HYPER-CALCEMIA OF GENITO-URINARY MALIGNANCY

Hypercalcemia of malignancy has been a difficult problem seen not infrequently by urologists. Although Albright reported the first case of hypercalcemia associated with a hypernephroma in 1941 there are reports in 1935, 1927 and 1950 of patients who underwent neck exploration for hyperparathyroidism who, in fact, had occult urologic malignancies. Hypercalcemia has been associated with numerous urologic malignancies, including those of the penis, testis, renal pelvis, prostate and adrenal, as well as the kidney and bladder. We herein review the current literature involving this problem, demonstrate the management of these patients with clinical material and add a modality of management not described previously for refractory cases of hypercalcemia in genitourinary malignancies. Prior to 1960 it had been assumed that bony metastases, just by their presence, caused hypercalcemia. However, this assumption is a fallacy for several reasons 1) the amount of hypercalcemia does not correlate with the size or number of metastases, 2) the osteoclasts, not the metastatic cells, are found active at the margin of the bone lesion resorbing the bone, 3) theoretically, if the serum calcium were increased by metastases one would expect a secondary hypoparathyroidism (as manifest by the tubular resorption of calcium and phosphate) but this is not the case, 4) proved non-metastatic tumors of renal cell carcinonoma have been shown to cause hypercalcemia, 5) Tashjian and associates actually proved the production of parathormone by tumor and documented a significant number of patients with this syndrome and 6) Brereton and associates reported the first case of hypercalcemia caused by a prostaglandin-producing hypernephroma. Hence, it is important for the urologist to understand the mechanism of hypercalcemia of mailignancy if he is to treat urologic tumors. The management of hypercalcemia patients would change frequently if the hypercalcemia were attributed to metastatic carcinoma. Furthermore, the symptoms of lassitude, anorexia, constipation, nausea, vomiting, polyuria, poor renal concentrating ability and cachexia could be interpreted mistakenly as secondary to terminal disease instead of hypercalcemia with disasterous consequences. Aggressive treatment of this syndrome may provide the patient with long, asymptomatic periods, if not cure.