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Hirschprung's disease

P B Sullivan1

  • 1University Department of Paediatrics, Oxford Radcliffe Hospital.

Archives of Disease in Childhood
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

Hirschsprung's disease pathogenesis suggests an abnormal colon microenvironment hinders neural crest cell development. This leads to congenital aganglionosis and other enteric nervous system abnormalities, likely due to genetic factors.

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Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Genetics

Background:

  • Hirschsprung's disease is characterized by the congenital absence of ganglion cells in the colon.
  • Existing theories propose various causes, including neural crest cell migration defects.

Purpose of the Study:

  • To review current evidence on the pathogenesis of Hirschsprung's disease.
  • To elucidate the role of the microenvironment in enteric nervous system development.

Main Methods:

  • Review of current scientific literature and evidence on Hirschsprung's disease pathogenesis.
  • Analysis of the 'abnormal microenvironment' hypothesis.

Main Results:

  • Evidence favors the 'abnormal microenvironment' hypothesis for Hirschsprung's disease.

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  • This hypothesis explains both aganglionosis and other enteric neuronal abnormalities like dysplasia and hypoganglionosis.

    • Conclusions:

    • The colon's microenvironment plays a critical role in neural crest cell development and migration.
    • Genetic factors likely determine the abnormal extracellular matrix, necessitating further molecular genetic research for diagnostic advancements.