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We read with interest the article by Castaño-Rodríguez et al,1 describing the role of Helicobacter pylori and Campylobacter spp in inflammatory bowel disease (IBD). While H. pylori infection has been shown to be protective against IBD, there is some ambiguity about the biological underpinnings of this effect. There is a spectrum of H pylori exposure across Caucasian populations with lower rates identified in Australian and USA studies.2 Importantly, Australia and other ‘new world’ regions such as the USA currently have some of the highest published incidence and prevalence rates for IBD.3–5
Multiple strains of H. pylori are observed, most notably, those with an active cytotoxin-associated gene A (cagA) and those without. The prevalence of the cagA gene in H. pylori is reported to be between 60% and 100% in western and eastern populations, respectively,6 potentially confounding any analysis on the …
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