There is an inverse association between infection with Helicobacter pylori and esophageal adenocarcinoma.
The mechanism of the apparent protection against esophageal adenocarcinoma by H pylori infection and, in particular, the role of gastric atrophy is disputed.
Dr Anderson and colleagues from the United Kingdom explored the relationship between all stages of the esophageal inflammation, metaplasia, adenocarcinoma sequence, H pylori infection and gastric atrophy.
|Gastric atrophy was uncommon, occurring in 5% of all subjects|
The team evaluated 260 population controls, 227 esophageal adenocarcinoma, 224 Barrett's esophagus, and 230 reflux esophagitis patients recruited within Ireland.
H pylori and cytotoxin-associated gene product A (Cag A) infection was diagnosed serologically by western blot.
The researchers measured pepsinogen I and II levels were measured by enzyme immunoassay.
Gastric atrophy was defined as a pepsinogen I/II ratio of less than 3.
The researchers found that H pylori seropositivity was inversely associated with esophageal adenocarcinoma, Barrett's esophagus, and reflux esophagitis.
Gastric atrophy was uncommon, occurring in 5% of all subjects, but was inversely associated with non-junctional esophageal adenocarcinoma, Barrett's esophagus and reflux esophagitis.
Inverse associations between H pylori and the disease states remained in gastric atrophy-negative patients.
Dr Anderson's team concluded, "H pylori infection and gastric atrophy are associated with a reduced risk of esophageal adenocarcinoma, Barrett's esophagus, and reflux esophagitis."
"While use of the pepsinogen I/II ratio as a marker for gastric atrophy has limitations, these data suggest that although gastric atrophy is involved it may not fully explain the inverse associations observed with H pylori infection."