gaslr_top.jpg (8903 bytes)

GASTROENTEROLOGY LITERATURE ALERT!

LANDMARK ARTICLE - Required reading 

Uemura N, Okamoto S, Yamamoto S, et al.  Helicobacter pylori infection and the development of gastric cancer.  N Engl J Med 2001;345:784-9. 

Fox JG, Wang TCHelicobacter pylori – Not a good bug after all.  N Engl J Med 2001:829-831. (Editorial)

 Major findings:

This is one of the first long-term prospective studies looking at the relationship of H. pylori and gastric cancer

 Among 1526 patients followed for a mean of 7.8 years (range 1-10.6), 1246 were H. pylori positive, none receive antibiotics. 280 patients were H. pylori negative

 Gastric cancer developed in 2.9% of H. pylori-positive patients compared to no gastric cancer in the non-infected patients.  The risk for developing gastric cancer was 5% at 10 years.

 Among H. pylori (+) patients, gastric cancer developed in 4.7% of non-ulcer dyspepsia patients, 3.4% in those with gastric ulcers and in 2.2% of those with gastric polyps at baseline endoscopy. None of the patients with duodenal ulcer on baseline endoscopy developed cancer

 The presence of severe gastric atrophy, corpus-predominant gastritis and intestinal metaplasia was associated with a higher risk for cancer.

FACTS TO REMEMBER FOR BOARDS

 Corpus-predominant atrophy appears to be the critical initiating event in the progression to cancer.  This is followed by intestinal metaplasia, dysplasia and then carcinoma.

  A specific mutation or a molecular marker predicting progression to gastric cancer has not yet been found.

  Patients with H. pylori-related duodenal ulcers appear to be protected against gastric cancer.  The reason is unknown, but may reflect infection with a different strain of H. pylori.

  Dietary salt increases and gastric ascorbic acid decreases the risk of gastric cancer

 The World Health Organization and the International Agency for Research on Cancer classified H. pylori as a class I carcinogen in 1994.

 Clinical application

1.  This is a Japanese study.  Japan has traditionally had a high rate of gastric cancer.  Factors other than H. pylori (i.e. genetic, dietary, environmental) may be the cause.  This study needs to be repeated in the U.S. population.

 2.  The number of patients in the H. pylori-negative group was small, if 3% of them had developed cancer, that would have been only 8 patients.  This could have been missed by the small number of patients in that group.

 3.  At present, however, evidence of H. pylori infection should trigger a recommendation to eradicate.

Get The Article

Go Back