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    Nitric oxide synthetase and Helicobacter pylori in patients undergoing appendicectomy.

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    Authors
    Kell, M R
    Winter, D C
    Ryan, D
    Lynch, M
    Brew, B
    Rajpal, P
    Kirwan, W O
    Redmond, H P
    Affiliation
    University Department of Surgery, Cork University Hospital, Wilton, Ireland.
    Issue Date
    2012-02-03T15:13:14Z
    MeSH
    Adolescent
    Adult
    *Appendectomy
    Appendicitis/*enzymology/microbiology
    Child
    Emergencies
    Enzyme-Linked Immunosorbent Assay
    Helicobacter Infections/complications/*enzymology
    *Helicobacter pylori
    Humans
    Immunohistochemistry
    Macrophages/enzymology
    Middle Aged
    Nitric Oxide Synthase/*metabolism
    Nitric Oxide Synthase Type II
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    Citation
    Br J Surg. 1999 Dec;86(12):1538X-1542.
    Journal
    The British journal of surgery
    URI
    http://hdl.handle.net/10147/209137
    DOI
    10.1046/j.1365-2168.1999.01268.x
    PubMed ID
    10594502
    Abstract
    BACKGROUND: 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.
    Language
    eng
    ISSN
    0007-1323 (Print)
    0007-1323 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1046/j.1365-2168.1999.01268.x
    Scopus Count
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    Cork University Hospital

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