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Comparison of Duodenal Strictures Between Crohn's and Non-Crohn's Diseases in Children
Ji Won Youn1, Jong Woo Hahn1,2, Hye Ran Yang1,2
1Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, Korea.
Insights
Pediatric duodenal strictures can stem from Crohn's disease (CD) or eosinophilic gastrointestinal disorder (EGID). Measuring serum anti-Saccharomyces cerevisiae antibody (ASCA) and fecal calprotectin aids in identifying these causes.
Area of Science:
- Pediatric Gastroenterology
- Gastrointestinal Motility Disorders
- Inflammatory Bowel Disease
Background:
- Duodenal strictures in children are uncommon but can significantly impact health.
- Identifying the underlying cause is crucial for effective treatment and management.
- Crohn's disease (CD) and eosinophilic gastrointestinal disorders (EGID) are potential causes.
Purpose of the Study:
- To compare clinical features and laboratory findings of pediatric duodenal strictures.
- To differentiate between strictures caused by Crohn's disease and other etiologies.
Main Methods:
- Retrospective analysis of clinical, laboratory, endoscopic, and radiological data.
- Inclusion of 11 pediatric patients diagnosed with duodenal strictures.
- Comparison of data between CD, EGID, and other etiological groups.
Main Results:
- Serum anti-Saccharomyces cerevisiae antibody (ASCA) was positive in 100% of CD and EGID cases.
- Fecal calprotectin levels were elevated in CD and EGID groups compared to others.
- Surgery was required for obstruction in one CD and three other cases; balloon dilation was used in two patients.
Conclusions:
- Acquired duodenal strictures can occur in pediatric patients with CD or EGID.
- Serum ASCA and fecal calprotectin measurements can help identify organic causes of duodenal strictures.
- Early identification aids in timely diagnosis and management of pediatric duodenal strictures.
Purpose:
This study aimed to compare the clinical features and laboratory findings of duodenal strictures caused by Crohn's disease (CD) with those of other etiologies in children.
Methods:
We recruited children diagnosed with duodenal strictures through a full investigation. Clinical, laboratory, endoscopic, and radiological data at diagnosis were collected retrospectively.
Results:
Of the 11 included patients, four were diagnosed with CD, four with eosinophilic gastrointestinal disorder (EGID), and the other three were grouped together (Helicobacter-associated in one and idiopathic disease in two). Serum anti-Saccharomyces cerevisiae antibody (ASCA) was positive in four of four (100%) CD cases, four of four (100%) EGID cases, and none (0%) of the other cases (p=0.011). The median fecal calprotectin concentration was 994 mg/kg in the CD group (range: 626-2,118 mg/kg), 548 mg/kg in the EGID group (range: 458-1,056 mg/kg), and 124 mg/kg in one patient in the other group (p=0.313). Surgery for duodenal obstruction was performed in four patients (one with CD and three with idiopathic and Helicobacter-associated conditions) (p=0.021), and balloon dilation was performed in one patient with CD and one other patient.
Conclusion:
Although acquired duodenal strictures are rare in children, they can develop in pediatric patients with CD or EGID. The measurement of serum ASCA and fecal calprotectin levels before endoscopic and histopathological investigations may identify the presence of organic causes of duodenal strictures in children.
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