4.7 Article

Association of Helicobacter pylori and gastric atrophy with adenocarcinoma of the esophagogastric junction in Taixing, China

Journal

INTERNATIONAL JOURNAL OF CANCER
Volume 150, Issue 2, Pages 243-252

Publisher

WILEY
DOI: 10.1002/ijc.33801

Keywords

adenocarcinoma of the esophagogastric junction; gastric atrophy; H; pylori; pepsinogens

Categories

Funding

  1. MOST [12]
  2. NAVA [12]
  3. National Key Research and Development Program of China [2016YFC0901403, 2017YFC0907000, 2019YFC1315804]
  4. National Natural Science Foundation of China [81973116, 82030101, 82073637, 91846302]
  5. Shanghai Municipal Science and Technology Major Project [2017SHZDZX01]
  6. Science and Technology Commission of Shanghai Municipality, China [20ZR1405600]
  7. ThreeYear Action Plan for Strengthening Public Health System in Shanghai [GWV-10.2-YQ32]

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The study found a positive association between Helicobacter pylori infection and gastric atrophy with the risk of adenocarcinoma of the esophagogastric junction (AEGJ). Specifically, the relationship between gastric atrophy and AEGJ risk may not be significantly modified by H. pylori infection.
Gastric atrophy caused by Helicobacter pylori infection was suggested to influence the risk of adenocarcinoma of the esophagogastric junction (AEGJ), however, the evidence remains limited. We aimed to examine the associations of H. pylori infection and gastric atrophy (defined using serum pepsinogen [PG] I to PGII ratio) with AEGJ risk, based on a population-based case-control study in Taixing, China (2010-2014), with 349 histopathologically confirmed AEGJ cases and 1859 controls. We explored the potential effect modification by H. pylori serostatus and sex on the association of serum PGs with AEGJ risk. We used unconditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). H. pylori seropositivity was associated with an elevated AEGJ risk (OR = 1.95, 95% CI: 1.47-2.63). Neither CagA-positive nor VacA-positive strains dramatically changed this association. Gastric atrophy (PGI/PGII ratio <= 4) was positively associated with AEGJ risk (OR = 2.36, 95% CI: 1.72-3.22). The fully adjusted ORs for AEGJ progressively increased with the increasing levels of PGII (P-trend <.001). H. pylori showed nonsignificant effect modification (P-interaction = .385) on the association of gastric atrophy with AEGJ. In conclusion, H. pylori and gastric atrophy were positively associated with AEGJ risk. These results may contribute evidence to the ongoing research on gastric atrophy-related cancers and guide the prevention and control of AEGJ.

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