American Journal of Epidemiology Vol. 144, No. 2: 142-149
Copyright © 1996 by The Johns Hopkins University School of Hygiene and Public Health
other |
Circulating Anti-Helicobacter pylori Immunoglobulin A Antibodies and Low Serum Pepsinogen I Level Are Associated with Increased Risk of Gastric Cancer
1National Public Health Institute, Helsinki, Finland
2Social Insurance Institution, Helsinki and Turku, Finland
3Department of Bacteriology and Immunology, University of Helsinki, Helsinki, Finland
4Finnish Cancer Registry, Helsinki, Finland
5Department of Public Health, University of Helsinki, Helsinki, Finland
6Department of Clinical Chemistry, Universrty of Helsinki, Helsinki, Finland
7Department of Public Health, Universrty of Tampere, Tampere, Finland
Reprint requests to Dr. Arpo Aromaa, National Public Health Institute (KTL), Mannerheimirrtie 166, FIN-00300 Helsinki, Finland.
Helicobacter pylori infection has been suggested to be associated with an increased risk of gastric cancer, and low levels of serum pepsinogen I (PG I) have been linked to atrophic gastritis, which is a risk factor for gastric cancer. In Finland, 39,268 persons from 25 cohorts participated during 1968–1972 in a health examination survey and were followed for up to 13 years. A nested case-control study was performed on 84 stomach cancer patients identified from the Finnish Cancer Registry and 146 controls matched for age, sex, and municipality. Serum samples drawn at the baseline study were analyzed. An elevated level of serum anti-H. pylori immunoglobulin A (IgA) antibodies (a titer >70) and a low serum PG I level (<49 µg/liter) were associated with an increased risk of gastric cancer. The odds ratios were 2.52 (95% confidence interval (Cl) 1.14–5.57) for high IgA and 2.68 (95% Cl 1.35–5.30) for low PG I. For high immunoglobulin G (>IgG) (>700), the odds ratio was only 1.50 (95% Cl 0.70–3.22). When both high IgA and low PG I were present, the odds ratio was 5.96 (95% Cl 2.02–17.57). The association of H. pylori infection with cancer became stronger with longer follow-up times, whereas that of low PG I was strongest at shorter follow-up times. Our findings support the hypothesis that H. pylori infection is a prevalent and potentially preventable cause of gastric cancer. They stress the value of IgA antibody determinations and provide new evidence for a pathogenesis leading from prolonged infection through atrophic gastritis to gastric cancer. Am J Epidemiol 1996; 144: 142–9.
Helicobacter pylori; IgA; IgG; longitudinal studies; pepsinogen; stomach neoplasms
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  F. Kamangar, S. M. Dawsey, M. J. Blaser, G. I. Perez-Perez, P. Pietinen, C. J. Newschaffer, C. C. Abnet, D. Albanes, J. Virtamo, and P. R. Taylor Opposing Risks of Gastric Cardia and Noncardia Gastric Adenocarcinomas Associated With Helicobacter pylori Seropositivity. J Natl Cancer Inst, October 18, 2006; 98(20): 1445 - 1452. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sasazuki, M. Inoue, M. Iwasaki, T. Otani, S. Yamamoto, S. Ikeda, T. Hanaoka, S. Tsugane, and for the Japan Public Health Center Study Group Effect of Helicobacter pylori Infection Combined with CagA and Pepsinogen Status on Gastric Cancer Development among Japanese Men and Women: A Nested Case-Control Study. Cancer Epidemiol. Biomarkers Prev., July 1, 2006; 15(7): 1341 - 1347. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. N. Weck and H. Brenner Prevalence of Chronic Atrophic Gastritis in Different Parts of the World. Cancer Epidemiol. Biomarkers Prev., June 1, 2006; 15(6): 1083 - 1094. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Oishi, Y. Kiyohara, M. Kubo, K. Tanaka, Y. Tanizaki, T. Ninomiya, Y. Doi, K. Shikata, K. Yonemoto, T. Shirota, et al. The Serum Pepsinogen Test as a Predictor of Gastric Cancer: The Hisayama Study Am. J. Epidemiol., April 1, 2006; 163(7): 629 - 637. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Helicobacter and Cancer Collaborative Group Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts Gut, September 1, 2001; 49(3): 347 - 353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Limburg, Y.-L. Qiao, S. D. Mark, G.-Q. Wang, G. I. Perez-Perez, M. J. Blaser, Y.-P. Wu, X.-N. Zou, Z.-W. Dong, P. R. Taylor, et al. Helicobacter pylori Seropositivity and Subsite-Specific Gastric Cancer Risks in Linxian, China J Natl Cancer Inst, February 7, 2001; 93(3): 226 - 233. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Yamagata, Y. Kiyohara, K. Aoyagi, I. Kato, H. Iwamoto, K. Nakayama, H. Shimizu, Y. Tanizaki, H. Arima, N. Shinohara, et al. Impact of Helicobacter pylori Infection on Gastric Cancer Incidence in a General Japanese Population: The Hisayama Study Arch Intern Med, July 10, 2000; 160(13): 1962 - 1968. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. T.K.-H. Stadtlander and J. W. waterbor Molecular epidemiology, pathogenesis and prevention of gastric cancer Carcinogenesis, December 1, 1999; 20(12): 2195 - 2208. [Abstract] [Full Text] [PDF]
|
|