This Article Full Text Full Text (PDF) Correction (v17,p2901) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by de Martel, C. Articles by Parsonnet, J. PubMed PubMed Citation Articles by de Martel, C. Articles by Parsonnet, J.

Helicobacter pylori Infection and Development of Pancreatic Cancer

Departments of ¹ Health Research and Policy and ² Medicine, Stanford University School of Medicine, Stanford, California; ³ Division of Research, Kaiser Permanente Medical Care Program, Oakland, California; ⁴ Orentreich Foundation for the Advancement of Science, Inc., Cold Spring-on-Hudson, New York; and ⁵ Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics and Cancer, Prevention Studies Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, Maryland

Requests for reprints: Catherine de Martel, Stanford University School of Medicine, 300 Pasteur Road, Stanford, CA 94305. Phone: 650-725-75-11; Fax: 650-725-6951. E-mail: prosper{at}stanford.edu

Background: Infection with Helicobacter pylori is an established risk factor for gastric cancer. Results from two studies suggest that it may also be a risk factor for pancreatic cancer.

Methods: We conducted a nested case control study among 128,992 adult subscribers to the Kaiser Permanente Medical Care Program who had been enrolled in a multiphasic health checkup from 1964 to 1969. Serum collected during the checkup was maintained frozen, and subjects were followed for cancer. Cases consisted of 104 randomly selected subjects among 507 who developed pancreatic cancer in the cohort. Controls consisted of 262 pancreatic cancer–free subjects from a pool of 730 controls previously tested for studies conducted on this cohort. Controls were individually matched to cases on age, gender, race, site, and date of multiphasic health checkup. Control sera were compared with cases for antibodies to H. pylori and the CagA protein. The effects of smoking, alcohol consumption, obesity, and years of education were also investigated.

Results: Neither H. pylori [odds ratio (OR), 0.85; 95% confidence interval (95% CI), 0.49-1.48] nor its CagA protein (OR, 0.96; 95% CI, 0.48-1.92) was associated with subsequent development of pancreatic cancer. Smoking (OR, 2.09; 95% CI, 1.17-3.74) and greater number of years of education (OR, 2.13; 95% CI, 1.23-3.69) were risk factors for pancreatic cancer, whereas alcohol consumption and obesity were not.

Conclusion: Our results suggest that H. pylori infection is not associated with development of pancreatic cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1188–94)

This article has been cited by other articles:

				Cancer Epidemiol. Biomarkers Prev., October 1, 2008; 17(10): 2901 - 2901. [Full Text] [PDF]