Gastric Adenocarcinoma and Helicobactor pylori

Gastric adenocarcinoma is the most common form of stomach cancer. Though rates of new cases of gastric cancer have been decreasing in North America in recent years, it is still among the leading causes of cancer death. The incidence of gastric cancers varies among countries and is much lower in North America than in Japan and some Scandinavian countries for example. Stomach cancer most commonly occurs in older populations and is very rare in people under the age of 30.

Historically, research has suggested an association between diets that include a lot of pickled and salty food and/or are low in vitamin C and an increase an individual's chance of getting stomach cancer. However, investigations examining diet alterations in at risk populations have revealed no ability to decrease cancer occurrence or risk.

The causative role of Helicobactor pylori (H.pylori) in ulcer disease is now widely accepted. There have been many studies in the past that showed some association between the presence of H.p. and certain forms of stomach cancer. Some small studies have even shown that treating patients suffering from a rare form of stomach cancer (not the common gastric adenocarcinoma described above) with drugs to kill the H. pylori has resulted in remission of their cancer. There has still been no evidence to show that H. pylori therapy can alter the disease course of gastric adenocarcinoma.

A recently published study by Uemura et al from the Fukuoka University School of Medicine in Japan offers strong new evidence associating the presence of H.p. and gastric adenocarcinoma1. This prospective study enrolled 1,526 patients with either duodenal ulcers, gastric ulcers, gastric hyperplasia (excessive formation of cells) or non-ulcer dyspepsia at the time of study enrolment and followed them for an average time of 8 years (min 1 max 10 years). Of those enrolled, 1246 of 1526 (81.7%) had H. pylori infection in addition to at least one of the conditions listed above.

Analysis indicated that gastric cancers developed in 36 (2.9 percent) of the infected and none of the uninfected patients. That is, this study showed gastric cancer developed in persons infected with H.p. but not in uninfected persons. Persons with H. pylori infection and non-ulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps (growth or nodule resulting from an excessive formation of cells) were also at risk, but those with duodenal ulcers were not.

This study combined with other recent research shows consistent increased risk of non-cardia stomach cancer in H.pylori positive individuals. (The stomach is composed of several areas including the antrum, the corpus or body, the pylorus and the cardia. The cardia is the part of the stomach that connects to the esophagus.) This would indicate that at least half of all non-cardia cancer could be attributable to the infection and possibly a great deal more. Apart from smoking, very few established causes of cancer have been associated with an identifiable risk now being attributed to H.p. There are some, now advocating the case for universal screening for H. pylori infection for people at risk from cancer2. However, the crucial question concerns the extent to which H. pylori pre-cancerous changes will regress or be prevented from progressing after the eradication of H. pylori from the stomach2. In order to prove that killing the H. pylori prevents gastric cancer, large numbers of patients (possibly several hundred thousand) would need to be recruited into clinical trials and followed for over 10 years2. It remains to be seen if this approach will be feasible or of any utility. This dilemma faces many researchers where infectious agents are suspected of triggering disease process (inflammatory bowel disease, cardiovascular disease). Fortunately, researchers in gastric cancer and these other disease areas can combine data and experience to model the best approaches to investigate these new and difficult questions.

Refs:
1) Helicobacter pylori Infection and the Development of Gastric Cancer
New England Journal of Medicine Volume 345:784-789 September 13, 2001 Number 11
Naomi Uemura, M.D., Shiro Okamoto, M.D., Soichiro Yamamoto, M.D., Nobutoshi Matsumura, M.D., Shuji Yamaguchi, M.D., Michio Yamakido, M.D., Kiyomi Taniyama, M.D., Naomi Sasaki, M.D., and Ronald J. Schlemper, M.D.

2) Remarks by Professor David Forman addressing the European Cancer Conference (ECCO 11) in Lisbon, Portugal October 24th 2001.

Past reports

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Non-ulcer Dyspepsia and Helicobacter Pylori Infection: To Treat or Not to Treat

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