Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.788612
Title: Studies of plasma gastrin and Helicobacter pylori infection in duodenal ulcer disease
Author: Chittajallu, Ravi Shankar
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1994
Availability of Full Text:
Access from EThOS:
Access from Institution:
Abstract:
Chronic Helicobacter pylori infection of the gastric antrum is seen in over 95% of duodenal ulcer patients. Eradication of this infection results in a lowering of circulating gastrin concentration. A considerable proportion of the population are infected with H. pylori but only some of them develop duodenal ulceration. In this thesis I looked at the possibility that the development of duodenal ulceration in subjects with H. pylori infection is determined by the degree of hypergastrinaemia induced. In addition, I attempted to determine the mechanism by which this hypergastrinaemia may be brought about. Consistent with earlier studies eradication of H. pylori infection in duodenal ulcer patients resulted in a fall in both basal and meal stimulated plasma gastrin concentrations. These values were similar in H. pylori positive duodenal ulcer patients and H. pylori positive asymptomatic volunteers. This suggests that factors in addition to elevated plasma gastrin are responsible for predisposition to duodenal ulceration in these patients. The mechanism by which H. pylori infection induces hypergastrinaemia is unclear. It has been postulated that by virtue of its high urease activity the organism produces ammonia locally at the gastric antrum and this may directly stimulate gastrin release by the G cells or may act indirectly by elevating antral surface pH. There was, however, no change in plasma gastrin concentrations with either increased bacterial ammonia production by intragastric urea infusion or suppression of bacterial urease activity by triple therapy (amoxycillin, metronidazole, tripotassium dicitrato bismuthate). In addition, examining the effect of gastric alkalinisation on basal and meal stimulated plasma gastrin concentrations before and after eradication of H. pylori did not support this hypothesis. It was also noted that reversal of the acute inflammatory component of the antral gastritis produced by the infection is not associated with a change in plasma gastrin concentrations. The possibility that the hypergastrinaemia is a physiological response to inhibition of parietal cell function by H. pylori was examined. There was no change in parietal cell sensitivity to pentagastrin after eradication of H. pylori. The mechanism by which chronic H. pylori infection of the gastric antrum induces hypergastrinaemia remains unclear. Further research is needed to elucidate this.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.788612  DOI: Not available
Share: