Clinical research

Constipation is a common complaint in pediatrics, accounting for 25% of all visits to a pediatric gastroenterologist. While most children improve with diet modification or medications, some suffer from severe constipation that does not respond to conventional therapy. These children often have abdominal pain and bloating, fecal incontinence, absence from school, frequent hospitalizations, and social withdrawal. One of the major causes of this intractable constipation is abnormal colonic motility, where the colon is unable to propel waste products out of the body. This problem is seen in slow transit constipation, irritable bowel syndrome, Hirschsprung disease, and other disorders of colonic function. Many individuals of all ages are affected by these conditions. However, despite its prevalence, little is known about the causes of abnormal colonic motility and therefore available treatments are limited.

Children with Hirschsprung disease can suffer from severe constipation and bloating even after they have had surgery to remove the part of the colon lacking nerve cells. Their symptoms, which can be very difficult to treat, are often due to abnormal colonic motility or abnormal anorectal function. In some cases, children with Hirschsprung can develop enterocolitis, a life-threatening inflammation of the intestine. As in other conditions caused by abnormal intestinal motility, the causes are unknown and treatment options few.

Current research studies include:

  • Examining the nerve cells, glial cells, and neurotransmitters in the intestine of children with Hirschsprung disease after they have surgery to understand the possible causes of persistent post-operative bowel problems.
  • Using metabolite profiling to identify novel serum biomarkers associated with colonic contractility in children.
  • Exploring minimally invasive approaches to visualize the enteric ganglia without the need for rectal or colonic biopsies.
  • Identifying potential causes for Hirschsprung-associate enterocolitis using a genetic mouse model of the disease.