The aging stomach: implications for NSAID gastropathy

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Abstract
The mechanisms by which aspirin and other NSAIDs produce acute and chronic gastroduodenal mucosal injury are incompletely understood. In general, gastric mucosal injury is thought to result when aggressive luminal factors (such as acid and pepsin) overwhelm local mucosal protective factors (such as mucus and bicarbonate).8 9Results from animal studies suggest that the production of mucosal lesions by aspirin is a result of two independent mechanisms: (a) cyclooxygenase inhibition by aspirin; and (b) topical effects induced by salicylate, the product of aspirin deacetylation.8 9 The salicylate induced toxic effects include changes in transmembrane permeability, electrical activity, metabolism, and ion transport; whereas cyclooxygenase inhibition and resultant changes in eicosanoid metabolism may result in alterations or reductions in gastric mucosal defensive functions, which include, but are not limited to, bicarbonate and mucus secretion, proliferation and repair, blood flow, and growth factor expression.8 9