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The association of vacA genotypes and Helicobacter pylori-related gastroduodenal diseases in the Middle East

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Abstract

The variations in the three regions of the Helicobacter pylori vacA gene, the signal (s1 and s2), intermediate (i1 and i2) and middle regions (m1 and m2), are known to cause the differences in vacuolating activities. However, it was unclear whether these vacA genotypes are associated with the development of gastric cancer and peptic ulcer in the Middle East. The aim was to identify the prevalence of vacA genotypes in the Middle East and the association with gastroduodenal diseases. We investigated the relationship of vacA genotypes to H. pylori-related disease development by meta-analysis using previous reports of 1,646 patients from the Middle East. The frequency of the vacA s1, m1 and i1 genotypes in the Middle Eastern strains was 71.5% (1,007/1,409), 32.8% (427/1,300) and 40.7% (59/145), respectively. Importantly, the frequency of vacA s- and m-region genotypes significantly differed between the north and south parts of the Middle East countries (P < 0.001). The vacA genotypes significantly increased the risk of gastric cancer (odds ratio [OR]: 4.02, 95% confidence interval [CI]: 1.98–8.14 for the s1 genotype; 2.50, 1.62–3.85 for m1; 5.27, 1.97–14.1 for s1m1; 15.03, 4.69–48.17 for i1) and peptic ulcers (OR: 3.07, 95% CI: 2.08–4.52 for s1; 1.81, 1.36–2.42 for m1). The cagA-positive genotype frequently coincided with the s1, m1 and i1 genotypes. The vacA s- and m-region genotypes may be useful risk factors for gastrointestinal diseases in the Middle East, similar to European and American countries. Further studies will be required to evaluate the effects of the i-region genotype.

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Acknowledgements

This material is based upon work supported in part by the National Institutes of Health (NIH) grant R01 DK62813 (to Y.Y.).

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Correspondence to Y. Yamaoka.

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Sugimoto, M., Zali, M.R. & Yamaoka, Y. The association of vacA genotypes and Helicobacter pylori-related gastroduodenal diseases in the Middle East. Eur J Clin Microbiol Infect Dis 28, 1227–1236 (2009). https://doi.org/10.1007/s10096-009-0772-y

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