Severe gastritis decreases success rate of Helicobacter pylori eradication

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dc.contributor.authorKalkan, Ismail Hakki
dc.contributor.authorSapmaz, Ferdane
dc.contributor.authorGuliter, Sefa
dc.contributor.authorAtasoy, Pinar
dc.date.accessioned2020-06-25T18:16:35Z
dc.date.available2020-06-25T18:16:35Z
dc.date.issued2016
dc.departmentKırıkkale Üniversitesi
dc.description.abstractIn several studies, different risk factors other than antibiotic resistance have been documented with Helicobacter pylori eradication failure. We aimed in this study to investigate the relationship of gastric density of H. pylori, the occurrence/degree of gastric atrophy, and intestinal metaplasia (IM) with success rate of H. pylori eradication. Two hundred consecutive treatment naive patients who received bismuth containing standart quadruple treatment due to H. pylori infection documented by histopathological examination of two antral or two corpal biopsies entered this retrospective study. The updated Sydney system was used to grade the activity of gastritis, density of H. pylori colonization, atrophy, and IM. Stages III and IV of operative link for gastritis assessment (OLGA) or the operative link on gastric intestinal metaplasia assessment (OLGIM) stages was considered as severe gastritis. H. pylori eradication was determined via stool H. pylori antigen test performed 4 weeks after the end of therapy. The presence of gastric atrophy and IM was significantly higher in patients with eradication failure (p = 0.001 and 0.01, respectively). Severe gastritis (OLGA III-IV and OLGIM III-IV) rates were higher in eradication failure group. A multiple linear regression analysis showed that OLGA and OLGIM stages were to be independent risk factors for eradication failure (p = 0.03 and 0.01, respectively). Our results suggested that histopathologically severe gastritis may cause H. pylori eradication failure. In addition, we found that H. pylori density was not a risk factor for treatment failure in patients who receive quadruple treatment.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1007/s00508-015-0896-2
dc.identifier.endpage334en_US
dc.identifier.issn0043-5325
dc.identifier.issn1613-7671
dc.identifier.issue9-10en_US
dc.identifier.pmid26637331
dc.identifier.scopus2-s2.0-84949501410
dc.identifier.scopusqualityQ1
dc.identifier.startpage329en_US
dc.identifier.urihttps://doi.org/10.1007/s00508-015-0896-2
dc.identifier.urihttps://hdl.handle.net/20.500.12587/6572
dc.identifier.volume128en_US
dc.identifier.wosWOS:000376607300004
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer Wienen_US
dc.relation.ispartofWiener Klinische Wochenschrift
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectH. pylorien_US
dc.subjectSydneyen_US
dc.subjectAtrophyen_US
dc.subjectIntestinal metaplasiaen_US
dc.subjectOLGAen_US
dc.subjectOLGIMen_US
dc.titleSevere gastritis decreases success rate of Helicobacter pylori eradicationen_US
dc.typeArticle

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