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Pathophysiology of reflux esophagitis

Author
Peter J Kahrilas, MD
Section Editor
Nicholas J Talley, MD, PhD
Deputy Editor
Shilpa Grover, MD, MPH, AGAF

INTRODUCTION

Some degree of reflux is physiologic [1]. Physiologic reflux episodes typically occur postprandially, are short-lived, asymptomatic, and rarely occur during sleep. Pathologic reflux often occurs nocturnally and is associated with symptoms or mucosal injury. In general, the term gastroesophageal reflux disease (GERD) is applied to patients with symptoms suggestive of reflux or complications thereof, but not necessarily with, esophageal inflammation. Reflux esophagitis describes a subset of patients with GERD who have endoscopic evidence of esophageal inflammation.

The pathophysiology of GERD will be reviewed here. The clinical manifestations and diagnosis of this disorder are discussed separately. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)

MECHANISMS OF GASTROESOPHAGEAL REFLUX DISEASE

The development of gastroesophageal reflux disease (GERD) reflects an imbalance between injurious or symptom-eliciting factors (reflux events, acidity of refluxate, esophageal hypersensitivity) and defensive factors (esophageal acid clearance, mucosal integrity) [2]. The extent of symptoms and of mucosal injury is proportional to the frequency of reflux events, the duration of mucosal acidification, and the caustic potency of refluxed fluid.

Esophagitis results from cytokine-triggered inflammation rather than a direct chemical effect of prolonged exposure to acid, pepsin, and bile on the esophageal epithelium [3-5]. This is substantiated by the observation that histopathological events in the development of esophagitis (lymphocytic inflammation, dilated intercellular spaces) occur deep in the epithelium, not at the luminal surface, and that regenerative changes (basal cell hyperplasia, papillary elongation) are initiated prior to the development of surface necrosis that was formerly hypothesized as the stimulus for those changes. Cytokine-triggered inflammation may also cause alterations in esophageal sensitivity in the absence of esophagitis.

Gastroesophageal junction incompetence — The antireflux barrier at the gastroesophageal junction is anatomically and physiologically complex and vulnerable to several potential mechanisms of reflux. The three dominant pathophysiologic mechanisms causing esophagogastric junction (EGJ) incompetence are:

                 
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Literature review current through: Nov 2017. | This topic last updated: Nov 28, 2017.
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