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Ralston SH, Alzaid AA, Gardner MD, et al. Treatment of cancer associated hypercalcaemia with combined aminohydroxypropylidene diphosphonate and calcitonin. Br Med J (Clin Res Ed). 1986;292(6535):1549-50doi: 10.1136/bmj.292.6535.1549.
Ralston, S. H., Alzaid, A. A., Gardner, M. D., & Boyle, I. T. (1986). Treatment of cancer associated hypercalcaemia with combined aminohydroxypropylidene diphosphonate and calcitonin. British medical journal (Clinical research ed.), 292(6535), 1549-50. https://doi.org/10.1136/bmj.292.6535.1549
Ralston, S H, et al. "Treatment of cancer associated hypercalcaemia with combined aminohydroxypropylidene diphosphonate and calcitonin." British medical journal (Clinical research ed.) vol. 292,6535 (1986): 1549-50. doi: https://doi.org/10.1136/bmj.292.6535.1549
Ralston SH, Alzaid AA, Gardner MD, Boyle IT. Treatment of cancer associated hypercalcaemia with combined aminohydroxypropylidene diphosphonate and calcitonin. Br Med J (Clin Res Ed). 1986 Jun 14;292(6535):1549-50. doi: 10.1136/bmj.292.6535.1549. PMID: 3087513; PMCID: PMC1340556.
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Br Med J (Clin Res Ed). 1986 Jun 14;292(6535):1549-50. doi: 10.1136/bmj.292.6535.1549.

Treatment of cancer associated hypercalcaemia with combined aminohydroxypropylidene diphosphonate and calcitonin.

British medical journal (Clinical research ed.)

S H Ralston, A A Alzaid, M D Gardner, I T Boyle

PMID: 3087513 PMCID: PMC1340556 DOI: 10.1136/bmj.292.6535.1549
Free PMC Article

Abstract

Eight patients with cancer associated hypercalcaemia were treated with the combination of aminohydroxypropylidene diphosphonate and salmon calcitonin for six days. Serum calcium concentration fell significantly within 24 hours of starting treatment due to a reduction in bone resorption and renal tubular calcium reabsorption. In the longer term hypercalcaemia was controlled by a further progressive reduction in bone resorption, which persisted for six days after treatment was stopped. Renal tubular calcium reabsorption, however, remained suppressed only during drug treatment. The rapid fall in serum calcium was attributable to the acute renal and skeletal effects of calcitonin, whereas in the longer term control of hypercalcaemia was due to diphosphonate mediated suppression of bone resorption. In view of the rapid effect and lack of toxicity, combined treatment with aminohydroxypropylidene diphosphonate and calcitonin would be of particular value in patients with severe hypercalcaemia in whom a quick but sustained reduction in the serum calcium concentration is desired.

References

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