Urine and serum calcium studies often provide a practical, accurate indication of the extent of breast carcinoma in patients in whom metastasis to bone has taken place. The quantity and rate of osteolysis in the metastatic lesions is directly correlated with urinary calcium excretion in most of these patients. Although in breast carcinoma metastasis is usually osteolytic, it is predominantly osteoblastic in 8 per cent of the cases. Even in patients with roentgenographic evidence of primarily osteoblastic metastasis, serum alkaline phosphatase has been inversely related to serum calcium levels. 1 Increasing serum alkaline phosphatase activity was associated with decreasing serum calcium levels in 94 per cent of 32 cases, and decreasing serum alkaline phosphatase activity, with increasing serum calcium levels, in 91 per cent of 33 cases. These findings suggested the possibility of relating chemical changes in urine and blood with osteoblastic bone involvement.

Precise measurement of calcium balance in patients is so complicated that it is practical only in special studies, but urinary excretion of calcium is readily studied. Excretion of excessive calcium takes place earlier and is a more sensitive indicator of bone destruction than is an increase in serum calcium. Hypercalcemia does not appear until urinary calcium excretion exceeds 500 mg. per day when the patient is on a low calcium diet (under 200 mg. per day). 2 It is at this level that the renal excretory capacity for calcium, in normal kidneys, is exceeded and hypercalcemia develops. A normal person on such a low calcium diet excretes approximately 50 mg. of calcium per day in his urine. According to Pearson, destruction of 1 gm. of bone per day, which releases about 100 mg. of calcium, probably represents the minimum rate of osteolysis that can be measured by studies of urinary calcium excretion in patients with destructive bone tumors. Causes of hypercalcemia and hypercalciuria, other than bone tumors, such as hyperparathyroidism, osteomalacia, and osteoporosis, are usually differentiated by the clinical picture, the laboratory data, and the skeletal radiographs. Numerous investigators have shown that in every case of prostatic carcinoma with metastasis to bone, microscopically the lesions show evidence of both bone destruction and bone repair. 3 According to Hellner, 4 and Axhausen, 5 every bone tumor, either primary or metastatic, begins with osteolysis. Von Recklinghausen6 in 1871 demonstrated that in metastasized prostatic tumors, bone formation