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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Strengths and limitations of this study
This study is unique in yielding evidence of the effects of Helicobacter pylori infection on gastric histopathology in a community setting where the study population is not restricted to individuals seeking medical care for symptoms.
It describes the H pylori-associated disease burden in a community in northern Canada.
It provides an example of how multidisciplinary research can address health concerns identified by communities.
The cross-sectional design limits inferences about determinants of severe gastritis and precancerous gastric conditions in this population.
Since the identification of Helicobacter pylori infection in 1983, research has revealed its associations with digestive diseases such as gastritis, peptic ulcer and gastric cancer,1–5 responsible for a large worldwide disease burden.6 ,7 Disease prevention strategies based on elimination of H pylori have not been widely implemented, however, and it is not fully clear whether specific infection control strategies are likely to result in net benefits to particular populations at risk. Since the late 1990s, a few reports, primarily from Alaska, Greenland and Canada, have shown H pylori prevalence and gastric cancer rates to be high among Arctic Indigenous communities, relative to elsewhere in North America and northern Europe,8 and similar to much of the developing world. Given that clinical guidelines recommend a test and treat approach for primary care patients presenting with dyspeptic symptoms,9 ,10 public awareness of H pylori infection and its link to gastric cancer has emerged in high-prevalence communities. In northern Canada, some communities and health officials have sought H pylori prevention research, calling attention to the scant evidence on the impact of H pylori among Arctic Canadians.
Reported estimates of H pylori seroprevalence in Canada vary between 21% and 95%, with prevalence of 50% or more estimated exclusively in Aboriginal communities.8 Beyond these seroprevalence studies, little evidence of the H pylori-associated disease burden in Canada has been reported. Furthermore, seroprevalence is not an optimal measure of current prevalence, given that serological testing for H pylori does not distinguish between past and current infection11; due to widespread treatment of H pylori infection in recent decades, many seropositive Canadians will not have an active infection. As harm from chronic H pylori infection is often silent until serious disease such as a bleeding ulcer or invasive cancer occurs, full elucidation of the H pylori-associated disease burden at the community level requires screening people who do not seek healthcare for digestive symptoms. Active H pylori infection can be detected non-invasively with breath or stool testing, but use of upper gastrointestinal endoscopy is required to detect disease manifestations of this infection. Endoscopy permits detection of visible abnormalities such as gastric ulcers and collection of gastric biopsies for histological examination to grade the density of H pylori and the severity of gastric mucosal pathology.
H pylori-induced gastric carcinogenesis starts with chronic H pylori infection accompanied by chronic gastritis.12 ,13 Superficial inflammation of the gastric mucosa can persist with or without symptoms or complications. In some cases, peptic ulcers develop, and with varied frequency depending on population characteristics, chronic gastritis can progress to atrophic gastritis, which involves loss of gastric glands. Subsequent stages in disease progression include intestinal metaplasia and dysplasia, conditions associated with a high risk of carcinoma. Progression through these steps is influenced by host susceptibility, virulence of infecting H pylori strains and environmental exposures.12 ,13
The Aklavik H pylori Project is an ongoing research endeavour conducted in a Northwest Territories (NT) hamlet, where residents and healthcare providers have advocated for research to address concerns about cancer risks from H pylori infection. In Canada's NT (2006 population ∼41 000),14 50% of the population is Aboriginal, including Inuit, First Nations and Metis peoples.15 The objectives of this analysis were to estimate the prevalence of H pylori infection and associated gastrointestinal pathology, as well as associations between prevalent H pylori and selected social and clinical factors, in a northern Canadian Aboriginal community.
