Systematic reviews of the clinical effectiveness and cost-effectiveness of proton pump inhibitors in acute upper gastrointestinal bleeding

Abstract

PPI treatment compared with placebo or H2RA reduces mortality following PU bleeding among patients with high-risk endoscopic findings, and reduces re-bleeding rates and surgical intervention. PPI treatment initiated prior to endoscopy in UGI bleeding significantly reduces the proportion of patients with SRH at index endoscopy but does not reduce mortality, re-bleeding or the need for surgery. The strategy of giving oral PPI before and after endoscopy, with EHT for those with major SRH, is likely to be the most cost-effective. Treatment of H. pylori infection was found to be more effective than antisecretory therapy in preventing recurrent bleeding from PU. H. pylori eradication alone or eradication followed by misoprostol (with switch to PPI, if misoprostol is not tolerated) are the two most cost-effective strategies for preventing bleeding ulcers among H. pylori-infected NSAID users, although the data cannot exclude PPIs also being cost-effective. Further large randomised controlled trials are needed to address areas such as PPI administration prior to endoscopic diagnosis, different doses and administration of PPIs, as well as the primary and secondary prevention of UGI bleeding.

NSAIDs and Peptic Ulcer Disease

“…Indeed, the eradication of H. pylori in highrisk patients prior to the initiation of NSAID therapy has been shown to significantly reduce the risk of subsequent ulceration (Bazzoli et al, 2001;Malfertheiner et al, 2002). Two systematic reviews have clearly shown that eradication of H. pylori is superior to placebo therapy in the primary prevention of peptic ulcers among NSAID users (risk ratio (95 % CI) 0.35 (0.20 -0.61)) (Leontiadis et al, 2007). Using a Markov model, Leontiadis et al (Leontiadis et al, 2007) showed that the most cost-effective strategy for primary prevention of NSAID-associated ulcers was H. pylori eradication in patients over age 50.…”

“…Systematic reviews have shown that double-dose (e.g., famotidine 40 mg two times daily) but not single-dose H2 receptor antagonists are effective at reducing the risk of NSAID-induced endoscopic gastric ulcers (Leontiadis et al, 2007;Rostom et al, 2002). In patients taking low-dose aspirin, famotidine 20 mg twice daily can reduce the development of oesophagitis, gastric and duodenal ulcers by 80% in an average-risk population, when compared with placebo therapy (Taha et al, 2009).…”

“…Two systematic reviews have clearly shown that eradication of H. pylori is superior to placebo therapy in the primary prevention of peptic ulcers among NSAID users (risk ratio (95 % CI) 0.35 (0.20 -0.61)) (Leontiadis et al, 2007). Using a Markov model, Leontiadis et al (Leontiadis et al, 2007) showed that the most cost-effective strategy for primary prevention of NSAID-associated ulcers was H. pylori eradication in patients over age 50. Interestingly, sensitivity analysis showed that eradication therapy remained cost-effective even when the H. pylori prevalence was as low as 5%.…”

Upper Gastrointestinal Bleeding and the Importance of an Early Endoscopic Study for Diagnosis: A Retrospective Study

“…The most known treatment in management of UGIB since their introduction is the proton pump inhibitor is the most effective as its reduces mortality following peptic ulcer bleeding and also in preventing low dose aspirin use associated to upper gastrointestinal ulcers and bleedings but also as preventing GI disease in relation with NSAIDS use, which are a common auto medicated drug in our population being most common in elderly from the total, 114 patients were treated with proton pump inhibitor as literature says and 86.96% had an effective discharge [12][13][14].…”

The type 2 CCK/gastrin receptor antagonist YF476 acutely prevents NSAID-induced gastric ulceration while increasing iNOS expression

“…Histamine H 2 -receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) prevent this (Leontiadis et al 2007). However, chronic suppression of acid secretion by H2RAs or PPIs causes hypergastrinaemia.…”