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Esophageal motor abnormalities in children with gastroesophageal reflux and peptic esophagitis
Insights
Severe gastroesophageal reflux in children causes esophageal motor dysfunction due to inflammation. Treatment improved symptoms and normalized esophageal motility, suggesting a link between inflammation and motility disorders.
Area of Science:
- Pediatric Gastroenterology
- Gastrointestinal Motility Disorders
- Esophageal Physiology
Background:
- Gastroesophageal reflux (GER) is common in children.
- Esophageal inflammation (esophagitis) can be associated with GER.
- The impact of GER-induced esophagitis on esophageal motility is not fully understood.
Purpose of the Study:
- To investigate esophageal motility in children with GER.
- To determine if esophageal inflammation severity correlates with motility abnormalities.
- To assess the effect of anti-reflux therapy on esophageal motility.
Main Methods:
- Esophageal manometry was performed on 26 children with GER (11 severe esophagitis, 15 mild/no esophagitis) and 16 controls.
- Measurements included lower esophageal sphincter pressure, wave amplitude, velocity, and duration.
- Patients received a 12-week antacid course, followed by repeat manometry.
Main Results:
- Lower esophageal motor wave amplitude was significantly reduced in children with severe esophagitis compared to controls (P<0.01).
- Nonspecific motor defects were more frequent in severe esophagitis.
- Therapy led to symptom resolution, endoscopic healing, and normalized manometric findings in previously severe cases.
Conclusions:
- Severe gastroesophageal reflux disease in children causes esophageal motor dysfunction secondary to inflammation.
- Esophageal motility abnormalities are linked to the severity of esophagitis.
- Resolution of inflammation through therapy normalizes esophageal motor function.
Abstract:
Esophageal motility was studied in 26 children with gastroesophageal reflux. In 11 patients (group A), esophagitis was severe; in the remaining 15 (group B), either mild or no microscopic changes were found. Lower esophageal sphincter pressure and amplitude, as well as velocity and duration of esophageal pressure waves, were manometrically measured. All patients underwent a 12-week intensive antacid course. Manometric tracings, blindly read, were compared with those of 16 age-matched children with emesis without proven reflux (group C). Among the variables analyzed, amplitude of the motor waves was significantly lower in patients with severe esophagitis than in group B and C patients (P less than 0.01). Nonspecific motor defects (simultaneous, broad-based, double-peaked waves) were more commonly present in group A. At the end of therapy, symptoms had either disappeared or significantly improved. Endoscopic and histologic studies showed disappearance of the severe inflammatory changes. Manometry, repeated in patients with cured severe esophagitis, showed normalization of the amplitude and significant decrease of the nonspecific motility abnormalities. We conclude that severe gastroesophageal reflux disease in children causes esophageal motor dysfunction, resulting from esophageal inflammation. The occurrence of esophageal motility disorders only in patients with severe esophagitis and its disappearance after therapy may account for the favorable course of reflux disease in infancy.