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Hypophosphataemia in infants with CHD treated with amino acid infant formula

Part of: Metabolic

Published online by Cambridge University Press:  15 August 2018

Luise V. Marino*
Affiliation:
Department of Dietetics/SLT, University Hospital Southampton NHS Foundation Trust, UK NIHR Biomedical Research Centre Southampton, University Hospital Southampton NHS Foundation Trust and University of Southampton, UK Faculty of Health Sciences, University of Southampton, Southampton, UK
Prathana Venkatesh
Affiliation:
Faculty of Medicine, University Hospital Southampton, NHS Foundation Trust, University of Southampton, UK
Andy Ho
Affiliation:
Paediatric Cardiology, University Hospital Southampton NHS Foundation Trust, UK
R. Mark Beattie
Affiliation:
NIHR Biomedical Research Centre Southampton, University Hospital Southampton NHS Foundation Trust and University of Southampton, UK Faculty of Medicine, University Hospital Southampton, NHS Foundation Trust, University of Southampton, UK Paediatric Gastroenterology, University Hospital Southampton NHS Foundation Trust, UK
Tara Bharucha
Affiliation:
Faculty of Medicine, University Hospital Southampton, NHS Foundation Trust, University of Southampton, UK Paediatric Cardiology, University Hospital Southampton NHS Foundation Trust, UK
*
Author for correspondence: L. V. Marino, Department of Dietetics/SLT, University Hospital Southampton NHS Foundation Trust, Southampton S016 6YD, UK. Tel: +44 (0) 23 8079 6000; Fax: (0) 23 8120 8665; E-mail: [email protected]

Abstract

Objective

Growth among infants with CHD is poor, and is multifactorial with multiple contributing factors. Unexplained hypophosphataemia has been reported among infants and children with complex medical needs consuming amino acid infant formula as the sole source of nutrition. The aim of this audit was therefore to review the incidence of hypophosphataemia among infants with CHD.

Methods

The use of an electronic patient record search for “amino acid infant formula”, “CHD”, and “cardiac” yielded 136 infants <12 months of age. Preterm infants (n=24), children with chromosomal abnormalities (n=4), those >1 year of age (n=11) and infants with a structurally normal heart (n=31) were excluded from the study. The remaining 66 infants with CHD were given amino acid infant formula.

Measurements and main results

In all, 1059 serum phosphate measures were available. After the introduction of amino acid infant formula, significantly more infants with CHD had episodes of hypophosphataemia: 15% (n=10/66) before treatment versus 29% (n=19/66) after treatment (p=0.049). Mean serum phosphate levels were significantly lower in infants with CHD following consumption of amino acid infant formula (2.0±0.5 versus 1.5±0.5 mmol/L following treatment (p<0.0001)). Infants with CHD and hypophosphataemia, associated with amino acid infant formula, use demonstrated significantly lower weight gain compared with those with normal phosphate levels (weight-for-age z scores −2.1±1.4 versus –0.9±1.5; p<0.0001).

Conclusion

After the introduction of an amino acid formula, weight gain was significantly lower among those infants with low phosphate levels. There was a significantly higher prevalence of hypophosphataemia among infants with CHD after the introduction of amino acid infant formula. Lower phosphate levels were associated with lower weight-for-age z scores. Infants with CHD are susceptible to poor weight gain; it is therefore, crucial the nutritional status of infants prescribed amino acid infant formula is more closely monitored to ensure adequate growth.

Type
Brief Report
Copyright
© Cambridge University Press 2018 

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