Is a normally functioning gastrointestinal tract necessary for normal growth in late gestation?

Byline: R. Blakelock (1), V. Upadhyay (2), R. Kimble (1), P. Pease (2), A. Kolbe (2), J. Harding (3) Keywords: Key words Gastroschisis; Fetal growth; Growth retardation; Intestinal atresia Abstract: It is known that neonates with congenital abnormalities of the intestine tend to be growth-retarded. We wished to explore the hypothesis that normal fetal gut function is needed for normal growth in late gestation. If this is true, then different populations of babies with different congenital gut abnormalities would be expected to have similar impairments of growth and be small at birth. This growth retardation would be more marked in term than in preterm babies and would be independent of other congenital anomalies. To test these hypotheses, we examined 43 babies born with gastroschisis (GS) in Auckland, New Zealand 69 babies born with GS in Birmingham, England and 60 babies born with intestinal atresia (IA) in Auckland. For Auckland babies with GS, the mean weight standard deviation score (WSDS) (i.e., birth weight relative to the mean birth weight for gestation) for term babies was lower than that for preterm babies (-0.932+-0.180 vs -0.064+-0.237, P=0.014). This was also true for Birmingham babies with GS (-0.991+-0.193 vs -0.36 +-0.153, P=0.028). For babies with IA, the mean WSDS for term babies was lower than that for preterm babies (-0.627+-0.266 vs 0.057+-0.211, P=0.034). There was no significant difference between the mean WSDS of babies with and without major congenital abnormalities (-0.402+-0.201 vs -0.271, P=0.70). Our results demonstrate that term babies born with GS are significantly growth-retarded compared with premature babies born with GS. Term babies born with a proximal IA are also growth-retarded. This strongly suggests that in late gestation, the normal growth is dependent on a normally functioning gastrointestinal tract that allows exposure of the proximal intestinal mucosa to ingested amniotic fluid. Author Affiliation: (1) Department of Paediatrics, University of Auckland, and Department of Paediatric Surgery, Starship Children's Health, Auckland, New Zealand, NZ (2) Department of Paediatric Surgery, Starship Children's Health, Park Road, Private Bag 92024, Auckland, New Zealand, NZ (3) Department of Paediatrics, University of Auckland, Private Bag 92019, Auckland, New Zealand, NZ Article note: Accepted: 9 December 1996