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dc.contributor.authorWaldum, Helge Lyder
dc.contributor.authorKleveland, Per Martin
dc.contributor.authorSørdal, Øystein Finset
dc.date.accessioned2020-06-08T13:35:47Z
dc.date.available2020-06-08T13:35:47Z
dc.date.created2016-11-18T18:53:23Z
dc.date.issued2016
dc.identifier.citationTherapeutic Advances in Gastroenterology. 2016, 9 (6), 836-844.en_US
dc.identifier.issn1756-283X
dc.identifier.urihttps://hdl.handle.net/11250/2657232
dc.description.abstractHelicobacter pylori (Hp) is the main cause of gastritis, peptic ulcer disease and gastric cancer. There are still unanswered questions related to the interaction between Hp and man, like what determines the susceptibility for the initial infection and the mechanisms for the carcinogenic effect. The initial infection seems to require a temporal gastric hypoacidity. For Hp to survive in the gastric mucous layer, some acidity is necessary. Hp itself is probably not directly carcinogenic. Only when inducing oxyntic mucosal inflammation and atrophy with hypoacidity, Hp predisposes for gastric cancer. Gastrin most likely plays a central role in the Hp pathogenesis of duodenal ulcer and gastric cancer.en_US
dc.language.isoengen_US
dc.publisherSAGE Publicationsen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleHelicobacter pylori and gastric acid: An intimate and reciprocal relationshipen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.pagenumber836-844en_US
dc.source.volume9en_US
dc.source.journalTherapeutic Advances in Gastroenterologyen_US
dc.source.issue6en_US
dc.identifier.doi10.1177/1756283X16663395
dc.identifier.cristin1401963
dc.description.localcodeCreative Commons Non Commercial CC-BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage)en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal