Abstract
BackgroundHypergastrinaemia occasionally indicates the presence of a gastrinoma. However it is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to influence fasting serum gastrin concentrations remains incompletely understood.Materials and MethodsFasting serum gastrin concentrations were measured by radioimmunoassay in 1,400 patients attending for diagnostic oesophagogastro-duodenoscopy. After exclusions, 982 patients were divided into four groups and their results analysed. We compared gastrin concentrations in normal patients (no H. pylori infection, no PPI use and no histological evidence of gastric preneoplasia (n=233)), with those in patients who were taking regular PPIs (H. pylori negative with no gastric preneoplasia (n=301)), patients who had active H. pylori infection but no gastric preneoplasia (n=164) and patients with histologically confirmed gastric preneoplasia (n=284).ResultsMedian fasting gastrin concentration in the normal group was 20pM and was significantly increased in PPI users (46pM, p<0.0001), patients with active H. pylori infection (27pM, p<0.0001), and patients with antral (25pM, p<0.01) or corpus (48pM, p<0.0001) gastric preneoplasia. PPI use resulted in further significant increases in fasting serum gastrin concentrations in patients who were infected with H. pylori (50pM, n=56) or who had antral gastric preneoplasia (53pM, n=87), but did not significantly alter serum gastrin concentrations in patients with corpus preneoplasia (90pM, n=66).ConclusionsPPI use, H. pylori infection and atrophic gastritis all caused significant elevations of median fasting gastrin concentrations. However, several patients who had potential risk factors for hypergastrinaemia still demonstrated fasting serum gastrin concentrations within the normal range.
Highlights
Gastrin is the major gastric hormone responsible for regulating gastric acid secretion and growth of the oxyntic mucosa [1]
More than half the total cohort (52.3%) reported pump inhibitor (PPI) use, 21.8% were H. pylori positive by histology, and 43.3% were positive by IgG serology
No patients were diagnosed as having a gastrinoma, Zollinger Ellison syndrome or multiple endocrine neoplasia (MEN)-1. 443 patients were reported as having no macroscopic upper gastrointestinal abnormality and the other patients had various benign pathologies such as oesophagitis, gastritis, duodenitis, benign polyps or vascular lesions
Summary
Gastrin is the major gastric hormone responsible for regulating gastric acid secretion and growth of the oxyntic mucosa [1]. Pyloric antral mucosal G-cells synthesise gastrin as a 101-amino acid precursor (preprogastrin) that is processed to yield biologically active amidated gastrin-17 and gastrin-34 [2, 3] These amidated forms of gastrin bind to cholecystokinin (CCK) receptors on gastric enterochromaffin-like (ECL)-cells, stimulating the release of histamine which acts in a paracrine manner, binding to histamine H2-receptors on parietal cells and resulting in acid secretion. A number of other clinical conditions can lead to elevated fasting serum gastrin concentrations. These include atrophic gastritis, either caused by autoimmune disease or chronic H. pylori infection, which results in hypochlorhydria and compensatory hypergastrinaemia. Hypergastrinaemia occasionally indicates the presence of a gastrinoma It is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to influence fasting serum gastrin concentrations remains incompletely understood
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