Relation of Thyroid and Parathyroid Glands to Cal- Cium

In a series of investigations on the relation of the thyroid to calcium and phosphorus metabolism Aub and his coworkers (1) have demonstrated that increased thyroid activity is associated with an increased excretion of calcium and phosphorus. In exophthalmic goiter there is an increased output of calcium not only in the urine but in the feces. In normal individuals who are fed thyroid there is a similar increase in calcium and phosphorus excretion, and in myxedema there is a diminished excretion which rises toward normal following thyroid therapy. This increase in negative calcium and phosphorus balance is dissimilar to that produced by overactivity of the parathyroid glands. In hyperparathyroidism the fecal calcium excretion is not increased in the absence of kidney damage (2). The blood levels of both calcium and phosphorus are altered in hyperparathyroidism while in hyperthyroidism they are usually within normal limits. These workers have also demonstrated improvement in tetany of hypoparathyroid origin from thyroid medication with an elevation of the lowered blood calcium level toward that of normal (3). Careful total acid-base balance experiments have excluded in their opinion acidosis as a cause of this altered metabolism (4). Vitamin D deficiency has also been studied as a possible cause and has been considered excluded (5). The conclusion of these workers is that if the blood calcium level is below normal before medication an increased amount of the thyroid hormone releases calcium and phosphorus from the bones with a consequent rise of the blood calcium level and an increased excretion of both calcium and phosphorus by the kidney and large bowel. The usual absence of altered blood levels of both calcium and phosphorus, together with the increased fecal calcium excretion, lead them to believe that in hyperthyroidism a concomitant overactivity of the parathyroid glands is not present. These conclusions have recently been challenged by Hansman and Wilson (6) in a series of studies on patients with hyperthyroidism, two of whom also had postoperative hypoparathyroidism. These Australian workers believe that in thyrotoxicosis there is an associated overactivity of the parathyroid glands and that the alterations in calcium and phosphorus metabolism are directly due to the excessive parathyroid secretion. The appearance of a patient in the Thyroid Clinic with postoperative parathyroid tetany and a recrudescence of her exophthalmic goiter presented us with an unusual opportunity to study the interrelation of the thyroid and parathyroid glands in their control of calcium and phosphorus metabolism.