Article Text
Abstract
Objective: A number of studies have shown an inverse association between infection with Helicobacter pylori (H. pylori) and oesophageal adenocarcinoma (OAC). The mechanism of the apparent protection against OAC by H. pylori infection and, in particular, the role of gastric atrophy is disputed. We explored the relationship between all stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence and H. pylori infection and gastric atrophy. Design and patients: Case-control study involving 260 population controls, 227 OAC, 224 Barrett¡¯s oesophagus (BO) and 230 reflux oesophagitis (RO) patients recruited within Ireland. H. pylori and CagA infection was diagnosed serologically by Western Blot and pepsinogen I and II levels were measured by enzyme immunoassay. Gastric atrophy was defined as a pepsinogen I/II ratio of <3. Results: H. pylori seropositivity was inversely associated with OAC, BO and RO; adjusted odds ratios (95% CIs), 0.49 (0.31-0.76), 0.35 (0.22-0.56), and 0.42 (0.27-0.65), respectively. Gastric atrophy was uncommon (5.3% of all subjects), but was inversely associated with non-junctional OAC, BO and RO; adjusted odds ratios (95% CIs), 0.34 (0.10-1.24), 0.23 (0.05-0.96) and 0.27 (0.08-0.88), respectively. Inverse associations between H. pylori and the disease states remained in gastric atrophy negative patients. Conclusion: H. pylori infection and gastric atrophy are associated with a reduced risk of OAC, BO and RO. 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.
- Barrett's oesophagus
- Helicobacter pylori
- oesophageal adenocarcinoma
- pepsinogen
- reflux oesophagitis