The mechanism of hypergastrinemia in achlorhydria. Effect of food, acid, and calcitonin on serum gastrin concentrations and component pattern in pernicious anemia, with correlation to endogenous secretin concentrations in plasma.

The effect of protein-rich food, intravenous calcitonin injections, and intragastric instillation of hydrochloric acid on serum gastrin concentrations and gastrin component pattern was studied in hypergastrinemic patients (pernicious anemia) and matched control subjects. Moreover, plasma secretin concentrations were measured during intragastric acidification. The intragastric acidification resulted in rapid fall in serum gastrin concentrations, although not below the upper limit of normal range. The small components, III (gastrin-17-like) and IV (gastrin-13-like), almost disappeared, whereas the concentrations of component I and component II (gastrin-34-like) were less affected. The increase in secretin concentrations after intragastric acidification was smaller in patients with pernicious anemia than in normal subjects, although the difference was not significant. In contrast to the results in normal control subjects, neither food nor calcitonin produced significant variations in serum gastrin concentrations and gastrin component pattern of pernicious anemia patients. The failure of food to stimulate and of calcitonin to inhibit release of gastrin in the majority of pernicious anemia patients might suggest that gastrin secretion in these patients is autonomous. However, considering the recently recognized slow metabolic clearance rate of big gastrins, the effect of intragastric acidification suggests that the mechanism for acid inhibition of the antral gastrin secretion is intact in patients with achlorhydria.