Eosinophilic mucosal infiltrate in infants with congenital gastrointestinal obstruction

A D Olson1, K Fukui-Miner

  • 1Department of Pediatrics, C. S. Mott Children's Hospital, University of Michigan, Ann Arbor.

Insights

Eosinophilic gastroenteritis (EGE) can cause duodenal obstruction in infants, but not always due to eosinophilic infiltration. Surgical correction of anatomical defects, not EGE treatment, resolved symptoms in this case.

Area of Science:

  • Pediatric Gastroenterology
  • Gastrointestinal Motility Disorders
  • Allergic Inflammatory Conditions

Background:

  • Eosinophilic gastroenteritis (EGE) is a rare condition characterized by eosinophilic infiltration of the gastrointestinal tract.
  • Intestinal obstruction in EGE is typically attributed to eosinophil infiltration of the bowel wall.
  • Congenital duodenal obstruction can present with similar symptoms in infants.

Observation:

  • An 8-month-old infant presented with severe hematemesis and signs of duodenal obstruction.
  • The infant exhibited elevated eosinophil counts and eosinophilic infiltration in upper GI biopsies, consistent with EGE.
  • Surgical findings revealed anatomical abnormalities including intestinal malrotation, Ladd's bands, duodenal stenosis, and annular pancreas.

Findings:

  • Despite EGE diagnostic markers, the infant's obstructive symptoms were primarily caused by congenital duodenal anomalies.
  • Surgical correction of the anatomical duodenal obstruction led to a rapid and complete clinical recovery.
  • This case highlights that eosinophilic infiltration is not the sole cause of obstructive symptoms in pediatric EGE.

Implications:

  • Challenges the assumption that all obstructive symptoms in pediatric EGE are solely due to eosinophilic infiltration.
  • Emphasizes the importance of thoroughly investigating anatomical causes of duodenal obstruction in infants, even with concurrent EGE.
  • Suggests a need for careful differential diagnosis in pediatric EGE cases presenting with obstruction, considering both inflammatory and structural etiologies.

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