Parathyroids and Gastric Secretion

Abstract

Summary The short-term injection of 13 normal subjects with parathyroid hormone in a total dose of 1000 units in 24 hours produced a significant increase in gastric secretory volume and total pepsin over control levels. The existence of this depends upon the assumption of a first day effect in explaining a portion of the data. The withdrawal of long-term parathyroid stimulation from 4 out of 5 hyperparathyroid patients by removal of parathyroid adenomas did not change gastric secretion. The 1 patient of the 5 who had a duodenal ulcer showed a postoperative decrease in gastric secretion. This finding raises the question of a varying response between individuals to hyperparathyroidism and keeps open the possibility of a secretory mechanism in the production of peptic ulcer in this disease; in general, however, gastric secretion is not changed by removal of a parathyroid adenoma. In 1 hypoparathyroid patient, gastric secretion was depressed at low levels of serum calcium; free acid was entirely absent when serum calcium was below 7.0 mg. per 100 ml. Free acid and pepsin activity were increased when the serum calcium was restored to normal levels. The findings in a series of 5 subjects made hypercalcemic with intravenous calcium gluconate suggest that hypercalcemia augments the production of pepsin, gastric secretory volume, and free acid, possibly by increasing the blood supply to the mucosa. In summary, notwithstanding the stimulatory effects of acute hypercalcemia and parathyroid hormone, the unaltered secretion in our patients with hyperparathyroidism leads us to believe that the ulcerogenic factor in this disease is not hypersecretion.