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CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2007;5:e33–e34

BSTRACTS FROM AROUND THE WORLD

Click on citations to link to these articles and additional papers of interest.

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Helicobacter Pylori and Gastricalignancy

akenaka R, Okada H, Kato J, et al. Helicobacter pylori eradica-ion reduced the incidence of gastric cancer, especially of thentestinal type. Aliment Pharmacol Ther 2007;25:805– 812.

su P-I, Lai K-H, Hsu P-N, et al. Helicobacter pylori infection andhe risk of gastric malignancy. Am J Gastroenterol 2007;102:25–730.

Summary. The link between gastric adenocarci-oma and Helicobacter pylori are strong. These twotudies further demonstrate such a link. Takenakat al, enrolled 1807 patients in a prospective one-yearollow-up study after H. pylori eradication. At the endf one year, 6 of 1519 (0.0039%) patients eradicated of. pylori, and 5 of 288 (0.0174 %) patients with persis-

ent H. pylori infection, developed gastric cancer with 4f the eradicated patients developing the intestinalype cancer. This incidence was statistically lower inhe eradicated patients. Similarly, but with a longerollow-up, Hsu et al, followed 1225 patients with up-er gastrointestinal complaints, of whom 50% had H.ylori infection. Patients underwent endoscopy at base-ine and at 1- and 3-year intervals. During a meanollow-up of 6.3 years, gastric adenocarcinoma devel-ped in 7 of the 618 H. pylori-infected patients0.011%) but in none of the 607 uninfected patients.ikewise, the incidence of gastric lymphoma was 0.2%nd 0%, respectively. Among H. pylori-infected subjects,he incidence of gastric malignancy was comparableetween those receiving, and those not receiving, erad-

cation therapy. Multivariate analysis showed that in-estinal metaplasia was the only independent factorredicting subsequent development of gastric malig-ancy.

Editor’s comment. These studies further underscorehe strong association of Helicobacter pylori infection andastric malignancy. Eradication decreases the likelihoodf subsequent cancer, although these reports nicely showhat it is not totally preventative, likely, because patientslready have developed intestinal metaplasia.This associ-tion is further demonstrated by the long-term follow-upn the study by Hsu et al, where no patients who were notnfected developed gastric cancer. Again, H. pylori eradi-ation was not totally protective. In summary, eradica-ion of H. pylori infection, when identified, is appropriateiven the potential reduction in the subsequent incidencef gastric malignancy. Nevertheless, eradication is not

otally protective perhaps in those who have developed 2

he footprints of longstanding H. pylori–intestinal meta-lasia.

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Omeprazole Before Endoscopy inpper GI Bleeders: Looking Good

au JY, Leung WK, Wu JCY, et al. Omeprazole before endoscopyn patients with gastrointestinal bleeding. N Engl J Med 2007;56:1631–1640.

Summary. Proton-pump inhibitors(PPI) are routinelyrovided for patients with upper GI bleeding. Whileany studies suggest an improved outcome of PPI treat-ent after endoscopic therapy, there is little information

n its impact prior to endoscopy. This prospective trialandomized 638 patients to continuous infusion of ome-razole (80 mg bolus followed by 8 mg infusion/hour) orlacebo at the time of admission followed later by en-oscopy. Outcomes included endoscopic stigmata ofleeding, need for endoscopic therapy, and outcome. Theuthors demonstrated that for those patients receiving IVmeprazole on admission, there was less need for endo-copic therapy, less active bleeding, and more clean basedesions at the time of endoscopy, and reduced hospitaltay. No difference was shown in need for surgery orecurrent bleeding.

Editor’s comment. This study to demonstrates thatontinuous IV infusion of omeprazole, at admission,educes bleeding stigmata and thus the need for endo-copic therapy, as well as duration of hospital stay. Itould have been interesting to know the time fromdministration of omeprazole to endoscopy, but presum-bly this was within 12 hours. The mechanism of such anffect of PPI is presumably clot stabilization, althoughhis would not necessarily explain the differences inleeding stigmata. Based on these studies, IV proton-ump inhibitor infusion should be administered at theime of admission for patients with significant UGIleeding.

dditional Papers of Interest

Christensen S, Riis A, Nørgaard M, et al. Short-termortality after perforated or bleeding peptic ulcer among

lderly patients: A population-based cohort study. BMCeriatrics 2007;7:1– 8.

Study. Rau BM,. Kemppainen EA, Gumbs AA, et al.arly assessment of pancreatic infections and overallrognosis in severe acute pancreatitis by procalcitonin

pct). A prospective international multicenter. Ann Surg

007;245:745–754.

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e34 ABSTRACTS FROM AROUND THE WORLD CLINICAL GASTROENTEROLOGY AND HEPATOLOGY Vol. 5, No. 8

Arvanitakis M, Koustiani G, Gantzarou A, et al. Stagingf severity and prognosis of acute pancreatitis by computedomography and magnetic resonance imaging–A compara-ive study. Dig Liver Dis 2007;39:473–482.

Vaira D, Zullo A, Vakil N, et al. Sequential therapy vstandard triple-drug therapy for helicobacter pylori eradi-ation: A randomized trial. Ann Intern Med 2007;146:

56 –563. 1

Müller S, Pühl S, Vieth M, Stolte M. Analysis ofymptoms and endoscopic findings in 117 patients withistological diagnoses of eosinophilic esophagitis. En-oscopy 2007;39:339 –344.

Flossman E, Rothwell PM. Effect of aspirin on long-erm risk of colorectal cancer: Consistent evidence fromandomized and observational studies. Lancet 2007;369:

603-13.