This study analyses data from the initial components of the community-based participatory Aklavik H pylori Project previously described.16 Study participants were residents of Aklavik, NT, a primarily Aboriginal hamlet of ∼600 people in Arctic Canada, with an ethnic distribution of ∼55% Inuvialuit (western Canadian Inuit), ∼35% Gwich'in Dene (Athabaskan First Nations), ∼2% other Aboriginal and ∼8% non-Aboriginal Euro-Canadian. Aklavik is located in the Mackenzie River delta, ∼100 km south of the Arctic coast, 60 km east of the Yukon border and 676 km east of Fairbanks, Alaska. For eligibility purposes, ‘resident’ was defined broadly as being present in Aklavik during the study period (and included 3 temporary visitors and 22 people who resided across the river in Inuvik but had relatives residing in Aklavik). All Aklavik residents were invited to undergo non-invasive screening for H pylori infection by 13C-urea breath test17 and complete a structured questionnaire-based clinical interview (November 2007–February 2008). For the endoscopy component (February 2008), all Aklavik residents aged 15 years and older were encouraged to participate; younger children were included on parental request at the discretion of the endoscopists. Inclusion required written informed consent for the survey and endoscopy components; assent and parental consent were required for children under 17 years of age. Individuals were excluded if they had severe cardiovascular disease, uncontrolled hypertension or were unable or unwilling to complete the endoscopy procedure.
In accordance with community-based participatory research methods, the research goals and protocols were developed with input from a community project planning committee; the clinical questionnaire, in particular, was reviewed and modified by the planning committee to ensure local understanding and appropriateness. English was used for the questionnaire, as none of the participants preferred to respond in another language. Questionnaires were administered by trained interviewers. The interviewer team included Aklavik residents and University of Alberta graduate students, and the participants were offered their choice of interviewer. Interviews were conducted at the local health centre or participants’ homes or place of work, with the location decided by the participant.
Transnasal gastroscopy (or transoral when the transnasal approach was contraindicated) was performed in temporary endoscopy units at the Aklavik Health Centre by seven physicians experienced in upper gastrointestinal endoscopy and with prior training in transnasal gastroscopy.18 ,19 The participants underwent unsedated endoscopy using Olympus GIF-N180 (Olympus, Tokyo, Japan) 4.9 mm diameter endoscopes with a working length of 110 cm and a 2 mm single instrument channel, after administration of topical anaesthetics as described previously.19 Five gastric biopsies (from antrum close to the pylorus, antrum greater curvature, antrum lesser curvature adjacent to the incisura angularis, corpus lesser curvature and corpus greater curvature) were taken for histopathology and evaluated according to the updated Sydney protocol20 ,21 by a single tertiary-care centre gastrointestinal pathologist (SG), blinded to endoscopic findings. Sections were stained with H&E for regular histology and with Giemsa to detect H pylori. Histopathological assessment graded the severity (normal/absent, mild, moderate, severe) of acute and chronic inflammation by stomach subsite (antrum, body), as well as glandular atrophy, intestinal metaplasia, other neoplasias and H pylori density.
To compare the H pylori-associated disease burden in the Aklavik population with that of the southern Canadian metropolitan area that provides advanced healthcare for NT residents, we searched the University of Alberta Hospital (Edmonton, Alberta) pathology department computerised database to identify gastric biopsy evaluations of patients examined during one 12-month period from 1 April 2010 through 31 March 2011. We identified reports that stated relevant pathological diagnoses, restricting the denominator of prevalence estimates to reports that explicitly mentioned assessment for the relevant diagnostic category; we also excluded duplicate reports for the same individual.
