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Esophageal dysmotility elicited by acid perfusion in children with esophagitis
J V Ganatra1, M S Medow, S Berezin
1Department of Pediatrics, New York Medical College, Valhalla, USA.
Insights
Acid reflux can cause esophageal dysmotility in children, leading to noncardiac chest pain. Treating acid reflux with H2-receptor antagonists resolved symptoms, indicating a link between reflux, motility, and pain.
Area of Science:
- Pediatric Gastroenterology
- Gastrointestinal Motility Disorders
- Esophageal Physiology
Background:
- Noncardiac chest pain is a common complaint in children.
- Gastroesophageal reflux and esophagitis are frequently implicated but the underlying mechanisms remain unclear.
- Acid reflux-induced esophageal dysmotility is a potential contributor to pediatric chest pain.
Purpose of the Study:
- To investigate the role of acid reflux in causing esophageal dysmotility.
- To determine if acid-induced motor abnormalities contribute to noncardiac chest pain in children.
- To assess the efficacy of acid suppression therapy in resolving these symptoms.
Main Methods:
- Esophageal manometry was performed in 19 children with gastroesophageal reflux and daily chest pain.
- Intraesophageal perfusion with saline or hydrochloric acid (HCl) was used to simulate acid reflux.
- Changes in esophageal motility patterns and symptom reporting were recorded during perfusion.
Main Results:
- Acid perfusion induced chest pain in 42% of children.
- Three children exhibited esophageal dysmotility during acid perfusion, characterized by increased contraction duration and amplitude.
- Esophageal acid exposure significantly altered esophageal motility compared to saline perfusion (p < 0.05).
Conclusions:
- This study provides the first evidence of acid-induced esophageal dysmotility in pediatric patients with chest pain.
- Reflux-induced motor abnormalities are implicated in the onset and/or exacerbation of chest pain in children with GERD and esophagitis.
- Symptomatic relief following H2-receptor antagonist therapy supports the role of acid reflux in this condition.
Objective:
To determine the importance of acid reflux-induced dysmotility in the genesis of noncardiac chest pain in children.
Method:
We performed esophageal manometries during intraesophageal perfusion with 0.9% NaCl or 0.1 N HCl in 19 children (age, 14.5 +/- 0.5 yr) with gastroesophageal reflux, biopsy-proven esophagitis, and complaints of at least one episode of chest pain per day.
Results:
Baseline esophageal motilities were normal in all patients. Eight of 19 children (42%) complained of chest pain during intraesophageal acid perfusion. In three of these eight patients, complaints of chest pain during acid perfusion were temporally associated with "conversion" of previously normal motility patterns to manometric tracings, indicating esophageal dysmotility. Compared with findings during saline perfusion, esophageal acid exposure in these three children resulted in significant increases in both the duration (13.6 +/- 4.0 vs 3.2 +/- 0.2 s, p < 0.05) and amplitude (105.2 +/- 7.8 vs 61.2 +/- 2.1 mm Hg, p < 0.05) of esophageal contractions during wet swallows. Symptoms of chest pain resolved in all patients after therapy with H2-receptor antagonists.
Conclusions:
These data represent the first demonstration of acid-induced esophageal dysmotility in children with chest pain and suggest that reflux-induced motor abnormalities contribute to the onset and/or exacerbation of chest pain in pediatric patients with gastroesophageal reflux and esophagitis.