1.   Therefore acid inhibition is not a prerequisite for the hyperplasia.

2.   Serum gastrin concentrations may also rise with age, probably because of the increased prevalence of gastric atrophy with consequent loss of acid mediated inhibition of gastrin release.

3.   Gastritis with atrophy and the consequent loss of acid mediated inhibition of gastrin release contributes most to this increase.

4.   This finding may have clinical importance in the few patients who have pronounced hypergastrinaemia because of profound long acting acid inhibition.

5.   Profound acid inhibition, however, results in increases in serum gastrin because of interference in the feedback mechanism between intragastric acidity and antral gastrin release.

6.   This finding may be of clinical importance in the few patients who have severe hypergastrinaemia as a result of long acting profound acid inhibition.