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Histopathological changes in the oesophageal mucosa in Egyptian children with corrosive strictures: A single-centre
Ayman Eskander1, Carolyne Ghobrial1, Nabil A Mohsen1
1Department of Paediatrics, Kasr Alainy School of Medicine, Cairo University, Cairo 11562, Egypt.
Insights
Caustic ingestion can lead to esophageal strictures and an increased risk of cancer. This study found chronic inflammation and dysplasia in children with post-corrosive esophageal strictures after prolonged dilatation.
Area of Science:
- Gastroenterology
- Pediatric Endoscopy
- Histopathology
Background:
- Caustic ingestion is a global health issue, particularly in developing nations.
- Long-term consequences include esophageal strictures and a significantly elevated lifetime risk of esophageal carcinoma.
Purpose of the Study:
- To investigate the occurrence of esophageal mucosal dysplasia in children with post-corrosive strictures following extended endoscopic dilatation.
- To assess histopathological changes in esophageal biopsies after prolonged treatment.
Main Methods:
- Observational study at Cairo University Children's Hospital involving children over 2 years old with post-corrosive esophageal strictures.
- Patients underwent repeated endoscopic dilatation for over 6 months.
- Histopathological examination of esophageal mucosal biopsies was performed to detect chronic esophagitis, inflammation, and dysplasia.
Main Results:
- 85% of patients showed chronic esophagitis (basal cell hyperplasia, hyperkeratosis, subepithelial fibrosis).
- 13% exhibited reactive atypia with severe neutrophilic infiltration.
- 2% (2 patients) were diagnosed with mild squamous dysplasia.
Conclusions:
- Histopathological analysis of esophageal biopsies from post-corrosive stricture patients reveals chronic esophagitis, inflammation, and dysplasia.
- Dysplasia is identified as a complication of post-corrosive esophageal strictures.
Background:
The caustic ingestion continues to be a major problem worldwide especially in developing countries. The long-term complications include stricture and increased life time risk of oesophageal carcinoma. Patients suffered from corrosive induced oesophageal strictures have more than a 1000-fold risk of developing carcinoma of the oesophagus.
Aim:
To determine the possibility of oesophageal mucosal dysplasia after prolonged dilatation in post corrosive stricture.
Methods:
This observational study was conducted at the Paediatric Endoscopy Unit in Cairo University Children's Hospital. It included children of both sexes older than 2 years of age who had an established diagnosis of post-corrosive oesophageal stricture and repeated endoscopic dilatation sessions for more than 6 mo. All patients were biopsied at the stricture site after 6 mo of endoscopic dilatation. A histopathological examination of an oesophageal mucosal biopsy was performed for the detection of chronic oesophagitis, inflammatory cellular infiltration and dysplasia.
Results:
The mean age of the enrolled children was 5.9 ± 2.6 years; 90% of the patients had ingested an alkaline corrosive substance (potash). The total number of endoscopic dilatation sessions were ranging from 16 to 100 with mean number of sessions was 37.2 ± 14.9. Histopathological examination of the specimens showed that 85% of patients had evidence of chronic oesophagitis (group A) in the form of basal cell hyperplasia, hyperkeratosis and subepithelial fibrosis. Thirteen percent of the patients had evidence of reactive atypia (group B) in the form of severe neutrophilic intraepithelial inflammatory cellular infiltration, and 2 patients (2%) had mild squamous dysplasia (group C); we rebiopsied these two patients 6 mo after the initial pathological assessment, guided by chromoendoscopy by Lugol's iodine.
Conclusion:
The histopathology of oesophageal mucosal biopsies in post-corrosive patients demonstrates evidence of chronic oesophagitis, intraepithelial inflammatory cellular infiltration and dysplasia. Dysplasia is one of the complications of post-corrosive oesophageal stricture.
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