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The gastroesophageal junction (GEJ) acid pocket is a physiological phenomenon characterized by a layer of unbuffered, highly acidic gastric juice (pH 1.0–2.0) that forms in the proximal stomach following a meal (Fletcher et al., 2001, Gastroenterology). While the bulk of the meal buffers the rest of the stomach, this pocket remains unbuffered and sits near the GEJ, serving as the primary reservoir for acid reflux into the esophagus (Kahrilas et al., 2013, American Journal of Gastroenterology). In patients with gastroesophageal reflux disease (GERD), the acid pocket is often larger or more frequently positioned above the diaphragm, especially in the presence of a hiatal hernia (Beaumont et al., 2010, Gut). Therapeutic intervention focuses on neutralizing this acidity or physically displacing the pocket to prevent mucosal damage. Alginate-based therapies are particularly effective as they form a neutral-pH raft that floats atop the gastric contents, while proton pump inhibitors (PPIs) and potassium-competitive acid blockers (P-CABs) reduce the overall production of the acid that constitutes the pocket (Rohof et al., 2013, Clinical Gastroenterology and Hepatology).
Drugs target the acid pocket through physical displacement, neutralization, or secretion inhibition. Alginates react with gastric acid to form a neutral-pH raft that floats on top of the stomach contents, physically displacing the acid pocket away from the gastroesophageal junction or acting as a mechanical barrier to reflux (Rohof et al., 2013, Clinical Gastroenterology and Hepatology). Proton pump inhibitors (PPIs) and potassium-competitive acid blockers (P-CABs) reduce the volume and acidity of the pocket by inhibiting the H+/K+-ATPase pump in parietal cells (Kahrilas et al., 2013, American Journal of Gastroenterology).
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