Presented at the Neonatal Society 2006 Autumn Meeting.
Kidwai S1, Julka D1, Sturrock D2, Hancock M2, Uthaya S1, Modi N1
1 Division of Medicine, Imperial College London
2 Department of Chemical Pathology, Chelsea & Westminster Hospital, London
Background: Compromised growth during early development appears to be a risk factor for the constellation of abnormalities termed the “metabolic syndrome”. Preterm babies are at considerable risk of intrauterine and early postnatal growth deceleration and thus might be particularly vulnerable to adverse metabolic consequences. We have previously demonstrated increased intra-abdominal adiposity (1) and increased intra-hepatocellular lipid (2) by the age of term-equivalent in infants born below 32 weeks gestation.
Aims: We aimed to compare pre-feeding insulin, glucose and insulin sensitivity, calculated using the Quantitative Insulin Sensitivity Check Index (QUICKI) (3), in preterm infants at term-equivalent (PTT) with healthy, appropriate weight for gestational age term-born infants (T). In the PTT group we also aimed to investigate the impact of parenteral nutrition, illness severity and growth velocity between birth and term on these indices.
Methods: A pre-feed blood sample, taken when a clinical sample was required, was analysed for insulin and glucose. These were used to calculate QUICKI. Patient characteristics, parenteral nutrition, expressed as the percentage of time parenteral nutr ition was received between birth and investigation, and illness severity, expressed as the percentage of time in level 1 intensive care, were recorded. Growth velocity was expressed as the change in weight standard deviation score (SDS, UK 1990 Growth Reference). Data were analysed using SPPS version 13. Data are expressed as medians with interquartile ranges in parentheses. The study was approved by the Riverside Research Ethics Committee.
Results: A total of 15 PTT and 7 T infants have been recruited. The fasting glucose concentration was significantly higher in the PTT than the T infants (84.6 (73.8, 92.3 mg/dl) vs 68.4 (51.3, 76.5 mg/dl); p=0.015 (Mann-Whitney). The PTT infants also had a higher insulin concentration (PTT: 2.55 (1.1, 5.0) ; T 2.00 (0.8, 6.0) mU/l) and a lower QUICKI (PTT 0.43 (0.38, 0.49); T 0.46 (0.39, 0.55), though the difference was not statistically significant. Within the PTT group there was a highly significant positive association between the extent of parenteral nutrition exposure and pre-feed insulin (r=0.68; adjusted R2=0.42, p=0.007), and a significant negative correlation with QUICKI (r=-0.61, adjusted R2=0.32, p=0.026). The PTT infants showed a deceleration in growth velocity between birth and term. Neither illness severity nor growth velocity were associated with insulin, glucose or QUICKI.
Conclusion: These data indicate that by the age of term, infants born extremely preterm display signs of reduced insulin sensitivity and that this is related to the extent of parenteral nutrition received. If confirmed, our findings would have implications for the management of preterm infants in intensive care.
References
1. Uthaya et al Pediatr Res 2005; 57:211-251
2. Uthaya et al Pediatr Res 2005; 58, 354-428 (abstr)
3. Katz et al J Clin Endocrinol Metab 2000; 87:2402-2410