Experimental Chronic Hyperparathyroidism in Dogs Without Hypercalcemia.

Abstract

The rate at which the elimination of tissue and bone calcium proceeds in the dog under the influence of parathormone depends, among other factors, upon the dosage. However, the dose of parathormone that may be administered to the dog is limited by the danger of fatal hypercalcemia.

Serum calcium is obviously one term in an equilibrium. Some of the other terms affecting it, under given physico-chemical conditions of the blood, are: tissue calcium and other salts, bone salts, their availability, and the rate of calcium excretion, particularly by the kidneys. The rapid rate of excretion of calcium, as well as dietary factors, are probably largely responsible for the phenomena observed by us in the guinea pigs after parathormone. We have shown 1 , 2 that this animal tolerates large doses of parathormone, although it reacts to the extract both by an elevation of serum calcium and by formation of bone lesions. In our belief, this “tolerance” is the reason for the ease with which the typical changes of ostitis fibrosa were produced in guinea pigs. We have succeeded, after having depleted bone and tissue calcium in dogs, in administering to them relatively large doses of parathormone without producing hypercalcemia. By thus increasing the “tolerance” of the dog to parathormone it was possible to produce ostitis fibrosa cystica in this animal. 3

This report is based on a study of 11 growing dogs in which experimental chronic hyperparathyroidism was produced by daily injections of parathormone. The diet of the dogs consisted of an adequate quantity of fresh raw meat with additions of cod-liver oil, bone meal, calcium lactate and tomato juice. Parathormone was injected at first in a daily dose of 2 units per kilo, which was raised gradually in some dogs to as high as 5 units toward the end of the experimental period of 5 to 6 months.