Phosphate metabolism in red blood cells of critically ill neonates

Citation
G. Kalan et al., Phosphate metabolism in red blood cells of critically ill neonates, PFLUG ARCH, 440(5), 2000, pp. R109-R111
Citations number
8
Categorie Soggetti
Physiology
Journal title
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
ISSN journal
00316768 → ACNP
Volume
440
Issue
5
Year of publication
2000
Supplement
S
Pages
R109 - R111
Database
ISI
SICI code
0031-6768(2000)440:5<R109:PMIRBC>2.0.ZU;2-D
Abstract
Very few data exist on phosphate metabolism in critically ill neonates. The refore we studied the incidence of hypophosphataemia, the intracellular met abolism of phosphate by measuring adenosine 5'-triphosphate (ATP) and 2,3-d iphosphoglycerate (2,3-DPG) in rod blood cells, and excretion of phosphate in urine. The aims of the study were early detection of changes in phosphat e metabolism as possible diagnostic markers of sepsis and defining the caus e of hypophosphataemia. Neonates, treated in multidisciplinary paediatric intensive care unit (PICU ), included in the study, were less than three days of age. Eighteen of the m had respiratory distress syndrome (RDS) and 16 had microbiologically conf irmed or clinical sepsis. The overall incidence of hypophosphataemia in cri tically ill neonates was over 80%, and was more common (88%) and more profo und in those with sepsis than in those with RDS (79%). Therefore the septic neonates needed significantly larger amounts of phosphate to maintain norm ophosphataemia. In septic neonates ATP concentration in red blood cells was significantly lower than in neonates with RDS and controls, while the 2,3- DPG concentration was increased as a result of compensation. In septic neon ates urinary losses of inorganic phosphate (Pi) were significantly higher t han in neonates with RDS. Hypophosphataemia in critically ill neonates is a t least partly due to higher urinary losses of phosphate.