Abstract. Approximately two-thirds ofpatients who receive the anticancer drug gallium nitrate develop mild hypocalcemia. To evaluate the mechanism of druginduced hypocalcemia, we tested the effects of gallium nitrate upon in vitro release of "5Ca"+ from explanted fetal rat bones. The drug significantly inhibited 45Ca`+ release in response to stimulation with both parathyroid hormone and a lymphokine preparation with osteoclast activating factor activity. The inhibitory effects on bone resorption were both time-and dose-dependent. Later, in a pilot study, we treated 10 patients who had cancerrelated hypercalcemia with gallium nitrate administered by continuous infusion. All patients responded by a reduction of total serum calcium to normal or subnormal concentrations (13.8±1.05 mg/dl, mean±SD pretreatment, to 8.03±1.03 mg/dl, mean posttreatment nadir). Our results indicate that gallium nitrate effectively treats cancer-related hypercalcemia and that it probably acts by inhibiting calcium release from bone.

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