Introduction A negative association exists between H. pylori infection and both gastroesophageal reflux disease and oesophageal adenocarcinoma. The great majority of the H. pylori infected population are asymptomatic, so we studied healthy volunteers to determine if the infection is associated with changes to the acid secretory capacity of gastric mucosa which may protect individuals from acid reflux.

Methods We studied 31 H . pylori positive and 29 H . pylori negative volunteers, matched for age and gender. Jumbo biopsies were taken at eleven pre-determined gastric locations. High resolution pHmetry (12 sensors at 11 mm intervals) and manometry (36 sensors at 7.5 mm intervals) was performed fasted and after a standardised meal. The position of the squamocolumnar junction, marked with two endoscopically placed radio-opaque clips, was visualised radiologically relative to the probes. The biopsy specimens were scored for inflammation and stained with monoclonal antibody to H⁺/K⁺ATPase for counting parietal cell (PC) density.

Results In the fasting period, at all sensors more than 1.1 cm below the peak LES pressure the median pH was less acidic in H. pylori positives (Table 1). After a meal, intragastric acidity was less in H. pylori positives compared to negatives at sensors 2.2 to 4.4 cm below the peak LES pressure (all p < 0.05), which are the sensors closest to the gastroesophageal junction (GOJ).

Median PC density (IQR) at mid-greater curve of gastric body was 233 (96) for H. pylori positives and 352 (76) for negatives (p < 0.001). PC density was lower in H. pylori positives in 10 out of the 11 gastric locations (all p < 0.01).

Positive CagA status was associated with reduced intragastric acidity, but had no effect on PC density or mucosal inflammation when compared to CagA negative H. pylori positives.

Conclusion The majority of H. pylori infected subjects have reduced intragastric acidity and PC density compared to the uninfected population and the reduction in acidity is most marked close to the GOJ. This may explain the negative association between H. pylori infection and both gastroesophageal reflux disease and oesophageal adenocarcinoma.

Disclosure of Interest None Declared