111.   H pylori infection was confirmed in the duodenal ulcer patients by microscopic examination of antral biopsy rapid urease test on antral biopsy, and by C urea breath test.

112.   It was increased in the H pylori positive duodenal ulcer patients, however, compared with both the H pylori negative healthy volunteers and H pylori positive healthy volunteers.

113.   The basal acid output in the one duodenal ulcer subject in whom H pylori infection was not eradicated was similar before and after the triple treatment.

114.   The median pepsin output in the H pylori positive duodenal ulcer patients was higher than both the H pylori positive and negative healthy volunteers.

115.   This study shows that chronic H pylori infection is accompanied by appreciably increased gastric acid output in both healthy volunteers and duodenal ulcer patients.

116.   The exaggerated acid response to gastrin can be explained by the increased parietal cell mass present in duodenal ulcer patients.

117.   The second finding is consistent with our previous study showing that the response to pentagastrin stimulation in duodenal ulcer patients is not changed after eradication of H pylori.

118.   This hypothesis was tested by two ongoing trials of H pylori eradication treatment, one in patients with duodenal ulcer disease and the other in patients with intestinal metaplasia.

119.   The primary aim of the first trial was to discover if, after conventional healing of duodenal ulcers, eradication of H pylori prevented ulcer relapse.

120.   The main selection criterion in the DU trial was a duodenal ulcer, freshly healed by standard acid supressive treatment.