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Article: Interaction of Helicobacter pylori eradication and non-steroidal anti-inflammatory drugs on gastric epithelial apoptosis and proliferation: Implications on ulcerogenesis

TitleInteraction of Helicobacter pylori eradication and non-steroidal anti-inflammatory drugs on gastric epithelial apoptosis and proliferation: Implications on ulcerogenesis
Authors
Issue Date2000
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2000, v. 14 n. 7, p. 879-885 How to Cite?
AbstractBackground: Apoptosis is associated with loss of gastric mucosal integrity and may play an important role in ulcer development. Aim: To examine how Helicobacter pylori and NSAIDs interact to effect apoptosis and proliferation of the gastric mucosa. Methods: Patients presenting with musculoskeletal pain requiring NSAID treatment and without previous exposure to NSAID or pre-existing ulcers were recruited. Patients were divided into three groups: (A) H. pylori-infected; (B) H. pylori-eradicated; and (C) non-infected patients. They were given naproxen for 8 weeks. Patients with non-ulcer dyspepsia and H. pylori infection who were given anti-Helicobacter therapy were recruited as controls (D). Endoscopy was performed at baseline and 8-weeks after receiving naproxen. Gastric antral biopsies were obtained to assess apoptosis by terminal uridine deoxynucleotidyl nick end-labelling (TUNEL) and proliferation by Ki67 immunostaining. Results: A total of 55 patients were studied. H. pylori-positive patients had a higher apoptosis and proliferation index at baseline than non-infected patients (P < 0.0001), and eradication of H. pylori resulted in a significant reduction in these parameters. The NSAID induced apoptosis in non-infected subjects (P = 0.03) whilst apoptosis was reduced in H. pylori-positive patients receiving NSAID (P = 0.02). After 8 weeks of NSAID, post-treatment apoptosis was significantly higher in patients with persistent H. pylori infection than in non-infected patients (P = 0.01). Conclusions: Eradication of H. pylori prior to NSAID therapy significantly reduces the level of apoptosis in the gastric mucosa, which may contribute to maintaining mucosa integrity and preventing ulcer development.
Persistent Identifierhttp://hdl.handle.net/10722/162399
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorChan, FKLen_US
dc.contributor.authorLee, TLen_US
dc.contributor.authorChung, SCSen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:19:35Z-
dc.date.available2012-09-05T05:19:35Z-
dc.date.issued2000en_US
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2000, v. 14 n. 7, p. 879-885en_US
dc.identifier.issn0269-2813en_US
dc.identifier.urihttp://hdl.handle.net/10722/162399-
dc.description.abstractBackground: Apoptosis is associated with loss of gastric mucosal integrity and may play an important role in ulcer development. Aim: To examine how Helicobacter pylori and NSAIDs interact to effect apoptosis and proliferation of the gastric mucosa. Methods: Patients presenting with musculoskeletal pain requiring NSAID treatment and without previous exposure to NSAID or pre-existing ulcers were recruited. Patients were divided into three groups: (A) H. pylori-infected; (B) H. pylori-eradicated; and (C) non-infected patients. They were given naproxen for 8 weeks. Patients with non-ulcer dyspepsia and H. pylori infection who were given anti-Helicobacter therapy were recruited as controls (D). Endoscopy was performed at baseline and 8-weeks after receiving naproxen. Gastric antral biopsies were obtained to assess apoptosis by terminal uridine deoxynucleotidyl nick end-labelling (TUNEL) and proliferation by Ki67 immunostaining. Results: A total of 55 patients were studied. H. pylori-positive patients had a higher apoptosis and proliferation index at baseline than non-infected patients (P < 0.0001), and eradication of H. pylori resulted in a significant reduction in these parameters. The NSAID induced apoptosis in non-infected subjects (P = 0.03) whilst apoptosis was reduced in H. pylori-positive patients receiving NSAID (P = 0.02). After 8 weeks of NSAID, post-treatment apoptosis was significantly higher in patients with persistent H. pylori infection than in non-infected patients (P = 0.01). Conclusions: Eradication of H. pylori prior to NSAID therapy significantly reduces the level of apoptosis in the gastric mucosa, which may contribute to maintaining mucosa integrity and preventing ulcer development.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_US
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Pharmacology - Therapeutic Useen_US
dc.subject.meshAnti-Ulcer Agents - Therapeutic Useen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastric Mucosa - Drug Effects - Pathologyen_US
dc.subject.meshHelicobacter Infections - Complications - Drug Therapy - Pathologyen_US
dc.subject.meshHelicobacter Pylorien_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshStomach Ulcer - Etiology - Pathologyen_US
dc.titleInteraction of Helicobacter pylori eradication and non-steroidal anti-inflammatory drugs on gastric epithelial apoptosis and proliferation: Implications on ulcerogenesisen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2036.2000.00783.xen_US
dc.identifier.pmid10886043-
dc.identifier.scopuseid_2-s2.0-0033937926en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033937926&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume14en_US
dc.identifier.issue7en_US
dc.identifier.spage879en_US
dc.identifier.epage885en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridChan, FKL=7202586434en_US
dc.identifier.scopusauthoridLee, TL=35292432600en_US
dc.identifier.scopusauthoridChung, SCS=19642462800en_US
dc.identifier.scopusauthoridSung, JJY=24473715000en_US

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