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dc.contributor.authorKell, M R
dc.contributor.authorWinter, D C
dc.contributor.authorRyan, D
dc.contributor.authorLynch, M
dc.contributor.authorBrew, B
dc.contributor.authorRajpal, P
dc.contributor.authorKirwan, W O
dc.contributor.authorRedmond, H P
dc.date.accessioned2012-02-03T15:13:14Z
dc.date.available2012-02-03T15:13:14Z
dc.date.issued2012-02-03T15:13:14Z
dc.identifier.citationBr J Surg. 1999 Dec;86(12):1538X-1542.en_GB
dc.identifier.issn0007-1323 (Print)en_GB
dc.identifier.issn0007-1323 (Linking)en_GB
dc.identifier.pmid10594502en_GB
dc.identifier.doi10.1046/j.1365-2168.1999.01268.xen_GB
dc.identifier.urihttp://hdl.handle.net/10147/209137
dc.description.abstractBACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.
dc.language.isoengen_GB
dc.subject.meshAdolescenten_GB
dc.subject.meshAdulten_GB
dc.subject.mesh*Appendectomyen_GB
dc.subject.meshAppendicitis/*enzymology/microbiologyen_GB
dc.subject.meshChilden_GB
dc.subject.meshEmergenciesen_GB
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_GB
dc.subject.meshHelicobacter Infections/complications/*enzymologyen_GB
dc.subject.mesh*Helicobacter pylorien_GB
dc.subject.meshHumansen_GB
dc.subject.meshImmunohistochemistryen_GB
dc.subject.meshMacrophages/enzymologyen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshNitric Oxide Synthase/*metabolismen_GB
dc.subject.meshNitric Oxide Synthase Type IIen_GB
dc.titleNitric oxide synthetase and Helicobacter pylori in patients undergoing appendicectomy.en_GB
dc.contributor.departmentUniversity Department of Surgery, Cork University Hospital, Wilton, Ireland.en_GB
dc.identifier.journalThe British journal of surgeryen_GB
dc.description.provinceMunster
html.description.abstractBACKGROUND: This study was designed to determine whether Helicobacter pylori forms part of the normal microenvironment of the appendix, whether it plays a role in the pathogenesis of acute appendicitis, and whether it is associated with increased expression of inducible nitric oxide synthetase (iNOS) in appendicular macrophages. METHODS: Serology for H. pylori was performed on 51 consecutive patients undergoing emergency appendicectomy. Appendix samples were tested for urease activity, cultured and stained for H. pylori, graded according to the degree of inflammatory infiltrate, and probed immunohistochemically for iNOS expression. RESULTS: The mean age of the patients was 21 (range 7-51) years. Seventeen patients (33 per cent) were seropositive for H. pylori but no evidence of H. pylori was found in any appendix specimen. However, an enhanced inflammatory cell infiltration was observed in seropositive patients (P < 0.04) and the expression of macrophage iNOS in the mucosa of normal and inflamed appendix specimens was increased (P < 0.01). CONCLUSION: H. pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. Priming effects on mucosal immunology downstream from the foregut may occur after infection with H. pylori.


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