1.   In conclusion, using the freeze fracture method, we have shown significantly fewer gap junctions between gastric surface mucous cells in ulcer patients than in healthy volunteers.

2.   A slight shift in the age distribution would be expected because of the increasing prevalence of non-operated peptic ulcer patients in the population.

3.   Numerous studies have shown that Helicobacter pylori infection of the gastric antrum raises circulating gastrin concentrations in duodenal ulcer patients and healthy volunteers.

4.   We have show, however, that there is no change in parietal cell sensitivity to gastrin after eradication of H pylori in duodenal ulcer patients.

5.   Raised basal gastrin and exaggerated meal stimulated gastrin responses have been described in infected duodenal ulcer patients.

6.   This hypergastrinaemia may account for the increased acid secretion seen in some duodenal ulcer patients and may be one mechanism whereby H pylori contributes to the ulcer diathesis.

7.   It has also been found that duodenal ulcer patients on continuous pharmacological acid suppression exhibit a lower prevalence of gastric metaplasia in comparison with intermittently treated patients.