Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely than population controls to have evidence of past Helicobacter pylori infection, reported in the issue of Gastroenterology.
The association persisted independently of known esophageal cancer risk factors, such as reflux and smoking, and also was independent of genetic factors, including polymorphisms in genes coding for interleukin-1B and tumor necrosis factor-alpha.
The findings add to a growing body of evidence suggesting that H. pylori might somehow be protective against esophageal cancers, even as it increases the risk of gastric cancer.
The head of the Cancer Control Laboratory at the Queensland Australia Institute of Medical Research, studied 794 patients aged 18-79 years with a primary invasive cancer of the esophagus or esophagogastric junction. Overall, 269 patients had esophageal adenocarcinoma, 307 had esophagogastric junction adenocarcinoma, and 218 had esophageal squamous cell carcinoma.
The 1,355 controls were randomly selected from the Australian Electoral Roll and were roughly matched to the patients by age, sex, and state of residence.
“Patients with [esophageal adenocarcinoma, or EAC] and [esophagogastric junction adenocarcinomas, or EGJAC] were significantly less likely than were controls to have antibodies to H pylori.”
Among the EAC patients, the odds ratio of being seropositive was 0.44 (95 percent confidence interval, 0.29-0.67) after researchers adjusted for age, sex, smoking history, education, and several other environmental factors. In the EGJAC population, the OR was 0.40 (95 percent CI, 0.27-0.59), there was no association between H. pylori and esophageal squamous cell carcinoma.
Also investigated whether esophageal cancer patients shared any common mutations in the genes coding for IL-1B and TNFalpha, but they “found no evidence that the inverse associations between H. pylori infection and [esophageal adenocarcinomas or esophagogastric junction adenocarcinoma] were modified by the presence of polymorphisms at IL-1B-31, IL-1B511, NF-A 308, and TNF-A 238.”
“Several potential mechanisms have been proposed to explain the association, including hypoacidity subsequent to prolonged infection, dysregulation of host cytokine or immune responses, disturbances to microbial flora, and changes in the expression of locally acting hormones relating to obesity pathways (notably leptin and ghrelin). “Each of these hypotheses is plausible, and all may indeed play a role.”