Gastric acid secretion, serum gastrin and parietal cell histology in hyperthyroidism

A decrease in MAO by gastrin stimulation was observed in 13 of 20 hyperthyroid patients. Five of these 13 cases had achlorhydria. The decrease in gastric acid secretion had no relation to the duration of symptoms, serum T3 and T4 levels, serum antithyroglobulin antibody levels and serum antithyroid microsomal antibody levels. Gastroscopy with biopsy was performed in 17 cases. In patients with achlorhydria, macroscopic and histological atrophy was not observed in the body, and parietal cells were present and their succinic dehydrogenase activity was normal. Electron microscopy of the parietal cells of patients with achlorhydria showed that their cells were similar to those in the resting state of healthy subjects with the ability to secrete normal amounts of gastric acid. These findings demonstrate that the decrease in gastric acid secretion in hyperthyroidism is not caused by any structural changes in the gastric mucosa but by functional suppression. In the present experiment, this suppression was found resistant to gastrin. A rise in serum gastrin level was observed in 8 cases. Either achlorhydria or marked hypoacidity was found in 6 cases with the level more than 400 pg/ml. The HCl administration temporarily lowered elevated gastrin levels, and feedback inhibition by HCl was found to be maintained. A rise in gastric pH was considered to be one of the prerequisites for an increase in serum gastrin level.