Cancer Research Lab

The risk of esophageal cancer differs in patients with gastric and duodenal ulcers, according to a report in the April issue of Gut.

Epidemiological evidence suggests that Helicobacter pylori infection is associated with a reduced risk of esophageal adenocarcinoma, the authors explain, but few studies have explored the risk of esophageal cancer according to histology in relation to peptic ulcer disease.

Dr. Shahram Bahmanyar at the Karolinska Institute, Stockholm, Sweden and associates investigated the risk of esophageal cancer by histology among patients hospitalized for gastric ulcer (n= 81,379) or duodenal (n= 61,548) ulcer between 1965 and 2003 in Sweden, compared with the general population.

Patients with duodenal ulcer had a 70% higher risk of esophageal adenocarcinoma than people in the general population, the authors report. Duodenal ulcer was only marginally associated with an increased risk of esophageal squamous cell carcinoma, the results indicate.

In contrast, the researchers note, gastric ulcer was not associated with a significantly increased risk of esophageal adenocarcinoma, but was associated with a significant 80% increased relative risk of esophageal squamous cell carcinoma.

“With due reservations, our finding of a positive association between gastric ulcer and risk of esophageal squamous cell carcinoma adds some further support for the hypothesis that the intragastric environment fostered by corpus atrophy may play a role in esophageal squamous cell carcinoma etiology,” the investigators say.

“This study suggests that the repeatedly confirmed strong inverse relation between H. pylori seropositivity and risk of esophageal adenocarcinoma does not pertain to all infections,” Dr. Bahmanyar and colleagues conclude. “It appears as if the pattern of gastric colonization and/or the clinical consequences in the stomach plays an important role.”

“The new challenge facing us is to clarify the mechanism of the positive association between atrophic gastritis and esophageal squamous cell carcinoma,” writes Dr. Kenneth E. L. McColl from the Western Infirmary, Glasgow, UK in a related editorial.

“This observation supports the hypothesis that it is not H. pylori itself which may influence reflux disease and its complications but the effects of the infection on acid secretion,” Dr. McColl adds.