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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.

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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.
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.
Division of Molecular Diagnostics of Oncogenic Infections, Research Program in Infection, Inflammation, and Cancer, German Cancer Research Center, Heidelberg, Germany.
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Department of Epidemiology, Shanghai Cancer Institute, China; and.
Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health, Rockville, Maryland.



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.


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.


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]).


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.


Helicobacter pylori; inflammation.; serology; stomach neoplasms

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