Author(s): Yeomans ND, Skeljo MV, Giraud AS
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Abstract Gastric acid probably exacerbates mucosal injury caused by non-steroidal anti-inflammatory drugs (NSAIDs) in two ways: first, by increasing absorption of NSAIDs, which are weak acids and predominantly in their undissociated form at low pH--this is probably mainly relevant for salicylates; then, by a 'second wave' of injury that leads to deeper erosions, as gastric acid accesses the partially denuded mucosa. Regulation of gastric acid secretion by acid-inhibitory drugs has been shown to decrease acute NSAID-induced injury to varying extents, depending on the drug used and the method of assessing mucosal damage. Healing of chronic NSAID-induced ulcers is slow if NSAID therapy is continued, but is facilitated by treatment with H2-receptor antagonists or prostaglandins. One study of the acid pump inhibitor omeprazole has shown a high rate of healing, even though NSAID therapy was continued.
This article was published in Digestion
and referenced in Journal of Gastrointestinal & Digestive System