[Extraparathyroid hypercalcemias. Physiopathological and therapeutic aspects].
An increase in plasma calcium concentration is always the consequence of at least one of the following events: an increase in the net calcium input in extracellular fluid, a decrease in glomerular filtration rate, and an increase in the tubular reabsorption of the filtered calcium. In parathyroid hormone-related hypercalcemia, that is typically stable with time, the main determinant is the rise in parathyroid hormone-induced tubular calcium reabsorption. By contrast, in parathyroid hormone-independent hypercalcemia, usually steadily progressive (the main cause being hypercalcemia of cancer), the primary event is almost always a rapid increase in the net calcium input in extracellular fluid. The attendant hypercalcemia is commonly poorly tolerated and induces a renal sodium leak and a decrease in extracellular fluid volume. The latter leads to a fall in glomerular filtration rate and a rise in tubular calcium reabsorption which, in turn, worsen hypercalcemia. Treatment includes a reexpansion of extracellular fluid volume and the inhibition of bone calcium release.
Houillier
P
P
Service de Physiologie, Hôpital Broussais, Paris.
Blanchard
A
A
Paillard
M
M
D002118:Calcium / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D009369:Neoplasms / Q000150:complications
D002118:Calcium