thromboxane B2 / Q000031:analogs & derivatives* / Q000652:urine; D013997:Time Factors; D001620:beta-Thromboglobulin / Q000652:urine*
D001620:beta-Thromboglobulin; D013929:Thromboxane B2; C049235:11-dehydro-thromboxane B2; D000641:Ammonia