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Do we know the cause of reflux disease?
1Department of Gastroenterology, The Cleveland Clinic Foundation, Ohio 44195, USA.
European Journal of Gastroenterology & Hepatology
|August 12, 1999
Summary
Gastroesophageal reflux disease (GERD) involves lower esophageal sphincter (LES) pressure, hiatal hernias, and ineffective esophageal clearance. Gastric factors, including delayed emptying and Helicobacter pylori, also play crucial roles in GERD pathophysiology.
Area of Science:
- Gastroenterology
- Esophageal Physiology
- Microbiome Research
Background:
- Gastroesophageal reflux disease (GERD) pathophysiology involves multiple factors affecting the anti-reflux barrier.
- Key components include the lower esophageal sphincter (LES) pressure and the crural diaphragm, with hiatal hernias significantly impacting LES function and acid clearance.
- Esophageal acid clearance relies on gravity, peristalsis, and saliva, with ineffective peristalsis being a major impairment.
Purpose of the Study:
- To review the multifactorial pathophysiology of GERD.
- To highlight the roles of esophageal and gastric factors in GERD.
- To explore the emerging influence of Helicobacter pylori on GERD severity and complications.
Main Methods:
- Review of existing literature on GERD pathophysiology.
- Analysis of factors contributing to GERD, including LES pressure, hiatal hernia, esophageal clearance, and gastric emptying.
- Examination of the role of acid, pepsin, bile acids, and Helicobacter pylori in esophageal mucosal injury.
Main Results:
- Low LES pressure and transient LES relaxations are critical for gastroesophageal reflux (GER).
- Hiatal hernias impair acid clearance by displacing the LES.
- Ineffective esophageal peristalsis is a primary cause of impaired acid clearance.
- Gastric factors like delayed emptying and subtle postprandial abnormalities contribute to GERD.
- Acid and pepsin are injurious to the esophageal mucosa; bile acids are also implicated.
- Helicobacter pylori colonization, particularly cagA-positive strains, may be protective against severe esophagitis and Barrett's esophagus via hypoacidity mechanisms.
Conclusions:
- GERD pathophysiology is complex, involving esophageal and gastric factors.
- Gastric factors may offer more treatable targets in GERD management.
- Helicobacter pylori's role in GERD is complex, with potential protective effects against severe esophageal conditions, while its eradication may worsen GER in some individuals.