Tunio, Ali Murad; (1995) Duodenal ulcer, Helicobacter pylori and epidermal growth factor. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

This thesis examines the role of epidermal growth factor (EGF) and Helicobacter pylori (H pylori) in the pathogenesis of duodenal ulcer (DU). EGF concentration was measured in 60 subjects, controls (n=20) and in patients with non-ulcer dyspepsia (NUD, n=20) and DU (n=20), in saliva and in gastric juice during basal conditions and after maximal histamine stimulation. EGF concentrations in gastric juice were similar during basal conditions in all three groups. Salivary concentrations were similar in the DU and control groups, but lower in the NUD group. After histamine stimulation EGF concentrations increased in gastric juice and saliva, DU subjects producing much more than the control group and patients with NUD. H pylori status was determined by measuring urea and ammonia in the gastric juice (ammonia test). EGF concentration was not related to H pylori status. The ammonia test was compared with the 13C-urea breath test in nine control subjects: there was complete concordance in the results. The prevalence of H pylori in 100 healthy controls, 39%, was strongly age- dependent and there was a trend suggesting that smokers had less chance of having H pylori infection. Prevalence was significantly higher in men than in women, a finding not explained by socio-economic status, age, race or smoking habits. The prevalence of H pylori in controls was compared with that in dyspeptic subjects previously studied here. In dyspeptics there was no influence of smoking or gender. The prevalence of H pylori in DU was significantly higher than controls in two age groups (36-45 and 56-65) Using EGF as a marker of swallowed saliva, Whitfield's hypothesis that the aspirated gastric juice is composed of three distinctive components, primary gastric secretion (Vacid), duodenogastric reflux (Vreflux) and swallowed saliva (Vsal) has been validated. This thesis does not confirm the roles of H pylori, or of lack of EGF, in causing DU, but the higher EGF in DU subjects may aid the healing of the ulcer.

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