Frequency distributions of demographic and clinical variables were summarised in tables, along with the proportion of participants in each category that were H pylori positive. Prevalence of each endoscopic and histopathological diagnosis was estimated by dividing the number with the diagnosis by the total number of participants who had biopsies examined; 95% CIs were calculated for these prevalence proportions; prevalence estimates were also calculated for subgroups stratified by H pylori status. To estimate the association between H pylori prevalence and variables selected based on clinical or sociodemographic relevance, ORs and 95% CIs were estimated from multivariable logistic regression as an appropriate measure of association for cross-sectional data.22 ,23 The set of adjustment variables was selected using a change-in-estimates approach, beginning with all of the preselected variables in the full model and excluding each one at a time. Likelihood ratio tests were performed to compare the model with each variable missing to the full model. For each estimated OR, we excluded from the set of adjustment variables those for which exclusion did not result in a greater than 10% change in the OR compared with the estimate from the full model. Likelihood ratio tests were used to select the optimal functional form for continuous variables (age, years of education) and care was taken to collapse categories only when this did not alter the dose–response pattern. The number of participants with data for particular variables is indicated in table notes. Participants with data missing from variables included in the multivariable logistic regression model were excluded from the analysis that estimated unadjusted and adjusted ORs. Statistical analysis was performed using STATA/IC V.10 statistical software (StataCorp, USA).
Of 379 participants in the Aklavik H pylori Project, 332 had results from breath tests to detect H pylori and 58% were positive. Among 200 individuals who consented to endoscopy, 4 could not tolerate the procedure and 2 were taking anticoagulant coumadin which precluded biopsy. Thus, 194 participants completed gastroscopy with biopsies (including 2 temporary visitors and 7 residents of Inuvik). The participants’ ages ranged from 10 to 80 years; 91% were Aboriginal (114 Inuvialuit, 54 Gwich'in and 8 other), and 58% were women. Table 1 shows the distribution of sociodemographic and clinical variables among endoscopy participants. Table 2 shows the distribution of age, sex, ethnicity and education comparing endoscopy participants, all project participants and Aklavik census participants captured by Statistics Canada.24 Small variations are noted in the distributions of these variables, with the major difference being an over-representation of older residents among endoscopy participants (it should be noted that the census data were missing education status for a large proportion of the population). Table 3 compares endoscopy participants and project participants who did not undergo endoscopy on the prevalence of chronic dyspepsia and other health-related factors among participants with data on these factors.25 The prevalence of two or more chronic dyspepsia symptoms was 43% among project participants who participated in endoscopy and 41% among those who did not, while the proportion with no symptoms was 37% in the endoscopy group and 41% in the group that did not undergo endoscopy. Modestly higher proportions of endoscopy participants had a family history of H pylori infection or gastric cancer, had been tested for H pylori before enrolling in the Aklavik H pylori Project or were taking medications for stomach upset.
H pylori prevalence and associated demographic and clinical factors
The pathologist's assessment of gastric biopsies classified 66% of endoscoped participants as having H pylori. From the set of variables selected a priori for multivariable regression, selection criteria retained age, ethnicity, previous gastroscopy, previous antibiotic treatment for H pylori, aspirin use and alcohol use; each of these variables had likelihood ratio test p values <0.17 and the exclusion of each from the full model resulted in >10% change in estimates of at least four variables in the model. All variables excluded from the adjustment set used in all models had likelihood ratio p values >0.48. The change-in-estimates criterion identified two additional adjustment variables for ethnicity (smoking and education) and one additional adjustment variable for aspirin use (education; table 4). Regression results show lower prevalence odds among individuals of non-Aboriginal ethnicity compared with individuals of Aboriginal ethnicity (OR 0.07, CI 0.02 to 0.33) and among those reporting previous gastroscopy, H pylori therapy or aspirin use (OR 0.25, CI 0.09 to 0.65; OR 0.20, CI 0.07 to 0.56 and OR 0.35, CI 0.13 to 0.99, respectively), while higher odds were observed among the current consumers of alcohol compared with non-drinkers (OR 2.4, CI 1.1 to 5.0). Of individuals reporting previous H pylori therapy and gastroscopy, 39% (11/28) and 32% (12/38), respectively, were still positive for H pylori (14 individuals with previous gastroscopy also had previous H pylori therapy). Weak and imprecise adjusted ORs were observed for sex, family history of stomach cancer, stomach medication use and non-steroidal anti-inflammatory drug use. The OR for smoking reduced from 2.4 to 1.2 on adjustment; the adjustment variables with the largest impact on the change in this estimate were ethnicity, aspirin use and alcohol consumption. The adjusted OR for education shows odds of infection decreasing by 5% with each increasing year of education (OR 0.95, CI 0.83 to 1.1); this estimate, however, is imprecise, and it should be noted that only 22% of participants had more than 12 years of education, so it may not be accurate for effects beyond 12 years (although 16 of the 18 (89%) non-Aboriginal participants had more than 12 years of education, the adjusted OR for education does not appear to contain residual confounding by ethnicity given that the adjusted OR within the subgroup of Aboriginal participants was nearly identical (0.95 (CI 0.82 to 1.1)) to that of the total study population). To assess whether the effect of education might be mediated by clinical or substance use variables, we removed these variables from the model for the effect of education, but did not note that the estimated effect of education strengthened on doing so. H pylori prevalence did not increase monotonically with age in this population, unlike what has been reported elsewhere. This agrees with the age-specific prevalence pattern observed in the 332 project participants with breath test results: 54% in children under 20 years, 72% in 20–39-year-olds and 52% in people aged 40 or older. Of note, among participants aged 40 or older, 18% reported previous H pylori therapy, compared with 11% in participants under 40.
The most frequent endoscopic abnormalities were gastritis (14%), esophagitis (10%), gastric erosions (6.2%) and gastric ulcer (3.1%) with duodenal lesions occurring much less frequently (table 5); frequencies of these endoscopic diagnoses were similar in the subpopulation of H pylori-positive participants. There were no cases of duodenal ulcer or gastric cancer.
Among 176 participants with biopsies from both the gastric antrum and body, acute antral gastritis and acute pangastritis were seen in 25% and 37%, respectively. Chronic antral gastritis and chronic pangastritis were seen in 9.7% and 57%, respectively (table 6). Among the 194 endoscoped participants, the prevalence of acute and chronic gastritis was 63% and 68%, respectively, and nearly all individuals with either form of gastritis were H pylori-positive (94% and 100%, respectively; table 7). There were no cases of gastric dysplasia or adenocarcinoma. Among H pylori-positive participants, prevalence was 21% for gastric atrophy and 11% for intestinal metaplasia, while chronic inflammation severity was mild in 9%, moderate in 47% and severe in 43%. The percentage with H pylori infection was 100% for atrophy, 88% for intestinal metaplasia, 100% for severe inflammation, 100% for moderate inflammation and 77% for mild inflammation. Online supplementary figures S1–3 show magnified views of histological sections from a participant with severe chronic and acute inflammation and high H pylori density; all three views are from the same individual.
Table 7 compares the frequency of gastric histopathology diagnoses among Aklavik research participants with those of University of Alberta Hospital patients assessed for the same conditions. Of 3845 patient reports matching search terms ‘gastric’ or ‘Helicobacter pylori’, 413 (10.7%) were classified as positive for H pylori. Excluding 815 records with no mention of H pylori, the prevalence of H pylori-positive diagnoses was 13.6% (413/3030; 2612 were explicitly classified as H pylori-negative and 5 were classified as H pylori uncertain). The 413 H pylori-positive diagnoses corresponded to 401 individual patients. Of the 401 individuals, 98.8% were diagnosed with gastritis. Of 390 that specified whether the gastritis was acute or chronic, 89.2% were specified as chronic only, 1% as acute only and 9.7% had acute and chronic gastritis. Of 282 patients whose gastric inflammation was graded, 40.4% were graded mild, 55% were graded as mild-moderate or moderate and 4.6% of the patients were graded as moderate-severe or severe. All of the 401 H pylori-positive patients were assessed for glandular atrophy and intestinal metaplasia: 2.2% were diagnosed with atrophy and 15% with intestinal metaplasia. Thus, relative to University of Alberta Hospital patients assessed for relevant conditions, Aklavik residents have a much higher prevalence of H pylori (greater than fourfold), and H pylori-positive Aklavik residents have a much higher prevalence of severe gastric inflammation and gastric atrophy.
