ISPO

Published in Cancer Detection and Prevention 1999; 23(5):357-367.

Helicobacter pylori Infection on the Risk of Stomach Cancer and Chronic Atrophic Gastritis

Zuo-Feng Zhang, M.D, Ph.D.,a,b Robert C. Kurtz, M.D.,c David S. Klimstra, M.D.,d Guo-Pei Yu, M.D., M.P.H.,e Ming Sun, M.S.,a Susan Harlap, M.B., B.S.f and James R. Marshall, Ph.D.g

a Department of Epidemiology, School of Public Health, and b Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, California; c Gastroenterology and Nutrition Service, Department of Medicine, and d Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York; e Department of Otolaryngology, New York Eye and Ear Infirmary, New York, New York; f Kaplan Cancer Center and Department of OBGYN, NYU Medical Center, New York, New York; and g Cancer Center, University of Arizona, Tucson, Arizona

Address all correspondence and reprint requests to: Zuo-Feng Zhang. M.D., Department of Epidemiology, UCLA School of Public Health, 71-225 CHS, Box 951772, 10833 Le Conte Ave., Los Angeles, CA 90095-1772.

ABSTRACT: Helicobacter pylori infection is associated with gastric adenocarcinoma. However, the mechanisms of this interaction are still unclear. This study was conducted to explore the effects of H. pylori infection on early and late-stage gastric carcinogenesis. This study included 134 patients with adenocarcinoma of the stomach (ACS), 67 patients with chronic atrophic gastritis (CAG) and 65 normal controls recruited at Memorial Sloan-Kettering Cancer Center (MSKCC) from November 1, 1992, to November 1, 1994. Epidemiologic data were collected by a modified National Cancer Institute Health Habits History Questionnaire. H. pylori infection was diagnosed by pathological evaluation. Risk factors were analyzed using logistic regression. The odds ratio (OR) associated with H. pylori infection was 10.4 [95% conference interval (Cl), 2.6-41.6] for CAG and 11.2 (95% CI, range 2.5-50.3) for gastric cancer in comparison with normal controls, with adjustment for pack-year of smoking, alcohol drinking, body mass index, total calorie intake, dietary fat and fiber intake, and Barrett’s esophagus. But H. pylori infection was not associated with risk of stomach cancer when patients with stomach cancer were compared with patients with CAG (OR = 0.6, 95% CI, range 0.3-1.3) after controlling for potential confounding variables. This association was persistent when only patients with both gastric cancer and chronic gastritis were considered as cases and patients with CAG were considered as controls (OR = 0.7, 95% CI, range 0.3-2.0) in the multivariate analysis. Our results suggest that H. pylori infection may be involved in the early stage of development of CAG, but not in the development of stomach cancer from CAG, and indicate that strategies for prevention of stomach cancer should target the early stage to eliminate H. pylori infection in high-risk populations.

KEY WORDS: chronic atrophic gastritis, helicobacter pylori infection, neoplasia, risk factors, stomach.

For more information, contact zfzhang@ucla.edu

http://www.cancerprev.org/Journal/Issues/23/5/350