Background Hyperalimentation describes the increase in glucose, amino acid and lipid intake designed to overcome postnatal growth failure in preterm infants. Preterm infants are dependent on phenylalanine metabolism to maintain tyrosine levels because of tyrosine concentration limits in parenteral nutrition (PN). Phenylalanine hydroxylase activity is increased by increasing phenylalanine intake (preterm infants), steroids and diabetes (animal models). The latter is reversed by insulin administration. Hyperalimentation increases hyperglycaemia requiring insulin treatment1.
Aim To compare the plasma amino acid profiles in preterm infants receiving a hyperalimentation versus a control PN regimen.
Methods Infants <29 weeks gestation were randomised to receive hyperalimentation (25% more glucose, 4 g/kg/day versus 3 g/kg/day protein/lipid) or a control regimen within 5 days of birth with head growth as the primary outcome1. Metabolic markers of PN “intolerance” including hyperglycaemia, insulin use, urea and amino acid profiles and hyperlipidaemia were collected from routine laboratory testing and the electronic patient database. Amino acid levels were measured on day 9 (ion exchange chromatography).
Results 142 infants were randomised with 118 amino acid profiles obtained on day 8-10. There were no differences in birthweight or gestation between groups. Of the 22 individual plasma amino acid levels, 14 showed a rise (p<0.05) and 7 no change (p>0.05) when comparing hyperalimentation (n=57) with controls (n=61). Median (IQR) phenylalanine levels increased from 72 (63-79) mmol/l to 80 (65-89) mmol/l (p=0.03). Only tyrosine levels fell (p<0.01) with hyperalimentation resulting in suboptimal tyrosine levels (normal range 33-75 mmol/l). This was associated with the increase in insulin-treated hyperglycaemia seen in this group (table 1; all insulin versus no insulin comparisons: p<0.001).
Conclusion Hyperalimentation results in a paradoxical fall in plasma tyrosine levels associated with an increase in insulin-treated hyperglycaemia. We propose that insulin administration inhibits phenylalanine hydroxylase activity preventing the PN dependent preterm infant maintaining adequate tyrosine levels.
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