Medical treatment of hypercalcemia

Calcium homeostasis and the symptoms, etiology, and general medical management of hypercalcemia are reviewed. Hypercalcemia, an elevation in total serum calcium concentration, may produce neurologic, gastrointestinal, renal, and cardiovascular disturbances; it may also cause calcification in extraskeletal tissue. Hyperparathyroidism and malignancy cause more than 90% of cases of this potentially fatal disorder. When correction of the underlying cause of hypercalcemia is impossible, calcium-lowering therapy is necessary. Acute management of hypercalcemia often involves rehydration, mobilization of the patient, and furosemide-induced diuresis. These measures may be followed by intravenous administration of etidronate, plicamycin, or calcitonin. Agents used in the long-term management of hypercalcemia include oral phosphates, oral etidronate, intermittent intravenous plicamycin, and, in selected patients, corticosteroids and nonsteroidal anti-inflammatory agents. Investigational calcium-lowering agents include gallium nitrate, ethiofos, dichloromethylene diphosphonate, and aminohydroxyproline diphosphonate. Many agents are available for the treatment of hypercalcemia. Therapy can be individualized by integrating knowledge of the physiologic causes of hypercalcemia, the mechanism of action of calcium-lowering drugs, and the patient's other disease states. Further studies are needed to define the role of investigational calcium-lowering agents.