• ABSTRACT
    • Primary hyperparathyroidism is the most frequent cause of hypercalcemia in outpatients. In contrast, this electrolyte disorder is very often associated with cancer when detected in hospital, particularly in the frame of tumors of breast, lung or lympho-hematopoietic system. Hypercalcemia results from an imbalance between the fluxes of calcium entering and leaving the extracellular space. Theses fluxes, mainly those at the levels of bone and kidney, are the main regulators of calcium homeostasis. Depending on the etiology, increases in either bone resorption or renal tubular calcium reabsorption can predominate as the cause of elevated calcemia. Thus, an increment of renal tubular reabsorption of calcium plays a prominent role in hypercalcemia resulting from increased serum concentrations of parathyroid hormone, but can also be detected in 50% of malignant hypercalcemias. The ectopic production of authentic parathyroid hormone has convincingly been demonstrated in very few cases. The syndrome of pseudohyperparathyrodism encountered in malignant hypercalcemia can be accounted for by the tumoral secretion of an analog of parathyroid hormone, parathyroid hormone-related protein. Both proteins, which are produced by different genes located on different chromosomes, interact with the same cell membrane receptors and display identical spectrum of actions. Since they are immunologically quite distinct, there is no cross-reactivity in the various competitive or radiometric immunoassays actually available. The determination of circulating levels of parathyroid hormone is an essential step in the differential diagnosis of hypercalcemias, provided the assays offer adequate sensitivity and specificity. Nowadays, this appears to be generally the case.