THE FUNCTIONAL PATHOLOGY OF HYPER-PARATHYROIDISM

Abstract

A study of 3 cases of hyperparathyroidism, 2 with osteitis fibrosa cystica and the other with multiple myeloma, has presented certain abnormalities of Ca and P metabolism. Most characteristic of these were a high serum Ca, possibly accounting for many of the clinical features, and an excessive excretion of Ca by the kidneys, apparently explaining the urinary tract complications. The increase of Ca in the urine was sufficient to cause a negative Ca balance, although 2 patients showed, in addition, an excessive output in the stools. Low serum P was repeatedly found except in 1 patient with marked kidney insufficiency. Altered P metabolism was encountered but no specific abnormality presented. There was no indication that the total N metabolism or creatinine metabolism is abnormal in hyperparathyroidism. Although there were marked changes in Ca and P other serum electrolytes were normal. By the administration of orthophosphate it was possible to cause an increase in the serum phosphate, a decrease in serum Ca, a reduction of Ca in the urine to normal and establish a positive Ca balance. It appears, however, that a continuation of this procedure resulted in an excessive output of Ca in the stools. Following parathyroidectomy in 2 patients the disturbances of Ca and P metabolism were reversed. The Ca almost disappeared from the urine and large amounts of Ca and P were retained in the proportion in which they occur in bone. One patient reverted to tetany which was almost fatal. It was controlled with difficulty by the administration of large amounts of parathormone and Ca. The metabolism of hyperparathyroidism differs almost completely from that of osteomalacia. In the literature, however, great confusion exists in nomenclature. Cases have been called osteomalacia which probably were examples of hyperparathyroidism. This state is perhaps most often seen with von Recklinghausen''s disease of bones, but accompanies hyperplasia of the parathyroid from a variety of causes which include multiple myeloma, extensive carcinoma of bone and possibly other destructive bone processes. These studies indicate that improvement in the clinical state of hyperparathyroidism may be accomplished by the administration of orthophosphate. The possible dangers of such a procedure have been made evident. It would appear that the only effective method of treatment is the removal of parathyroid tissue.