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Radiologic features of gastric outlet obstruction in infants after long-term prostaglandin administration
1Department of Diagnostic Imaging, Hospital for Sick Children, Toronto, Ontario, Canada.
Insights
Long-term prostaglandin (PG) therapy may cause gastric mucosal hyperplasia in children with congenital heart disease, leading to feeding issues and characteristic stomach changes visible on imaging.
Area of Science:
- Pediatric Gastroenterology
- Cardiology
- Medical Imaging
Background:
- Long-term prostaglandin (PG) therapy is increasingly recognized for potential adverse effects.
- Gastric mucosal hyperplasia has been an emerging concern associated with PG use.
Purpose of the Study:
- To investigate the clinical and radiologic manifestations of prostaglandin-associated gastric mucosal hyperplasia.
- To assess the impact of PG therapy on gastric and skeletal structures in pediatric patients.
Main Methods:
- Retrospective review of clinical and radiologic records (including sonography and barium meal) of eight patients.
- Patients had complex congenital heart disease and were undergoing long-term PG therapy.
Main Results:
- Six patients experienced feeding problems, vomiting, or abdominal distension.
- Radiologic findings included antral narrowing (two suggestive of pyloric stenosis) and significant gastric mucosal lobulation/polypoid appearance on sonography.
- Three patients also exhibited cortical hyperostosis, another PG-related finding.
Conclusions:
- Prostaglandin-associated gastric mucosal hyperplasia can manifest with gastrointestinal symptoms and distinct sonographic findings.
- This condition should be considered in pediatric patients with congenital heart disease on long-term PG therapy presenting with feeding difficulties and gastric abnormalities.
Abstract:
Long-term prostaglandin (PG) therapy has recently been associated with gastric mucosal hyperplasia. We reviewed the clinical and radiologic (especially sonographic) records of eight patients with complex congenital heart disease who were on PG therapy. Feeding problems, vomiting, and abdominal distension were present in six patients. Barium meal revealed antral narrowing in three patients, suggestive of hypertrophic pyloric stenosis in two. Sonography showed a variable degree of increased gastric mucosal lobulation often accompanied by a marked polypoid or lobular appearance. Cortical hyperostosis related to PG therapy was seen in three patients. PG-associated gastric mucosal hyperplasia can cause feeding problems and pronounced gastric lobulation.