Pathophysiology of reflux esophagitis.
Prolonged (24 h) intra-esophageal pH measurements have shown that short-lasting reflux episodes regularly occur in normal subjects, especially in the postprandial period. This phenomenon has been called physiological reflux. When the reflux episodes become more frequent and last longer, symptoms and esophagitis ensue. The mechanism of symptom production (pyrosis and/or chest pain) is incompletely understood. Chemoreceptors are involved but manometric disturbances and irritability of the esophagus may play an important role. The pathogenesis of pathological reflux is multifactorial: 1. An ineffective anti-reflux barrier at the level of the gastroesophageal junction is the most important factor in the pathogenesis of reflux. 2. Once reflux has occurred, an appropriate clearing of the refluxed material is necessary to minimize the contact time of the noxious agent with the esophageal mucosa. This clearing function is a two-step operation. In the refluxed material the concentration of H+ is the most irritant factor although pepsine increases its noxious character. Bile acid reflux decreases the epithelial resistance. The mucosal resistance to noxious agents is determined by the mucous layer, the cytoprotective properties of the epithelium, the regeneration capacity of the cells and by a number of post-epithelial factors.
Janssens
J
J
Internal Medicine and Gastroenterology, Hospital St. Raphael, Leuven, Belgium.
Vantrappen
G
G
D004942:Esophagitis, Peptic / Q000503:physiopathology*; D004943:Esophagogastric Junction / Q000503:physiopathology*; D005764:Gastroesophageal Reflux / Q000503:physiopathology*; D006801:Humans; D006863:Hydrogen-Ion Concentration