STIMULATION OF CALCIUM REABSORPTION OBSERVED IN ADVANCED BREAST-CANCER PATIENTS WITH HYPERCALCEMIA AND MULTIPLE BONE METASTASES

  • 1 January 1985
    • journal article
    • research article
    • Vol. 76  (4) , 308-314
Abstract
In an attempt to analyze the pathological processes which lead to hypercalcemia in patients with multiple bone metastases, 23 advanced breast cancer patients with multiple bone metastases, 3 hypercalcemic patients with other malignancies and 7 early breast cancer patients without any distant metastasis were studied. Of the 23 patients with advanced breast cancer, 9 showed serum calcium levels higher than 10 mg/dl. In 5 of the 9 hypercalcemic patients with advanced breast cancer, urinary cyclic AMP excretion was lower than 4 nmol/100 ml of glomerular filtrate (GF), indicating that the secretion of parathyroid hormone was suppressed. However, urinary cyclic AMP excretion was higher than 4 nmol/100 ml of GF in the other 4 hypercalcemic patients with advanced breast cancer and 3 hypercalcemic patients with other malignancies. In patients with higher urinary cyclic AMP excretion, fractional excretion of calcium (FECa) showed a negative correlation (r= 0.83, P < 0.05) with urinary cyclic AMP. Parathyroid hormone immunoreactivity was not detected in any of 6 patients showing serum calcium levels higher than 11 mg/dl. In about 1/2 of hypercalcemic patients with advanced breast cancer and multiple bone metastasis, there is apparently a factor which increases urinary cyclic AMP and enhances calcium reabsorption in the kidney, but which is different from parathyroid hormone. This factor may facilitate retention of calcium mobilized into the circulation by bone metastases and lead to hypercalcemia.