Mechanisms of nonsteroidal anti-inflammatory drug-induced gastric damage: Actions of therapeutic agents

摘要: Abstract All nonsteroidal anti-inflammatory drugs (NSAIDs) used in the treatment of rheumatic diseases may cause gastric mucosal damage. Although best-studied agent is aspirin, mechanisms by which it damages mucosa are not fully understood. However, thought that drug Impairs defenses penetrating protective mucous and bicarbonate layers damaging epithelial lining cells. In turn, acid permitted to pour through breached defenses. This "back-diffusion" further injures cells destroys capillaries venules. local effect pH dependent contributed secretion stomach. Other aspirin induce or contribute injury include inhibition prostaglandin synthesis, reduction alteration mucus secretion, interference with cell turnover, as well systemic effects such platelet dysfunction. The mechanism nonaspirin NSAIDs gastrointestinal damage uncertain. known inhibit could their toxicity since prostaglandins found stomach both have defensive effects. Partial protections against aspirin-induced other NSAID-induced has been demonstrated, at least some studies, sucralfate, prostaglandins, omeprazole histamine (H 2 )-receptor antagonists. Sucralfate appears act primarily on mechanisms; its antisecretory minimal. Prostaglandins exert a nonantisecretory (cytoprotective) doses, indicating either be involved. most recently studied agent, omeprazole, potent all inhibitors; also cytoprotective, possibly result sulfhydryl groups. available United States potential side limit use patients chronic diseases. Protection H -receptor antagonists mostly related though cytoprotective occur.