MJA
MJA

Prevalence of Helicobacter pylori in Indigenous Western Australians: comparison between urban and remote rural populations

Naomi R Mayers, Sophie Couzos, Richard Murray and John Daniels
Med J Aust 2005; 182 (10): 544. || doi: 10.5694/j.1326-5377.2005.tb00026.x
Published online: 16 May 2005

To the Editor: We read with interest the recent cross-sectional survey of Helicobacter pylori infection in remote and urban Aboriginal populations in Western Australia.1 The prevalence of H. pylori was shown to be consistent with that in developing countries. This is not surprising, given the high prevalence of diseases such as chronic suppurative otitis media, rheumatic fever, scabies, and tuberculosis affecting Aboriginal peoples — all of which relate to poverty and overcrowding.2 Aboriginal and Torres Strait Islander people have a massively disproportionate share of the overcrowded households in Australia. In the 2001 Census, Aboriginal people in WA accounted for 53% and 93% of the two-bedroom and three-bedroom households that accommodated seven to nine and ten or more people, respectively (from 3% of the population).3

Windsor et al speculate that high H. pylori infection rates may be the result of children not wearing nappies and of poor personal hygiene — even though these matters (and housing standards, the presence of functional washing facilities and the degree of overcrowding) were not investigated. We are concerned that such conclusions reflect negatively on the Aboriginal population who took part in the survey in good faith with good will.

Moreover, it is misleading to suggest that H. pylori is a cause of poor growth among Aboriginal children. There is insufficient evidence to support screening for H. pylori infection in children, as no studies have demonstrated that treating H. pylori infections improves their growth.

It is expected that “some of the participants who tested positive for H. pylori have asked to be treated with antibiotics”. We assign considerable importance to research protocols that adhere to the criterion “no research proceeds without service”.4 Did those who were H. pylori positive with dyspepsia, a history of peptic ulcer complications, or a family history of gastric cancer5 receive treatment? Windsor et al do not describe what follow-up their survey participants received. Without clarity on this point (especially appropriate advice to those who were asymptomatic), we wonder what negative impacts a positive H. pylori finding had on participants’ social and emotional well-being.

We are concerned by the authors’ anthropological musings: “Indigenous people may have their own H. pylori strains”. Given Australia’s heterogeneous Indigenous population, this potential research question is of no strategic relevance.4 The promotion of expanded testing for H. pylori is not supported by the evidence.

Talley’s accompanying editorial prioritises a “randomised controlled trial to test the health benefits (and risks) of population-based screening and antibiotic treatment [for H. pylori] in Indigenous Australians”.5 In the absence of a clinical endpoint for an as-yet undefined health problem, there is no convincing argument for such a trial.

Narrow medical answers to health problems that ignore economic and environmental solutions are not evidence-based. Both articles should have argued strongly for political commitment to these solutions to address a wide range of existing poverty-related diseases which currently affect Abori-ginal and Torres Strait Islander people on a massive scale.

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