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Helicobacter pylori infection, atrophic gastritis, and pancreatic cancer risk A meta-analysis of prospective epidemiologic studies

Journal

MEDICINE
Volume 96, Issue 33, Pages -

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MD.0000000000007811

Keywords

atrophic gastritis; cytotoxin-associated gene A; epidemiology; Helicobacter pylori; pancreatic cancer

Funding

  1. National Natural Science Foundation of China [81301866]
  2. Scientific Research Program from the Sichuan Provincial Health and Family Planning Commission [16PJ362]
  3. Outstanding Young Scientific Scholarship Foundation of Sichuan University, from the Fundamental Research Funds for the Central Universities of China [2015SCU04A43]

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Background: To investigate the associations of Helicobacter pylori (Hp) infection and atrophic gastritis (AG) with pancreatic cancer risk. Methods: A literature search in PubMed was performed up to July 2017. Only prospective cohort and nested case-control studies enrolling cancer-free participants were eligible. Incident pancreatic cancer cases were ascertained during the follow-up. The risks of pancreatic cancer were compared between persons infected and noninfected with Hp, or between those with and without AG status at baseline. Odds ratios (ORs) or hazard ratios were combined. Subgroup and sensitivity analyses were performed, and publication bias was estimated. Results: Three cohort studies and 6 nested case-control studies, including 65,155 observations, were analyzed. The meta-analyses did not confirm the association between pancreatic cancer risk and Hp infection (OR=1.09, 95% confidence interval [CI]= 0.81-1.47) or AG status (OR=1.18, 95% CI=0.80-1.72). However, particular subpopulations potentially had increased risks of pancreatic cancer. Cytotoxin-associated gene A (CagA)-negative strains of Hp might be a causative factor of pancreatic cancer (OR=1.30, 95% CI=1.05-1.62), but a sensitivity analysis by leave-one-out method did not fully warrant it (OR=1.20, 95% CI= 0.93-1.56). In 1 nested case-control study, AG at stomach corpus in Hp-negative subpopulation might have increased risk of pancreatic cancer, but with a poor test power=0.56. Publication biases were nonsignificant in the present meta-analysis. Conclusion: Based on current prospective epidemiologic studies, the linkage of pancreatic cancer to Hp infection or AG status was not warranted on the whole. Nevertheless, prospective studies only focusing on those specific subpopulations are further required to obtain better power.

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