Effect of Calciferol-Induced Chronic Hypercalcemia on the Gastric Secretion from a Heidenhain Pouch

Abstract

THE OCCURRENCE of peptic ulceration in a variety of chronic clinical states where prolonged hypercalcemia is a major part of the metabolic alteration suggests that a sustained elevation of serum calcium may affect the acid-pepsin secretory mechanism of the stomach. Hyperparathyroidism is the primary example of such a disease, but ulcers have been reported following vitamin D intoxication, and with the hypercalcemia that sometimes accompanies sarcoidosis and Hodgkins disease.5–7, 11, 13 In our own clinical experience we have observed peptic ulcers in patients who become hypercalcemic from osteolytic neoplasin, and in fracture patients who have become osteoporeotic from prolonged immobilization. It is also possible that the unusual intractability of ulcers in the milk-alkali syndrome described by Burnett is related to the hypercalcemic state.2 Conflicting and inconclusive reports appear in the literature prior to the work of Schiffrin, in 1941.12 In a single acute experiment with a Heidenhain pouch dog he was able to demonstrate an abrupt increase in pouch volume output and acidity when sufficient parathormone was injected to raise the serum calcium level 2.0 mg.%. There was no appreciable change in pepsin content but the acid increase appeared to be commensurate with and correlative to the hypercalcemia since it gradually disappeared in a week as the serum calcium levels returned to normal. For nearly 20 years, however, no such similar investigations have been reported and there are no reports where a chronic hypercalcemic state has been successfully produced experimentally to study gastric secretion A recent histopathologic finding of Le-winter and Spiro lends added interest to this problem. They were able to demonstrate a marked chief cell hyperplasia in the gastric mucosa of hypercalcemic rats which had received acutely massive doses of vitamin D.8 Our report deals with gastric secretory studies on a Heidenhain pouch dog in which a state of chronic hypercalcemia has been sucessfully effected