41.   H pylori was not examined because its importance in duodenal ulcer disease was not widely recognised when this study was being planned.

42.   Indeed, there were fewer patients than expected taking NSAIDs, perhaps since intake had been reduced because of chronic duodenal ulcer disease.

43.   The effect of ulcer healing with eradication of Helicobacter pylori on gastric function was investigated in nine patients with duodenal ulcer disease.

44.   Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.

45.   We therefore studied acid secretory responses to gastrin in a series of patients with duodenal ulcer disease before and after treatment to eradicate H pylori.

46.   Thus H pylori infection combined with active ulceration may cause the increased basal acid secretion seen in duodenal ulcer disease.

47.   We also found the basal acid output to be significantly greater in patients with duodenal ulcers and with H pylori than in patients with duodenal ulcers without this infection.

48.   It is widely held that the increased basal acid secretion in patients with duodenal ulcer disease is determined by vagal drive rather than circulating gastrin.

49.   Iron deficiency was not proved in five patients who were found to have duodenal ulcer, myelomatosis, giardiasis with partial villous atrophy, hepatocellular carcinoma, and menorrhagia.

50.   Five patients had additional selective gastric vagotomy because of excessive gastric acid or a history of duodenal ulcer.