This study describes a high prevalence of active H pylori infection and associated gastric pathology among participants in the Aklavik H pylori Project. The pattern of endoscopically visible lesions occurring more frequently in the gastric body relative to the duodenum, along with the high prevalence of severe inflammation and gastric atrophy diagnosed in a project that screened community members not seeking healthcare for dyspeptic symptoms, is consistent with an elevated risk of gastric cancer in this community.
This research arose from public perception of a greater than expected number of gastric cancer cases in Aklavik in recent years. As the population of this hamlet is so small, this perception cannot be verified with official statistics, given that the NT cancer registry does not make public community-specific cancer frequencies when case counts are low to protect confidentiality. Statistics Canada suppresses the yearly number of gastric cancer cases diagnosed across the NT (2006 population ∼41 000) for the same reason.14 NT Health and Social Services reported, however, for the time period 1992–2000, that the age-adjusted gastric cancer incidence rate among men in outlying areas of the territory was ∼3 times the rate in men across Canada,26 and that gastric cancer was the second most frequently diagnosed cancer in Inuit men and third most frequently diagnosed cancer in Dene First Nations men compared with 10th in men across Canada. (These statistics are not reported for NT women due to small numbers.)
Using histological assessment, a large Canadian multicentre study reported a H pylori prevalence of 30% in patients with dyspepsia.27 The Aklavik H pylori Project used two methods to estimate prevalence of active H pylori infection; prevalence estimates were 58% in the breath-test screened sample and 67% in the sample that underwent endoscopy. The H pylori prevalence estimates observed in this study is in the range of other reported prevalence estimates for northern Aboriginal communities in Canada (51–95%), Alaska (80%) and Greenland (58%).8
Systematic searches of the literature yield little information on H pylori-associated histopathology in North American Aboriginal communities. In 1997, Yip et al28 reported that H pylori infection in an Alaska Native population with elevated faecal haemoglobin levels was accompanied by a high prevalence of grossly abnormal gastric mucosa with erythema and mucosal thickening, diffuse intraepithelial haemorrhages, gastric ulcers and multiple erosions (inflammation severity, gastric atrophy and intestinal metaplasia were not mentioned), while only 1% had duodenal ulcers. To place our findings in perspective, we performed a systematic literature search to locate studies of H pylori-associated histopathology frequencies for other populations. This search did not identify any other population-based studies. Nearly all studies identified were based on series of patients undergoing diagnostic evaluation, thus it is difficult to put the frequencies observed in Aklavik in perspective. Among 1040 patients investigated endoscopically for dyspepsia across Canada (H pylori prevalence=30%), the reported prevalence among H pylori-positive patients was 5.7% for gastric ulcer, 10.6% for gastric erosions, 6.6% for duodenal ulcer and 5.6% for duodenal erosions;27 this report did not include histopathology frequencies. Large studies conducted in Japan,29 Taiwan30 and China31 revealed high prevalence of atrophy and metaplasia among H pylori-positive patients, though reports did not mention the severity of chronic inflammation. A few smaller studies of patients undergoing medical care in diverse locations reported prevalence for subsets of the endoscopic and histopathological outcomes of interest;32–42 however, the diverse selection criteria across these studies impede meaningful summarisation of data patterns. An important limitation for comparing the frequencies observed in Aklavik to those reported in the literature is the much younger age distribution of the Aklavik population, given the mean age of 40 years compared with mean ages over 50 years in the published reports. Another limitation of comparisons across studies is the suboptimal degree of interobserver agreement on histopathological assessment of gastric biopsies, even among expert pathologists adhering to the Sydney system.43 ,44
Although the prevalence of peptic ulcer disease in Aklavik H pylori Project participants did not appear to be elevated compared with the multicentre Canadian dyspepsia study,27 it should be noted that a quarter of Aklavik participants reported taking antisecretory therapy, which provides protection against peptic ulcer disease. The low occurrence of duodenal lesions relative to gastric lesions in the Aklavik population is noteworthy, given that a relatively high ratio of gastric to duodenal ulcer is typical of populations with increased risk of gastric carcinoma.45 Our comparison of H pylori-positive NT research participants with H pylori-positive patients receiving care at a university hospital in Alberta provides evidence of a much higher prevalence of histopathology indicating an increased risk of gastric carcinoma in the northern Aboriginal community. While the Alberta hospital pathology data did not result from systematic assessment of gastric biopsies for relevant conditions, restricting the prevalence estimates to patients who were explicitly assessed for relevant conditions would not likely have underestimated the prevalence of these conditions, because it does not seem plausible that individuals who were less likely to have these conditions were more likely to be assessed for them.
