2010
DOI: 10.1016/s0016-5085(10)60495-7
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774 Renin-Angiotensin System and Risk of Peptic Ulcer and Ulcer Bleeding Induced by Low Dose Aspirin

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“…Recently, novel pathways, independent of COX inhibition, have been identified for some NSAIDs. Patients treated with angiotensin-1 receptor blockers or angiotensin-converting enzyme inhibitors and lowdose aspirin have a reduced risk of peptic ulcers or ulcer bleeding [15]. In vitro, exposure of gastric epithelial cells to different concentrations of NSAIDs resulted in altered cell membrane permeability with profound and rapid changes in cell morphology and cell size on confocal microscopy, suggesting that cytotoxicity and biological actions of NSAIDs are mediated by the cell membrane and not dependent on COX [13 ].…”
Section: Mechanisms Of Nsaid-induced Gastrointestinal Toxicitiesmentioning
confidence: 99%
“…Recently, novel pathways, independent of COX inhibition, have been identified for some NSAIDs. Patients treated with angiotensin-1 receptor blockers or angiotensin-converting enzyme inhibitors and lowdose aspirin have a reduced risk of peptic ulcers or ulcer bleeding [15]. In vitro, exposure of gastric epithelial cells to different concentrations of NSAIDs resulted in altered cell membrane permeability with profound and rapid changes in cell morphology and cell size on confocal microscopy, suggesting that cytotoxicity and biological actions of NSAIDs are mediated by the cell membrane and not dependent on COX [13 ].…”
Section: Mechanisms Of Nsaid-induced Gastrointestinal Toxicitiesmentioning
confidence: 99%