Pathophysiology of gastroesophageal reflux. Lower esophageal sphincter dysfunction in gastroesophageal reflux disease

LES dysfunction is the principal mechanism responsible for GER disease. Two main patterns of sphincter dysfunction have been identified: an abnormally high rate of transient LES relaxations, and defective basal LES pressure. Overpowering of a weak LES by pressure transients induced by straining is less common than previously thought, at least under conditions tested thus far. Current evidence suggests that LES dysfunction results primarily from defective neural control, although smooth muscle function may also be impaired. Extrinsic mechanisms, particularly the diaphragmatic crura, also appear to be important during straining. The role of hiatus hernia remains unclear but seems likely to contribute to the pathogenesis of reflux disease by impairing LES function.