Abstract

Hirschsprung disease (HD), or congenital intestinal aganglionosis, is characterized by absence of neurons in the distal colon resulting from a lack of migration of neural crest cells to the large intestine during fetal development.1 HD typically manifests in early childhood, but very rarely the diagnosis may be delayed for several years when ‘adult HD’ patients present with refractory constipation, intestinal obstruction, sigmoid volvulus or colonic perforation.2 While co-existing congenital genitourinary anamolies have been reported in ∼6% of HD cases, …

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