Q J Med 1999; 92: 373-377
© 1999 Association of Physicians
The rise in circulating gastrin with age is due to increases in gastric autoimmunity and Helicobacter pylori infection
From the Altnagelvin Hospital, Londonderry, Northern Ireland, The Regional Regulatory Peptide Laboratory, Royal Victoria Hospital, Belfast, and 1 Departments of Medicine and 2 Bacteriology, The Queen's University of Belfast, Belfast, UK
Received 28 January 1999 and in revised form 7 May 1999
Dr J.E.S. Ardill, Regional Regulatory Peptide Laboratory, Mulhouse Building, Royal Victoria Hospital, Grosvenor Road, Belfast BT12 6BJ
To assess the effect of increasing age on circulating gastrin, we surveyed serum gastrin, Helicobactor pylori seroantibody status and gastric autoimmunity in 366 hospitalized patients aged 15–90 years. Data were subjected to multivariate analysis, using logarithmic transformation to normalize the distribution of gastrin concentrations (presented as geometric means and 95%CIs). The frequency of H. pylori-positive antibody status increased with age from 28% in the second decade to >70% beyond the fourth decade. Fasting gastrin concentrations rose significantly from 44 ng/l (41–48) in the second decade to 95 ng/l (67–131) by the eighth decade (p=0.001) in the total group. Twenty-seven patients (6.8% of the total) tested positive for gastric auto-antibodies: 2% of patients in the second decade, rising to 15.9% in the eighth decade. These patients formed a distinct group with respect to circulating gastrin concentrations. Excluding these 27, fasting gastrin concentrations still rose significantly, from 44 ng/l (41–48) in the second decade, to 67 ng/l (50–89) in the eighth decade (p=0.003) in the remaining 341 patients. Fasting gastrin concentrations were significantly higher in patients who were H. pylori-seropositive (59 ng/l, 54–64 vs. seronegative 41 ng/l, 37–46) (p=0.002), and there was no increase in circulating gastrin concentrations with increasing age in either the H. pylori-positive or the H. pylori-negative group. The increase in circulating fasting gastrin observed with increasing age is due to an increased incidence of gastric antibodies associated with auto-immune atrophic gastritis, and an increased incidence of H. pylori infection.