[NSAID-induced gastrointestinal diseases: recent data on pathogenesis and prevention].
Our knowledge of the mechanism by which aspirin and traditional NSAIDs work and damage the gastrointestinal mucosa, recently markedly improved, has suggested a number of measures for the prevention of the NSAID-induced GI lesions. Among these, perhaps the most innovative approach seems to be the nitric oxide-releasing NSAIDs or compounds, like amtolmetin guacyl, that work by increasing the endogenous biosynthesis of NO selectively at gastric mucosa level. Further data, stemming from large RCTs and confirming the results of experimental studies and the initial clinical experiences, are needed to better define the true clinical impact of this approach.
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D000367:Age Factors; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000897:Anti-Ulcer Agents / Q000008:administration & dosage; D019610:Cytoprotection; D004381:Duodenal Ulcer / Q000139:chemically induced; D005260:Female; D005767:Gastrointestinal Diseases / Q000139:chemically induced* / Q000517:prevention & control; D005998:Glycine / Q000009:adverse effects / Q000031:analogs & derivatives; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006635:Histamine H2 Antagonists / Q000008:administration & dosage; D006801:Humans; D007410:Intestinal Diseases / Q000139:chemically induced; D008297:Male; D008875:Middle Aged; D016595:Misoprostol / Q000008:administration & dosage; D011758:Pyrroles / Q000009:adverse effects; D012307:Risk Factors; D013276:Stomach Ulcer / Q000139:chemically induced; D013392:Sucralfate / Q000008:administration & dosage; D014456:Ulcer / Q000139:chemically induced
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D006635:Histamine H2 Antagonists; D011758:Pyrroles; D016595:Misoprostol; C065762:ST 679; D013392:Sucralfate; D005998:Glycine