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Clin Infect Dis. 2017 May 15;64(10):1380-1386. doi: 10.1093/cid/cix106.

A Prospective Study of Urinary Prostaglandin E2 Metabolite, Helicobacter pylori Antibodies, and Gastric Cancer Risk.

Author information

1
Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital and Institute, Peking University Health Science Center, Beijing, China.
2
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.
3
Division of Molecular Diagnostics of Oncogenic Infections, Research Program in Infection, Inflammation, and Cancer, German Cancer Research Center, Heidelberg, Germany.
4
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
5
Department of Epidemiology, Shanghai Cancer Institute, China; and.
6
Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health, Rockville, Maryland.

Abstract

Background:

Previous studies suggest that a stable end-product of prostaglandin E2, the urinary metabolite PGE-M, is associated with colorectal cancer, and 1 study of relatively small sample size found an association with gastric cancer among women. In the present study we further investigate the PGE-M, Helicobacter pylori, and gastric cancer association.

Methods:

The present analysis included 359 prospectively ascertained gastric cancer cases and 700 individually matched controls from the Shanghai Women's and Men's Health Studies. Urinary PGE-M was measured by a liquid chromatography/tandem mass spectrometric method. Seropositivity to 15 H. pylori recombinantly expressed fusion proteins was detected by H. pylori multiplex serology.

Results:

Adjusting for H. pylori, increasing PGE-M was associated with higher risk of gastric cancer (quartile 4 vs 1: odds ratio [OR], 1.76 [95% confidence interval {CI}, 1.17-2.66], Ptrend = .004). This association remained after excluding those diagnosed within 2 years from sample collection (OR, 1.73 [95% CI, 1.12-2.65], Ptrend = .007). However it was no longer present among individuals with 10 or more years of follow-up (2-4.9 years: OR, 3.15 [95% CI, 1.11-8.91]; 5-9.9 years: OR, 2.23 [95% CI, 1.22-4.06]; ≥10 years: OR, 0.73 [95% CI, .31-1.70]). Compared to H. pylori-negative individuals with below-median PGE-M levels, H. pylori-positive individuals with above-median PGE-M levels had a 5-fold increase in the odds of gastric cancer (OR, 5.08 [95% CI, 2.47-10.43]).

Conclusions:

In China, higher PGE-M levels may indicate an increased risk of gastric cancer independent of the risk conferred by H. pylori infection status, particularly for cancers diagnosed within 10 years of sample collection.

KEYWORDS:

Helicobacter pylori; inflammation.; serology; stomach neoplasms

PMID:
28402440
PMCID:
PMC5411401
DOI:
10.1093/cid/cix106
[Indexed for MEDLINE]
Free PMC Article

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