Potentiation of calcitonin by corticosteroids during the treatment of the hypercalcaemia of malignancy.
Some patients treated for the hypercalcaemia of malignancy develop renal tubular resistance to the effects of calcitonin which is independent of concurrent changes in sodium excretion. This type of resistance can be overcome by the addition of corticosteroids. In other patients apparent renal resistance to calcitonin is a consequence of reduced sodium excretion and is unaffected by corticosteroids.
Hosking
D J
DJ
City Hospital, Nottingham.
Stone
M D
MD
Foote
J W
JW
D000368:Aged; D002116:Calcitonin / Q000378:metabolism / Q000627:therapeutic use*; D002118:Calcium / Q000378:metabolism*; D003907:Dexamethasone / Q000627:therapeutic use*; D004357:Drug Synergism; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000150:complications*; D011239:Prednisolone / Q000627:therapeutic use*; D013997:Time Factors
D003907:Dexamethasone; C028815:salmon calcitonin; D002116:Calcitonin; D011239:Prednisolone; D002118:Calcium