[Tumoral hypercalcemia: physiopathology and treatment]

The regulation of plasma calcium involves many factors acting at the gut, bone and kidney levels. The mechanism leading to hypercalcemia in malignant neoplasm may well differ according to the type of tumor, the presence or otherwise of bone metastasis, the stage of the disease as well as additional factors such as the state of hydration. Increased bone resorption would certainly play an important role. However, increased tubular reabsorption of calcium could be the main hypercalcemic mechanism in some types of malignant tumor. Therapeutically, the approach has so far been to reduce the input of calcium from gut and bone and/or improve its renal clearance. Until now, the most efficient action appears to be the blockage of bone resorption. Among several bone resorption inhibitors, the diphosphonate compounds have been shown in several reports to be quite efficient in normalising calcemia.