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Gastric acid is a digestive fluid primarily composed of hydrochloric acid (HCl), which is secreted by the parietal cells of the gastric mucosa in the stomach [1]. Its primary biological functions include the denaturation of dietary proteins, the activation of the proteolytic enzyme pepsin from its precursor pepsinogen, and providing a sterile environment by killing ingested microorganisms [1, 3]. While essential for normal digestion, the overproduction or reflux of gastric acid is a central factor in the pathogenesis of gastroesophageal reflux disease (GERD), peptic ulcer disease, and gastritis [4]. In the context of pharmacology, gastric acid serves as a direct chemical target for antacids, which are basic compounds that neutralize the acid to increase the pH of the gastric contents [2]. This neutralization provides rapid symptomatic relief for conditions like heartburn and dyspepsia by reducing the acidity that irritates the esophageal and gastric linings [2]. Unlike systemic medications such as proton pump inhibitors (PPIs) that inhibit the production of acid at the cellular level, antacids act locally within the stomach lumen through a simple acid-base reaction [2, 3]. Monitoring intragastric pH is the standard biomarker for evaluating the efficacy of these acid-neutralizing or acid-reducing therapies [1].
Chemical neutralization of hydrogen ions (H+) by basic compounds to form water and neutral salts, thereby increasing the pH of the gastric lumen.
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