Abstract
Hypercalcemia, osteolytic lesions, and bone pain occur frequently in patients with a wide variety of neoplastic diseases. Within the last few years it has become increasingly apparent that hypercalcemia in cancer may occur without direct bone metastasis but indirectly through humoral mediators that appear to stimulate osteoclastic bone resorption. The humoral mediator in some patients has been ectopic parathyroid hormone (PTH) or parathyroid-like substances produced by tumor tissues. Initial attempts to differentiate true ectopic PTH production from nonparathyroid substances have been hampered by the complexity of the measurement of immunoreactive PTH (iPTH) in the peripheral circulation. A review of the . . .