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Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
Raza A Patel1, Susan S Baker, Wael N Sayej
1Division of Pediatric Gastroenterology, Hepatology, and Nutrition, University of Utah and Primary Children's Medical Center, Salt Lake City, UT 84113, USA.
Insights
Gastric outlet obstruction (GOO) in children can occur without H. pylori infection. Surgical intervention offers definitive treatment for peptic ulcer disease-related GOO when other methods fail.
Area of Science:
- Pediatric Surgery
- Gastroenterology
- H. pylori Research
Background:
- Gastric outlet obstruction (GOO) in children is typically linked to hypertrophic pyloric stenosis.
- Historically, peptic ulcer disease (PUD) caused by H. pylori was a significant cause of GOO before advanced medical treatments.
- Proton pump inhibitors and H2 blockers are now standard for PUD management.
Observation:
- Two pediatric patients presented with symptoms of weight loss, vomiting, and abdominal pain, indicative of PUD and GOO.
- Esophagogastroduodenoscopy (EGD) and upper gastrointestinal (UGI) series confirmed PUD and GOO diagnoses.
- Despite repeated negative H. pylori tests, both patients received H. pylori eradication therapy.
Findings:
- GOO secondary to PUD can manifest even with negative H. pylori testing.
- Pharmaceutical management failed for both patients, necessitating alternative treatments.
- Patient 1 underwent surgery, while Patient 2 required six pyloric dilations followed by surgery for definitive treatment.
Implications:
- These cases highlight that PUD can cause GOO in children irrespective of H. pylori status.
- Surgical management, including pyloric dilation and surgery, provides effective definitive therapy for refractory GOO.
- Further research may explore non-H. pylori related PUD mechanisms in pediatric GOO.
Abstract:
Gastric outlet obstruction (GOO) in children is most commonly caused by idiopathic hypertrophic pyloric stenosis. Prior to proton pump inhibitors and H2 blockers, peptic ulcer disease (PUD) secondary to H. pylori was a cause of GOO. Both patients presented with a history of weight loss, vomiting, and abdominal pain. Their diagnosis of PUD and GOO was made by EGD and UGI. H. pylori testing was negative for both on multiple occasions but still received H. pylori eradication therapy. Patient 1 after failing pharmaceutical management underwent surgery for definitive treatment. Patient 2 underwent six therapeutic pyloric dilations before undergoing surgery as definitive treatment. These cases suggest that GOO secondary to PUD occurs in the absence of H. pylori infection and surgical management can provide definitive therapy.
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