Famotidine Is Inferior to Pantoprazole in Preventing Recurrence of Aspirin-Related Peptic Ulcers or Erosions

Ng, Fook‐Hong; Wong, Siu–Yin; Lam, Kwok–Fai; Chu, Wai-Ming; Chan, Pierre; Ling, Yuk–Hei; Kng, Carolyn; Yuen, Wai–Cheung; Lau, Yuk-Kong; Kwan, Ambrose; Wong, Benjamin C.Y.

doi:10.1053/j.gastro.2009.09.063

Cited by 111 publications

(77 citation statements)

References 20 publications

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“…In patients with LDA-related peptic ulcers, highdose famotidine therapy is inferior to pantoprazole in preventing recurrent bleeding ulcers continued to receive LDA [136]. Lansoprazole was superior to gefarnate in reducing the risk of gastric or duodenal ulcer recurrence in patients with a definite history of gastric or duodenal ulcers who required long-term LDA therapy [137].…”

Section: Commentmentioning

confidence: 99%

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

et al. 2016

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The Japanese Society of Gastroenterology (JSGE) revised the evidence-based clinical practice guidelines for peptic ulcer disease in 2014 and has created an English version. The revised guidelines consist of seven items: bleeding gastric and duodenal ulcers, Helicobacter pylori (H. pylori) eradication therapy, non-eradication therapy, drug-induced ulcer, non-H. pylori, non-nonsteroidal anti-inflammatory drug (NSAID) ulcer, surgical treatment, and conservative therapy for perforation and stenosis. Ninety clinical questions (CQs) were developed, and a literature search was performed for the CQs using the Medline, Cochrane, and Igaku Chuo Zasshi databases between 1983 and June 2012. The guideline was developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. Therapy is initially provided for ulcer complications. Perforation or stenosis is treated with surgery or conservatively. Ulcer bleeding is first treated by endoscopic hemostasis. If it fails, surgery or interventional radiology is chosen. Second, medical therapy is provided. In cases of NSAID-related ulcers, use of NSAIDs is stopped, and anti-ulcer therapy is provided. If NSAID use must continue, the ulcer is treated with a proton pump inhibitor (PPI) or prostaglandin analog. In cases with no NSAID use, H. pylori-positive patients receive eradication and anti-ulcer therapy. If first-line eradication therapy fails, second-line therapy is given. In cases of non-H. pylori, non-NSAID ulcers or H. pyloripositive patients with no indication for eradication therapy, non-eradication therapy is provided. The first choice is PPI therapy, and the second choice is histamine 2-receptor antagonist therapy. After initial therapy, maintenance therapy is provided to prevent ulcer relapse.

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Section: Commentmentioning

confidence: 99%

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

et al. 2016

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“…For prevention, dual antiplatelet therapy (DAPT) with aspirin and an ADP-receptor blocker such as clopidogrel is most effective [2][3][4][5][6] , and almost all patients undergo this therapy after coronary stent implantaKeiichiro Yamane and Yoshihiro Kato contributed equally to this work. the protective effects of PPIs are much stronger than those of H2 blockers 21) . Considering these data, ACCF/AGC/AHA have recently revised the expert consensus 19) .…”

Section: Introductionmentioning

confidence: 97%

Effects of PPIs and an H2 blocker on the Antiplatelet Function of Clopidogrel in Japanese Patients under Dual Antiplatelet Therapy

Yamane

Kato

Tazaki

et al. 2012

JAT

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Aim: Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel is essential after percutaneous coronary intervention (PCI).Clopidogrel is a prodrug and changed into active metabolite by cytochrome p450 enzymes (CYPs), especially CYP2C19. Proton pump inhibitors (PPIs) are used for the prevention of aspirin-induced gastrointestinal bleeding. PPIs are also metabolized by CYP2C19, although the degree of its contribution is dependent on the kind of PPI. Omeprazole, a PPI, has been reported to weaken the antiplatelet effects of clopidogrel. Famotidine, a histamine receptor type 2 (H2) blocker, could also be an alternative to PPIs. The aim of this study was to evaluate the effects of PPIs and an H2 blocker on the antiplatelet function of clopidogrel. Methods: Patients receiving DAPT due to prior PCI, who took either omeprazole or rabeprazole, were enrolled (n = 25). The initial PPI was changed to the other PPI as a crossover study. In another study, patients undergoing DAPT without taking PPIs or H2 blockers were enrolled (n = 30) and famotidine was added. Results: Platelet aggregability when taking omeprazole was higher than when taking rabeprazole, evaluated by an optical aggregometer using collagen as a stimulus (p= 0.0051) and by the VerifyNow P2Y12 assay (p= 0.0060). Platelet aggregability when taking rabeprazole was comparable to that in control patients (n= 15). Concomitant use of famotidine had no effect. Conclusion: Omeprazole significantly reduced the antiplatelet effect of clopidogrel and this effect on clopidogrel was stronger than that of rabeprazole. Concomitant use of famotidine had no effect on the antiplatelet effect of clopidogrel.

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“…PPIs are demonstrated to be more effective than H2RAs (Ng et al, 2010); however, although to a minor extent, H2RAs (other than cimetidine, because of its hepatic metabolism through CYP2C19) appear to be an alternative option in decreasing risk of gastric and duodenal ulcers (also among antiplatelet-receiving patients) (Lin et al, 2011). H2RAs, because of the low cost and low interaction, could be a good choice in patients with low risk for GI bleeding presenting peptic symptoms or NSAID-related dyspepsia.…”

Section: Keypoint II -Timing and Dosingmentioning

confidence: 99%