Intravenous pantoprazole as an adjuvant therapy following successful endoscopic treatment for peptic ulcer bleeding

内镜治疗消化性溃疡出血成功后,静脉注射泮托拉唑作为辅助治疗

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Abstract

BACKGROUND: Several studies have suggested that proton pump inhibitors are efficacious in preventing rebleeding when administered immediately after endoscopic treatments. However, there are limited clinical outcome data on the use of intravenous pantoprazole. OBJECTIVE: To evaluate the efficacy of intravenous pantoprazole after successful endoscopic treatment for peptic ulcer bleeding using evidence from randomized controlled trials (RCTs). METHODS: The Cochrane Library, MEDLINE, EMBASE and several Chinese databases up to July 2008 were searched. RCTs that compared the relative effectiveness of intravenous pantoprazole with placebo, H2 receptor antagonist or other agents for patients with peptic ulcer bleeding who were pretreated with successful endoscopic therapies were retrieved. RESULTS: Five RCTs comprising a total of 821 participants were included in the final meta-analysis. Overall, there were significant differences in ulcer rebleeding (RR 0.31; 95% CI 0.18 to 0.53; pooled rates were 4.7% for pantoprazole and 15.0% for control), surgical intervention (RR 0.28, 95% CI 0.09 to 0.83; pooled rates were 1.4% in pantoprazole group versus 6.5% in control) and total length of hospital stay (weighted mean difference -1.53; 95% CI -1.91 to -1.16), but not on mortality (RR 0.72, 95% CI 0.29 to 1.81; pooled mortality rates were 1.9% for pantoprazole versus 2.8% for control) and blood transfusion requirements (weighted mean difference -0.53; 95% CI for random effects -1.04 to -0.02) when compared with control treatments. A series of subgroup analyses supported the results from the main analysis. CONCLUSIONS: Intravenous administration of pantoprazole after endoscopic therapy for peptic ulcer bleeding reduces rates of ulcer rebleeding, surgical intervention and overall duration of hospital stay, but not mortality and blood transfusion requirements compared with placebo, H2 receptor antagonist or somatostatin.

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