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    Expressions of P-glycoprotein in treatment: Resistant Helicobacter pylori patients

    Access Status
    Fulltext not available
    Authors
    Omar, Marhanis
    Crowe, Andrew
    Tay, C.
    Hughes, Jeff
    Date
    2014
    Type
    Journal Article
    
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    Citation
    Omar, M. and Crowe, A. and Tay, C. and Hughes, J. 2014. Expressions of P-glycoprotein in treatment: Resistant Helicobacter pylori patients. Journal of Applied Biomedicine. 12 (4): pp. 263-269.
    Source Title
    Journal of Applied Biomedicine
    DOI
    10.1016/j.jab.2014.02.001
    ISSN
    1214-021X
    School
    School of Pharmacy
    URI
    http://hdl.handle.net/20.500.11937/4412
    Collection
    • Curtin Research Publications
    Abstract

    Objective: There is an increasing incidence of Helicobacter pylori eradication therapy failure secondary to antibiotic resistance. In this study, we aimed to assess the P-glycoprotein expression levels among subjects who were H. pylori-positive and received multiple courses of eradication therapy to understand factors that may associate with their non-responses. Methods: Eleven resistant subjects were recruited during their hospital visit for upper gastrointestinal endoscopies. H. pylori infection status was confirmed by rapid urease test and bacterial culture. P-glycoprotein expressions from the antral and duodenal biopsies were measured by Western blot. The data was compared with H. pylori-negative (n = 54) and H. pylori-positive-treatment naïve (n = 22) that were recruited earlier in another study. Results: The resistant group showed higher relative antral P-glycoprotein expression com-pared to the H. pylori-negative group ( p = 0.0361). Most subjects demonstrated resistance to clarithromycin (72%), metronidazole (63.6%) or both (54.5%). No significant difference was observed between the P-glycoprotein expression in H. pylori-treatment resistant and H. pylori-positive-treatment naïve groups ( p = 0.319). Conclusion: H. pylori infection induces the expression of P-glycoprotein in the antrum. This study shows a potential protective mechanism which may be exploited through the use of P-glycoprotein inducers, such as rifabutin, may be beneficial in eradication regimens.

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