The role of acid regulation in the treatment of NSAID-induced mucosal damage.
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.
Yeomans
N D
ND
Department of Medicine, University of Melbourne, Western Hospital, Australia.
Skeljo
M V
MV
Giraud
A S
AS
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D002986:Clinical Trials as Topic; D005744:Gastric Acid / Q000502:physiology*; D006635:Histamine H2 Antagonists / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D010437:Peptic Ulcer / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D011453:Prostaglandins / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D014945:Wound Healing
D000894:Anti-Inflammatory Agents, Non-Steroidal; D006635:Histamine H2 Antagonists; D011453:Prostaglandins