Slow-transit constipation in childhood

Abstract

Background/Purpose: Intestinal neuronal dysplasia (IND) as a cause for severe chronic constipation remains controversial. The authors have identified a deficiency of substance P (SP) immunoreactivity in the colonic nerve fibres of some children with severe constipation, and aim to correlate this with clinical features and transit studies.Methods: Over 100 children with intractable constipation with or without soiling have been assessed by clinical questionnaire, nuclear transit study, and laparoscopic seromuscular biopsy of the colon labelled with antibodies to SP and vasoactive intestinal peptide (VIP) using immunofluorescence.Results: More than 30% of children had delayed passage of meconium, and symptoms of constipation appeared by the age of 1 year in 63%. More than 80% had significant delay in colonic transit, and of these, about 80% had reduced SP immunoreactivity in the axons of the colonic circular muscle. A further 6% had heterotopic ganglion cells or hypoplastic ganglia on routine histology.Conclusions: In children with intractable constipation, features of early onset and delayed colonic transit correlated with deficiency of SP in myenteric axons. The authors propose that deficient SP immunoreactivity may be used as a histological marker for severe constipation. Defective excitatory neuromuscular transmission may be the cause of slow colonic transit.