Possible platelet contribution to pathogenesis of transient neonatal hyperammonaemia syndrome

C Van Geet; L Vandenbossche; E Eggermont; H Devlieger; J Vermylen; J Jaeken

doi:10.1016/0140-6736(91)90736-9

Possible platelet contribution to pathogenesis of transient neonatal hyperammonaemia syndrome

Lancet. 1991 Jan 12;337(8733):73-5. doi: 10.1016/0140-6736(91)90736-9.

Authors

C Van Geet¹, L Vandenbossche, E Eggermont, H Devlieger, J Vermylen, J Jaeken

Affiliation

¹ Center for Thrombosis and Vascular Research, University Hospital Gasthuisberg, Leuven, Belgium.

PMID: 1670726
DOI: 10.1016/0140-6736(91)90736-9

Abstract

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.

Publication types

Case Reports
Research Support, Non-U.S. Gov't

MeSH terms

Ammonia / blood*
Catheterization / adverse effects
Evaluation Studies as Topic
Female
Humans
Infant, Newborn
Infant, Premature, Diseases / blood*
Infant, Premature, Diseases / etiology*
Infant, Premature, Diseases / urine
Male
Metabolic Diseases / blood*
Metabolic Diseases / etiology*
Metabolic Diseases / urine
Platelet Activation / physiology*
Syndrome
Thromboxane B2 / analogs & derivatives*
Thromboxane B2 / urine
Time Factors
beta-Thromboglobulin / urine*

Substances

beta-Thromboglobulin
Thromboxane B2
11-dehydro-thromboxane B2
Ammonia