[Prostaglandins and the prevention of non-steroidal antirheumatic drug-induced gastric lesions].
By the mechanism of the inhibition of the endogenous prostaglandin synthesis by NSAIDs, and thus the attenuation of the protective factors in the gastrointestinal mucosa, gastric lesions frequently develop, and the healing of existing peptic ulcers is appreciably slowed. The combination of several risk factors increases the probability of peptic ulcers or ulcer complications developing under NSAID treatment. In such at-risk patients, treatment with NSAIDs should be accompanied by prophylactic measures. The use of various anti-ulcer drugs has shown that for the treatment of NSAID-induced gastropathies the prostaglandin analog, misoprostol is equally as good as the other anti-ulcer drugs, for the prevention of NSAID-induced lesions however it is superior to H2-receptor antagonists (cimetidine, ranitidine), antacids and sucralfate.
Miederer
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D000527:Alprostadil / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D005753:Gastric Mucosa / Q000187:drug effects; D006801:Humans; D016595:Misoprostol; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000517:prevention & control
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016595:Misoprostol; D000527:Alprostadil
Prostaglandine und die Prävention NSAR-induzierter gastraler Läsionen.