Role of acid suppressants in prophylaxis of NSAID damage.
Gastric acid contributes to the pathogenesis of non-steroidal anti-inflammatory drug (NSAID)-induced ulceration via several mechanisms, including conversion of superficial to deeper injury, impairment of haemostasis, and interference with ulcer healing. The suppression of acid secretion has been shown to reduce the severity of NSAID-induced mucosal damage in experimental models and clinical studies. Current evidence indicates that proton pump inhibitors (PPIs) are the preferred treatment for the healing of gastric ulcers when NSAIDs cannot be discontinued. PPIs are superior to standard-dose H(2)-receptor antagonists and equivalent to low-dose misoprostol in preventing NSAID-induced gastric ulcers. Whether there is any significant advantage of PPIs over higher doses of H(2)-receptor antagonists or misoprostol is unknown. The efficacy of PPIs is enhanced in the presence of H. Pylori infection. Omeprazole has been shown to be effective for the secondary prevention of ulcer bleeding in H. pylori -infected NSAID users. The efficacy of PPIs for the prevention of ulcer complications in H. pylori-negative NSAID users remains uncertain.
Chan
F K
FK
Department of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese University of Hong Kong.
Sung
J J
JJ
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D019072:Antibiotic Prophylaxis; D004359:Drug Therapy, Combination; D005744:Gastric Acid / Q000378:metabolism; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D010437:Peptic Ulcer / Q000139:chemically induced / Q000188:drug therapy / Q000517:prevention & control; D054328:Proton Pump Inhibitors; D017494:Proton Pumps / Q000627:therapeutic use; D016896:Treatment Outcome
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors; D017494:Proton Pumps