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[Role of Helicobacter pylori in drug-induced gastrointestinal bleeding].

TWO CO-FACTORS: Helicobacter pylori (Hp) infection and ingestion of NSAIDs are two factors which play a major role in the occurrence of gastric and duodenal ulcers, simple or complicated by perforation and GI bleeding. Hp increases the risk of ulcer in patients receiving an NSAID and the effects of Hp and NSAIDs are additive. Following GI bleeding in a patient receiving a conventional NSAID, the eradication of Hp does not make it possible to protect the patient from another episode of GI bleeding and proves to be a much less effective therapy than continuous therapy with proton pump inhibitors. ROLE OF COX-2 INHIBITORS: COX-2 inhibitors (celecoxib, rofecoxib) are associated with a major decrease in the number of symptomatic and/or complicated ulcers compared to a conventional NSAID. Two randomized studies using doses four times higher than those recommended, have demonstrated that serious GI complications associated with NSAIDs (perforation, GI bleeding) were decreased by half compared to those by use of a conventional NSAID at the usual therapeutic dosage. Considering the patient's previous history of GI disorders prior to initiation of treatment and Hp(+) serology, it appears that decreasing risk of symptomatic or complicated gastro-duodenal ulcer was higher in treatment with Rofexocib in patients who did not have a previous history of ulcer, whatever their Hp status. On the other hand, in the group with a history of GI disorders, the decrease in the risk of ulcer was lower than in patients who were Hp(+). ROLE OF ASPIRIN: The causal relationship between intake of aspirin and Hp appear to be more complex. Thus, it appears that eradication of Hp in patients who presented with GI bleeding and scheduled to resume low-dose aspirin had the same efficacy as a daily dose of 20 mg of omeprazole for a 6-month period.