Reasons for the high prevalence of H pylori infection in this and other northern Aboriginal populations remain unclear, though it should be noted that H pylori prevalence is equally high in many of the world's developing regions,46 as well as specific communities in developed regions: for example, immigrants to Canada from high-prevalence areas.47 In a large national survey of the USA, elevated prevalence was observed in immigrants as well as Mexican-American and African Americans, and among sociodemographic subgroups defined by poverty, high household density, low education levels and rural residence.48 Potentially important socioenvironmental factors unique to northern populations may include dispersed settlement that impedes access to organised social resources such as healthcare, geographical and climate challenges for sanitation and water supply, and increased concentration of people in indoor spaces. Multiple lines of evidence suggest that H pylori infection may have been ubiquitous in humans in earlier eras and that it has declined in modernised and affluent settings. Thus, the question about why H pylori prevalence is high in particular communities can be reframed as why it has not declined in these settings as it has elsewhere. In the Aklavik population, factors clearly associated with lower odds of H pylori infection were previous H pylori therapy, previous gastroscopy, aspirin use and non-Aboriginal ethnicity, which in this community equates with not having grown up in a small hamlet in Arctic Canada.
These results from the Aklavik H pylori Project demonstrate that H pylori is highly endemic in this community, and severe inflammation and precancerous lesions of the gastric mucosa are highly prevalent. Motivated by worries among Aklavik residents over cancer risk from H pylori infection, this analysis shows that community concern is justified and provides an example of how epidemiological research can address health priorities identified by communities. The reasons for a more severe course of infection in this and similar communities have become a major focus of the community-driven research carried out by the Canadian North Helicobacter pylori (CANHelp) Working Group, which now includes H pylori projects in additional Yukon and NT communities. These projects are unique in yielding evidence of the effects of H pylori infection on gastric histopathology in a community setting where the study population is not restricted to individuals seeking medical care for symptoms. Future analyses will focus on identifying determinants of gastritis severity, such as dietary factors, exposure to environmental contaminants and bacterial genotypes. Such determinants would be potential modifiers of gastric cancer risk among individuals with H pylori infection and may suggest effective cancer prevention strategies. Driven by the desire of residents of the participating communities to reduce health risks from H pylori infection, the CANHelp Working Group's community H pylori projects are also assessing the short-term and long-term effectiveness of available H pylori treatment regimens to generate information for use in policy analysis that will aid regional health officials in identifying optimal strategies for control of this infection.
The authors acknowledge the contributions of physicians Dr Mario Millan (Misericordia Hospital, Edmonton, Alberta) and Dr Tom Guzowski (Stanton Territorial Hospital, Yellowknife, Northwest Territories), Olympus Canada personnel Peter Bresee and Dale Kennedy, University of Alberta Hospital patient care manager Susan Derk; Royal Alexandra Hospital endoscopy program manager Brenda Holowaty, University of Alberta Hospital and Royal Alexandra Hospital (Edmonton, Alberta) endoscopy nurses Leanne Ellis, Jennifer Antonio, Sheila Berrisford, Kathy Korner, Cinnamon Landhauser, Paula Ledsham, Louise Steffan, and service aids Austin Babb, Tamara Bangs, Tammy Church, and Sharda Naidu; and Inuvik Regional Hospital endoscopy aid Louie Goose.
