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.

The addition of pyloromyotomy to pylorus-preserving pancreaticoduodenectomy is effective in preventing DGE. Results are supportive of the hypothesis that DGE may be caused by operative injuries of the vagus innervating the pyloric region.

Hemophagocytic lymphohistiocytosis (HLH) is an overwhelming inflammatory response, associated with an outpouring of cytokines and inappropriate activation of the macrophage system, causing severe morbidity and possible death. HLH has inherited and acquired forms. Secondary HLH can be related to any number of underlying conditions including infections, malignancy and autoimmune diseases. There are similarities between "cytokine storm" seen in HLH and the clinical findings of avian influenza. We report a patient with a history of sarcoidosis on chronic steroid treatment, who developed HLH secondary to an infection with Histoplasma capsulatum.