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      Disease manifestations of Helicobacter pylori infection in Arctic Canada: using epidemiology to address community concerns

      research-article
      1 , 2 , 2 , 3 , 2 , 4 , 5 , 2 , 2 , 2 , 2 , the CAN Help Working Group
      (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab), (Collab)
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          Abstract

          Objectives

          Helicobacter pylori infection, linked to gastric cancer, is responsible for a large worldwide disease burden. H pylori prevalence and gastric cancer rates are elevated among indigenous Arctic communities, but implementation of prevention strategies is hampered by insufficient information. Some communities in northern Canada have advocated for H pylori prevention research. As a first step, community-driven research was undertaken to describe the H pylori-associated disease burden in concerned communities.

          Design

          Participants in this cross-sectional study completed a clinical interview and gastroscopy with gastric biopsies taken for histopathological examination in February 2008.

          Setting

          Study procedures were carried out at the health centre in Aklavik, Northwest Territories, Canada (population ∼600).

          Participants

          All residents of Aklavik were invited to complete a clinical interview and gastroscopy; 194 (58% female participants; 91% Aboriginal; age range 10–80 years) completed gastroscopy and had gastric biopsies taken.

          Primary and secondary outcome measures

          This analysis estimates the prevalence of gastric abnormalities detected by endoscopy and histopathology, and associations of demographic and clinical variables with H pylori prevalence.

          Results

          Among 194 participants with evaluable gastric biopsies, 66% were H pylori-positive on histology. Among H pylori-positive participants, prevalence was 94% for acute gastritis, 100% for chronic gastritis, 21% for gastric atrophy and 11% for intestinal metaplasia of the gastric mucosa, while chronic inflammation severity was mild in 9%, moderate in 47% and severe in 43%. In a multivariable model, H pylori prevalence was inversely associated with previous gastroscopy, previous H pylori therapy and aspirin use, and was positively associated with alcohol consumption.

          Conclusions

          In this population, H pylori-associated gastric histopathology shows a pattern compatible with elevated risk of gastric cancer. These findings demonstrate that local concern about health risks from H pylori is warranted and provide an example of how epidemiological research can address health priorities identified by communities.

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          Most cited references39

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          Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

          The Sydney System for the classification of gastritis emphasized the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. To reappraise the Sydney System 4 years after its introduction, a group of gastrointestinal pathologists from various parts of the world met in Houston, Texas, in September 1994. The aims of the workshop were (a) to establish an agreed terminology of gastritis; (b) to identify, define, and attempt to resolve some of the problems associated with the Sydney System. This article introduces the Sydney System as it was revised at the Houston Gastritis Workshop and represents the consensus of the participants. Overall, the principles and grading of the Sydney System were only slightly modified, the grading being aided by the provision of a visual analogue scale. The terminology of the final classification has been improved to emphasize the distinction between the atrophic and nonatrophic stomach; the names used for each entity were selected because they are generally acceptable to both pathologists and gastroenterologists. In addition to the main categories and atrophic and nonatrophic gastritis, the special or distinctive forms are described and their respective diagnostic criteria are provided. The article includes practical guidelines for optimal biopsy sampling of the stomach, for the use of the visual analogue scales for grading the histopathologic features, and for the formulation of a comprehensive standardized diagnosis. A glossary of gastritis-related terms as used in this article is provided.
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            Unidentified curved bacilli on gastric epithelium in active chronic gastritis.

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              Carcinogenesis of Helicobacter pylori.

              Helicobacter infection is the leading cause of gastric cancer worldwide. Infection with this ubiquitous bacterium incites a chronic active immune response that persists for the life of the host, in the absence of antibiotic-induced eradication. It is the combination of bacterial factors, environmental insults, and the host immune response that drives the initiation and progression of mucosal atrophy, metaplasia, and dysplasia toward gastric cancer. Although it may seem intuitively obvious that removing the offending organism would negate the cancer risk, this approach is neither feasible (half of the world harbors this infection) nor is it straightforward. Most patients are infected in childhood, and present with various degrees of mucosal damage before any therapy. This review outlines the histologic progression of human Helicobacter infection from the early stages of inflammation through the development of metaplasia, dysplasia, and, finally, cancer. The effects of dietary and bacterial eradication therapy on disease progression and lesion reversibility are reviewed within the context of population studies and compared between study designs and populations tested. Eradication studies in the mouse model of infection prevents the formation of gastric cancer, and allows regression of established lesions, providing a useful model to study interaction between bacterium, environment, and host, without the difficulties inherent in human population studies. Recent advances in identifying the bone marrow-derived stem cell as the cell of origin of Helicobacter-induced gastric cancer in the murine model are discussed and interpreted in the context of human disease, and implications for future treatment are discussed.
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                Author and article information

                Journal
                BMJ Open
                BMJ Open
                bmjopen
                bmjopen
                BMJ Open
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2044-6055
                2014
                8 January 2014
                : 4
                : 1
                : e003689
                Affiliations
                [1 ]Division of Gastroenterology, Royal Columbian Hospital , New Westminster, British Columbia, Canada
                [2 ]Department of Medicine/Gastroenterology Division, University of Alberta , Edmonton, Alberta, Canada
                [3 ]Department of Pathology and Laboratory Medicine, University of Alberta , Edmonton, Alberta, Canada
                [4 ]Royal Alexandra Hospital , Edmonton, Alberta, Canada
                [5 ]Stanton Territorial Hospital , Yellowknife, Northwest Territories, Canada
                Author notes
                [Correspondence to ] Dr Karen J Goodman; karen.goodman@ 123456ualberta.ca
                Author information
                http://orcid.org/0000-0002-0743-8713
                Article
                bmjopen-2013-003689
                10.1136/bmjopen-2013-003689
                3902307
                24401722
                4d732b50-d744-4487-b1ea-ff4e623b0576
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

                History
                : 30 July 2013
                : 23 October 2013
                : 6 November 2013
                Categories
                Epidemiology
                Research
                1506
                1692
                1695

                Medicine
                Medicine

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