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. 2014 Jan;23(1):172-8.
doi: 10.1158/1055-9965.EPI-13-0447. Epub 2013 Nov 14.

Helicobacter pylori seropositivities and risk of pancreatic carcinoma

Affiliations

Helicobacter pylori seropositivities and risk of pancreatic carcinoma

Harvey A Risch et al. Cancer Epidemiol Biomarkers Prev. 2014 Jan.

Abstract

Background: Pathophysiologic actions of Helicobacter pylori colonization on gastric acidity have been hypothesized to modulate the effect of pancreatic carcinogens, through CagA-negative organism strain type, hyperchlorhydria and increased risk of pancreatic cancer, or CagA-positive strain, hypochlorhydria and decreased risk of pancreatic cancer. We aimed to determine H. pylori strain-specific associations with pancreatic cancer in a population in which colonization by CagA-positive strains is common.

Methods: We carried out a large population-based case-control study of pancreatic carcinoma in Shanghai, China. Venipuncture specimens were obtained from a representative sample of 761 case patients and 794 randomly selected control subjects matched by category of age and gender. Antibody seropositivity for H. pylori and its virulence protein CagA were determined by commercial enzyme-linked immunosorbent IgG assays.

Results: Compared with individuals seronegative for both H. pylori and CagA, decreased pancreas-cancer risk was seen for CagA seropositivity [adjusted OR, 0.68; 95% confidence interval (CI), 0.54-0.84], whereas some increased risk was suggested for CagA-negative H. pylori seropositivity (OR, 1.28; 95% CI, 0.76-2.13). No risk interactions were observed between CagA seropositivity and gender, cigarette smoking, or age-21 body mass index.

Conclusions: Similar to what has been seen in animal models, our results provide suggestive evidence in humans for the involvement of gastric acidity, through its bidirectional modification according to colonization by H. pylori CagA strain type, in the risk of pancreatic carcinoma.

Impact: H. pylori colonization may have diverse effects on cancer risk, depending on the organism strain type as well as on the particular cancer site.

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Conflict of interest statement

Disclosures: There were no apparent or real conflicts of interest for any of the authors.

References

    1. Gao Y-T, Lu W. Cancer incidence, mortality and survival rates in urban Shanghai (1973–2000) Shanghai: Second Military Medical University Press; 2007.
    1. Risch HA. Etiology of pancreatic cancer, with a hypothesis concerning the role of N-nitroso compounds and excess gastric acidity. J Natl Cancer Inst. 2003;95:948–960. - PubMed
    1. Risch HA, Yu H, Lu L, Kidd MS. ABO blood group, Helicobacter pylori seropositivity, and risk of pancreatic cancer: a case-control study. J Natl Cancer Inst. 2010;102:502–505. - PMC - PubMed
    1. Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev. 2006;19:449–490. - PMC - PubMed
    1. Shu H, Ge Z, Xiang Z, Liu Y, Ren W, Xiao S. Evaluation of detecting methods of Helicobacter pylori infection—histology, serology, 13C urea breath test, and rapid urease tests. Chin J Digestion. 1998;18:260–262.

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