Barrett's esophagus: participation of the esophageal wall.

The modern inhibitors of gastric acid secretion reduce very efficiently the aggressiveness of gastroesophageal reflux but they appear to modify the pathophysiological situation in a way that favours the development of Barrett's esophagus (BE). During the last two decades, the prevalence of BE in the population submitted to endoscopy has clearly increased while the peptic stricture of the esophagus is fast disappearing. With a reduced tendency to stricture and fibrosis, the esophagus seems more prone to the columnar metaplasia. This suggests that the factor that promotes the columnar metaplasia reaches the areas of esophagitis through the esophageal wall. In the conditions of an advanced reflux disease, the veins crossing the gastroesophageal junction would be well suited to the transport of this factor, provided they have not been obliterated by thrombosis or fibrosis. The veins do not normally participate in the metabolic activity but their permeability may be altered in a pathological environment. In the esophageal wall submitted to an important reflux, the environment cannot be normal, as evidenced by the alterations of the esophageal motricity. Furthermore, these veins are submitted to the peristaltic activity of the esophagus.