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Article: Effect of omeprazole on duodenal ulcer-associated antral gastritis and Helicobacter pylori

TitleEffect of omeprazole on duodenal ulcer-associated antral gastritis and Helicobacter pylori
Authors
Issue Date1991
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116
Citation
Digestive Diseases And Sciences, 1991, v. 36 n. 5, p. 577-582 How to Cite?
AbstractThis study set out to investigate the effects of omeprazole or ranitidine on the progression of antral gastritis and Helicobacter pylori in patients with active duodenal ulcer. A double-blind, double-dummy trial was performed in 270 patients, 241 of whom were studied histologically for the presence of H. pylori. Patients were randomized to receive omeprazole, 10 mg every morning, omeprazole, 20 mg every morning, or ranitidine, 150 mg twice a day, for four weeks. Endoscopy was performed on entry and at weekly intervals during the study; at least two antral biopsies were taken on each occasion to assess the activity and degree of chronic inflammation, as refected by the degree of polymorphonuclear leukocyte infiltration and mononuclear cell infiltration, respectively. Biopsy specimens also were assessed histologically for H. pylori. The sex, age and maximal acid output were comparable in the three treatment groups. The percentages of patients showing an improvement in the activity of gastritis in the four consecutive weeks of treatment were 9%, 40%, 51%, and 53% for omeprazole, 10 mg (N = 78); 14%, 42%, 49%, and 53% for omeprazole, 20 mg (N = 81); and 2%, 23%, 30%, and 33% for ranitidine, 150 mg twice a day (N = 82) (life table analysis gave P < 0.01 for both omeprazole regimens compared with ranitidine). The degree of chronic inflammation showed similar changes. The density of H. pylori decreased significantly after treatment with omeprazole, 10 mg or 20 mg, (both, P < 0.00001) but not with ranitidine. The reduction in bacterial density was significantly higher (P < 0.003) in those who showed improvement of gastritis than in those who did not. We conclude that effective acid inhibition with omeprazole improves antral gastritis and is accompanied by a reduction in antral bacterial density, suggesting that both acid and H. pylori may be involved in the pathogenesis of antral gastritis.
Persistent Identifierhttp://hdl.handle.net/10722/161855
ISSN
2015 Impact Factor: 2.516
2015 SCImago Journal Rankings: 0.995
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHui, WMen_US
dc.contributor.authorLam, SKen_US
dc.contributor.authorHo, Jen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorLok, ASFen_US
dc.contributor.authorNg, MMTen_US
dc.contributor.authorLau, WYen_US
dc.contributor.authorBranicki, FJen_US
dc.date.accessioned2012-09-05T05:15:32Z-
dc.date.available2012-09-05T05:15:32Z-
dc.date.issued1991en_US
dc.identifier.citationDigestive Diseases And Sciences, 1991, v. 36 n. 5, p. 577-582en_US
dc.identifier.issn0163-2116en_US
dc.identifier.urihttp://hdl.handle.net/10722/161855-
dc.description.abstractThis study set out to investigate the effects of omeprazole or ranitidine on the progression of antral gastritis and Helicobacter pylori in patients with active duodenal ulcer. A double-blind, double-dummy trial was performed in 270 patients, 241 of whom were studied histologically for the presence of H. pylori. Patients were randomized to receive omeprazole, 10 mg every morning, omeprazole, 20 mg every morning, or ranitidine, 150 mg twice a day, for four weeks. Endoscopy was performed on entry and at weekly intervals during the study; at least two antral biopsies were taken on each occasion to assess the activity and degree of chronic inflammation, as refected by the degree of polymorphonuclear leukocyte infiltration and mononuclear cell infiltration, respectively. Biopsy specimens also were assessed histologically for H. pylori. The sex, age and maximal acid output were comparable in the three treatment groups. The percentages of patients showing an improvement in the activity of gastritis in the four consecutive weeks of treatment were 9%, 40%, 51%, and 53% for omeprazole, 10 mg (N = 78); 14%, 42%, 49%, and 53% for omeprazole, 20 mg (N = 81); and 2%, 23%, 30%, and 33% for ranitidine, 150 mg twice a day (N = 82) (life table analysis gave P < 0.01 for both omeprazole regimens compared with ranitidine). The degree of chronic inflammation showed similar changes. The density of H. pylori decreased significantly after treatment with omeprazole, 10 mg or 20 mg, (both, P < 0.00001) but not with ranitidine. The reduction in bacterial density was significantly higher (P < 0.003) in those who showed improvement of gastritis than in those who did not. We conclude that effective acid inhibition with omeprazole improves antral gastritis and is accompanied by a reduction in antral bacterial density, suggesting that both acid and H. pylori may be involved in the pathogenesis of antral gastritis.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0163-2116en_US
dc.relation.ispartofDigestive Diseases and Sciencesen_US
dc.subject.meshAdulten_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDouble-Blind Methoden_US
dc.subject.meshDuodenal Ulcer - Complications - Drug Therapy - Microbiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastritis - Drug Therapy - Etiology - Microbiologyen_US
dc.subject.meshHelicobacter Infections - Drug Therapyen_US
dc.subject.meshHelicobacter Pylori - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshOmeprazole - Therapeutic Useen_US
dc.subject.meshPyloric Antrumen_US
dc.subject.meshRanitidine - Therapeutic Useen_US
dc.titleEffect of omeprazole on duodenal ulcer-associated antral gastritis and Helicobacter pylorien_US
dc.typeArticleen_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF01297022-
dc.identifier.pmid2022158-
dc.identifier.scopuseid_2-s2.0-0025729286en_US
dc.identifier.volume36en_US
dc.identifier.issue5en_US
dc.identifier.spage577en_US
dc.identifier.epage582en_US
dc.identifier.isiWOS:A1991FL22100007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHui, WM=7103196477en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US
dc.identifier.scopusauthoridHo, J=15029093800en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridLok, ASF=35379868500en_US
dc.identifier.scopusauthoridNg, MMT=7202076310en_US
dc.identifier.scopusauthoridLau, WY=7402933199en_US
dc.identifier.scopusauthoridBranicki, FJ=7003617514en_US

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