Do we know the cause of reflux disease?

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Abstract
Numerous factors are important in the pathophysiology of gastroesophageal reflux disease (GERD). The anti-reflux barrier consists of the lower esophageal sphincter (LES) and crural portion of the diaphragm. Absolute LES pressure less than 6 mmHg is required for gastroesophageal reflux (GER), but this is more frequently associated with increased episodes of transient relaxation than persistently low LES pressure. The vast majority of patients with complicated GERD have a hiatal hernia, because the gastric excursion into the chest displaces the LES segment of the distal esophagus above the crural diaphragm, promoting a pinch-cock effect that impairs acid clearance. Clearance of refluxed acid from the esophagus is dependent on gravity, peristalsis and saliva (pH > 6) to neutralize residual acid. Ineffective peristalsis, characterized by low amplitude contractions and dysmotility, represents the major impairment to normal acid clearance. Despite our great attention to these areas, gastric factors may be the most amenable abnormalities to treatment in GERD. Delayed gastric emptying is present in 10-15% of GERD patients, but more subtle postprandial abnormalities may contribute to gastric distension and transient LES relaxation. Although reflux patients are infrequently hypersecretors of acid, studies find acid combined with pepsin to be the most injurious agents to the esophageal mucosa. Recent studies also show increased amounts of bile acids in the refluxate of GERD patients, especially those with Barrett's esophagus. The influence of gastric colonization by Helicobacter pylori is just now being understood. Exciting studies suggest that H. pylori colonization, especially with the more virulent cagA-positive strains, may be protective against severe esophagitis and Barrett's esophagus. Increased intragastric ammonia production and pangastritis with gastric atrophy and intestinal metaplasia, both promoting hypoacidity, are the most likely mechanisms. Conversely, eradication of H. pylori may aggravate GER in some susceptible subjects.

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