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Chronic gastritis is not associated with gastric dysrhythmia or delayed solid emptying in children with dyspepsia

Craig A Friesen1, Zhiyue Lin, Robert Garola

  • 1Gastroenterology, Children's Mercy Hospital, Kansas City, Missouri 64108, USA. cfriesen@cmh.edu

Digestive Diseases and Sciences
|July 1, 2005
PubMed

Insights

Chronic gastritis in children with dyspepsia does not correlate with gastric dysrhythmia or delayed emptying. Inflammation and abnormal gut motility appear to be separate causes of pediatric dyspepsia.

Area of Science:

  • Pediatric Gastroenterology
  • Gastrointestinal Motility Disorders
  • Immunohistology

Background:

  • Dyspepsia is a common complaint in children.
  • Chronic gastritis (CG) and gastric dysrhythmia are potential causes of dyspepsia.
  • The relationship between CG and gastric dysrhythmia in pediatric patients is not well understood.

Purpose of the Study:

  • To investigate the association between chronic gastritis and gastric dysrhythmia or delayed gastric emptying in children presenting with dyspepsia.
  • To evaluate immune cell infiltration in the gastric antrum in relation to motility parameters.

Main Methods:

  • Twenty-two children (7-15 years) with dyspepsia and normal endoscopies underwent antral biopsies for CG and immunohistology (CD3+, CD20+, CD25+, tryptase).
  • Electrogastrography (EGG) and gastric scintiscans were performed to assess gastric motility.
  • Correlation analysis was used to examine relationships between inflammation markers and motility.

Main Results:

  • Chronic gastritis and increased immune cell densities were not associated with delayed gastric emptying.
  • Mean CD3+ cell counts showed a positive correlation with normal slow waves on EGG.
  • Patients with normal EGG findings had higher CD3+ cell densities.

Conclusions:

  • In children with dyspepsia and normal endoscopies, chronic antral inflammation is not linked to EGG abnormalities or delayed solid emptying.
  • Chronic gastritis and gastric dysrhythmia may represent distinct pathophysiological mechanisms contributing to pediatric dyspepsia.

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