[Hypercalcemia of cancer and myeloma]

Hypercalcemia secondary to malignancies can be divided into two groups according to their calcium elevating mechanism: solid tumors with bony metastases, most frequently originating from the breast or the bronchi, and solid tumors without bony metastases, associated with secretion by the tumor of a substance which increases the calcium level. This substance resembles parathormone in pseudo-hyperparathyroidism, prostaglandins, or other substances not yet identified. The most common tumors involved are bronchial or renal cancers. Diagnostic problems vary depending on whether the cancer has been identified or not, and if bony metastases have or have not been discovered. Primary hyperparathyroidism must also be considered since it is frequently associated with cancer. Hypercalcemia from blood dyscrasias (myeloma and lymphoma) originates from the same mechanisms. It may or may not be associated with bony lesions. The hypercalcemia could be due to a "parathormone like" substance, to prostaglandins, to a substance that stimulates osteoclasts (OAF), or to calcitriol (1,25-dihydroxycholecalciferol). The treatment of hypercalcemia due to malignancies is primarily through the use of antiosteoclastic agents: calcitonin, mithramycin, and more recently diphosphonates. Corticosteroids and the prostaglandin inhibitors can have an additional calcium lowering effect.