Moss, Steven Frank; (1993) Studies of the increased gastrin release associated with Helicobacter pylori infection in duodenal ulcer disease. Doctoral thesis (M.D), UCL (University College London).

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Abstract

Duodenal ulcer disease is strongly associated with infection of the gastric antrum by Helicobacter pylori (H. pylori), possibly through the exaggerated plasma gastrin response associated with this organism. The work described in this thesis investigates aspects of both the cause and the effect of this increase in gastrin secretion in duodenal ulcer patients. Chapter 2 provides further evidence that H pylori is responsible for the exaggerated gastrin response since when duodenal ulcers are healed by sucralfate, which does not eradicate H pylori, the gastrin response is unchanged. However, unexpectedly, this treatment decreased basal gastric acid secretion. The results of studies described in chapter 3 suggest that the exaggerated gastrin response occurs by a mechanism independent of luminal pH and with no apparent change in the meal-stimulated secretion of acid or pepsin. Despite the fall in meal-stimulated gastrin the peak acid output also remained unchanged a year after the eradication of H pylori (chapter 4) but the basal acid output appeared to decrease in this small study. The work described in chapter 5 confirms this fact; successful eradication of the organism decreased both basal plasma gastrin concentrations and basal acid secretion, without altering the sensitivity of the parietal cell to circulating gastrin. This may be how the eradication of H pylori prevents ulcer recurrences. The cause of the hypergastrinaemia was addressed in the final chapters. Methods were developed to measure somatostatin mRNA from endoscopic biopsies as a surrogate marker of local somatostatin release. It was then established that the hypergastrinaemia seen in pernicious anaemia is associated with a deficiency of somatostatin mRNA (chapter 6). Finally, an increase in both somatostatin-secreting cells and somatostatin mRNA was found after the eradication of H pylori, implying that this bacterium increases gastrin release by the depletion of somatostatin.

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