This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.
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Collaborators CANHelp Working Group —Aklavik, Northwest Territories: Rachel Munday (Aklavik Health Centre); Robert Buckle, Glen Gordon, Annie Buckle, Jerome Gordon, Andrew Gordon, Billy Archie (Aklavik Health Committee). Inuvik, Northwest Territories: Leah Seaman (Inuvik Regional Hospital), Crystal Lennie (Inuvialuit Regional Corporation). Yellowknife, Northwest Territories: Kami Kandola (Northwest Territories Health and Social Services), John Morse (formerly, Stanton Territorial Health Authority), Susan Chatwood (Institute for Circumpolar Health Research). Edmonton, Alberta: Karen Goodman, Justin Cheung, Richard Fedorak, Christopher Fletcher, Safwat Girgis, Monika Keelan, Sander Veldhuyzen van Zanten (University of Alberta investigators), Janis Geary, Katharine Fagan-Garcia, Hsiu-Ju Chang, Ashley Wynne, Laura Aplin, Katie Tweedie (University of Alberta research staff); Robert Bailey (Northern Health Services Network).
Contributors JC designed the endoscopy component of this research, performed endoscopic assessment of participants, analysed the gastric biopsy data and drafted the manuscript. KJG is the primary investigator of the CANHelp (Canadian North Helicobacter pylori) Working Group research programme; she designed and directed the Aklavik H pylori project, supervised JC's research methodology and edited the manuscript. SG designed the histopathology methods and carried out the assessment of gastric biopsies. RB supervised the design of the endoscopy methodology and performed endoscopic assessment of participants. JM supervised the implementation of the endoscopy project and performed endoscopic assessment of participants. RNF provided key input in the overall research design and implementation and performed endoscopic assessment of participants. JG designed the data management methods that supported the analysis. KF-G conducted the analysis of the University of Alberta pathology data, verified all of the analyses and the accuracy of the data presentation, and assisted with manuscript preparation. SVvZ supervised the overall clinical methodology of the research and performed endoscopic assessment of participants. All authors reviewed and approved the manuscript.
Funding The relevant phase of the Aklavik H pylori project was supported by grants from the Canadian Association for Gastroenterology in partnership with the Canadian Institutes for Health Research; the Social Sciences and Humanities Research Council of Canada and the University of Alberta Division of Gastroenterology. Additional financial support was provided by the Northwest Territories Health and Social Services Department and the Inuvialuit Regional Corporation, along with in-kind contributions from Olympus Canada, Canadian North Airlines, Alberta Health Services (formerly Capital Health), Inuvik Regional Hospital, Susie Husky Health Centre, Aklavik Community Corporation, and Aklavik residents and community groups who housed and fed endoscopy team members. Olympus Canada loaned and transported endoscopic equipment with technical support.
Competing interests At the time of the study, Dr JC was a clinical research fellow supported by two fellowships: (1) from the Canadian Association for Gastroenterology partnered with the Canadian Institutes for Health Research and Ferring Pharmaceuticals and (2) from the Alberta Heritage Foundation for Medical Research.
Ethics approval The study was approved by the University of Alberta Health Research Ethics Board, the Aurora Research Institute (Northwest Territories research licensing agency), the Aklavik Health Committee, the Hamlet of Aklavik council, the Aklavik Community Corporation (Inuvialuit governance) and the Ehdiitat Gwich'in Council.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement Decisions about sharing additional data are made on a case-by-case basis by the CANHelp Working Group in consultation with relevant project planning committees; direct inquiries to firstname.lastname@example.org.
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