Pathophysiology of Gastroesophageal Reflux Disease

Abstract

Gastroesophageal reflux disease pathophysiology is multifactorial and linked to a misbalance between the aggressiveness of the refluxate into the esophagus or adjacent organs and the failure of protective mechanisms associate or not to a defective valvular mechanism at the level of the esophagogastric junction incapable of dealing with a transdiaphragmatic pressure gradient. Antireflux mechanisms include the lower esophageal sphincter and abdominal esophagus, the diaphragm, the angle of His, the Gubaroff valve, and the phrenoesophageal membrane. Protective mechanisms include esophageal motility, saliva production, and epithelial protection. Disruption of this balance occurs most commonly due to the presence of a hiatal hernia, esophageal dysmotility, a rise in abdominal pressure (obesity), and decrease in thoracic pressure (chronic lung diseases).

Modulation of the oxidative plasmatic state in gastroesophageal reflux disease with the addition of rich water molecular hydrogen: A new biological vision

“…Wide quantities of nitric oxide were found in human gastro‐junction, and it can diffuse epithelial mucosa and contribute to the increase in the GERD pathological condition. ROS levels have been reported to be increased in oesophagitis compared to healthy controls in both patients and murine models and are hypothesized to mediate mucosal damage and drive disease progression . Administration of many antioxidants have been shown to prevent mucosal damage in models of oesophagitis suggesting that antioxidant treatment should be considered as a therapy in the treatment of oesophagitis .…”

Ten Things Every Gastroenterologist Should Know About Antireflux Surgery

“…Intact diaphragmatic crura augments the pressure at the LES, which is vital in preventing reflux of gastric contents. 3 Hiatal hernia, a pathologic displacement of the esophagus relative to the diaphragm, compromises the LES's ability to withstand the transdiaphragmatic pressure gradient and is a key contributor to GERD. The LES competency determines the volume of gastric refluxate entering the esophagus; the clearance of esophageal acid determines the duration of esophageal acid exposure.…”

In Defense of Four Decades of Esophageal Function Tests. Reply to Reaction to Articles on High Resolution Manometry, the Length of the Lower Esophageal Sphincter and the Diagnosis of Gastroesophageal Reflux Disease

“…The statement that 'If this study is correct, then during the opening of the LES, the bolus should move in a retrograde direction -from the stomach into the esophagus' is absolutely correct, unless a valve is interposed between the thorax and the abdomen (what happens in the basal state) or peristalsis pushes bolus down (what happens during swallows). The failure of peristalsis or the valvar mechanism or increase in the pressure gradient is actually the pathophysiology of gastroesophageal reflux disease (10) .…”