Role of the Parathyroids in Calcification,and Susceptibility of Parathyroidectomized Rats to Viosterol.

Abstract

The long continued administration of parathyroid extract to animals results in an increased excretion of calcium and phosphorus from the body. 1 , 2 , 3 Similarly, the presence of hyperfunctioning parathyroid glands results in a negative calcium and phosphorus balance and bone decalcification termed clinically, osteitis fibrosa cystica. Several observers noticed marked improvement when one or more of these glands was removed. Hence, in hypofunction a marked retention of calcium and phosphorus should result. Greenwald, 4 contrary to previous assumptions, demonstrated retention of these elements after thyroparathyroidectomy in dogs. The validity of Greenwald's conclusions may be questioned because the thyroid extirpation may have contributed to this retention. However, in metabolism experiments on rats, in which the parathyroids alone were removed, retention of calcium and phosphorus was observed, provided the diet contained a certain amount of these elements, 5 thus substantiating, in part, Greenwald's hypothesis. However, no attempts have as yet been made to determine the depots of retention of calcium and phosphorus. That their deposition is not always in the osseus tissue is evidenced by the observations of Erdheim, 6 Iselin, 7 and Toyofuku. 8 Leopold and Von Reuss 9 found that the combined soft tissues of parathyroidectomized rats contained more calcium than those of control rats.

In the course of study on the effect of calcium, phosphorus and viosterol intake on parathyroidectomized rats it was noted that they were much more susceptible to viosterol hypercalcification than normal animals. A dose of viosterol, which ordinarily would not produce calcification in a normal rat in a given length of time, may cause calcification in the organs of the parathyroidectomized animals, provided certain amounts of calcium and phosphorus be present in the diet.