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Trick or treatment: alternative medicine on trial by Singh S., Ernst E.

By Singh S., Ernst E.

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NSAIDs may also induce microvascular ischaemia, leading to adherence of cellular elements to the vascular endothelium. The accumulation of activated neutrophils, together with the reduced blood flow might ultimately lead to ischaemic cell damage predisposing to ulceration. In animal models, inhibition of nitric oxide (NO) synthesis promotes NSAID-induced injury, while NO donors reduce NSAID toxicity. Since COX-2 is induced by inflammatory stimuli, it is likely that the anti-inflammatory action of NSAIDs results from the inhibition of COX-2, while the sideeffects are largely owing to the inhibition of COX-1.

Sucralfate (4–6 g/day) is about as effective as antacids in the prevention of stress ulcer bleeding. Administration via nasogastric tube may be associated with technical difficulties. 31 with placebo or untreated controls. It is advised to give prophylaxis only to patients with coagulopathy and/or who are mechanically ventilated. In patients receiving continuous enteral feeding, usually after the most critical ICU period, stress ulcer prophylaxis may be discontinued. Prostaglandin analogues NSAID-INDUCED GASTROPATHY These have not been studied adequately in stress ulcer prophylaxis, as yet there are no data to support their use.

Antimicrob Agents Chemother 1995; 39(9): 2078–2083. 57. Goddard AF, Jessa MJ, Barrett DA, et al. Effect of omeprazole on the distribution of metronidazole, amoxicillin, and clarithromycin in human gastric juice [see comments]. Gastroenterology 1996; 111(2): 358–367. 58. Lind T, Megraud F, Unge P, et al. The MACH2 study: role of omeprazole in eradication of Helicobacter pylori with 1-week triple therapies [see comments]. Gastroenterology 1999; 116(2): 248–253. 59. Malfertheiner P, Bayerdorffer E, Diete U, et al.

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