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Malignant Hypercalcemia: The Choice of Therapy

Malignant Hypercalcemia: The Choice of Therapy Abstract Malignant hypercalcemia is the leading cause of hypercalcemia in hospital practice and is the most common life-threatening metabolic disorder associated with cancer.1,2 Left unattended, clinical deterioration is often rapid, resulting in profound volume depletion, azotemia, neuromuscular irritability, and progressive obtundation. When it is properly managed, however, responses may be gratifying, with symptomatic improvement achieved within days of initiation of treatment. The ideal treatment of patients with cancer-related hypercalcemia is cytoreductive therapy directed against the underlying malignancy. For the vast majority of patients, however, this is an unrealistic option, since most have advanced disease and have failed primary cytotoxic therapy. In the acute setting, measures to restore plasma volume and enhance calciuresis with vigorous intravenous hydration remain the cornerstone of therapy. Although this treatment is effective in the short term, fewer than 30% of patients can be expected to achieve normocalcemia with hydration alone,3,4 and most will require additional References 1. Fisken RA, Heath DA, Bold AM. Hypercalcemia: a hospital survey . Q J Med. 1980;49:405-418. 2. Mundy GR, Martin TJ. The hypercalcemia of malignancy: pathogenesis and management . Metabolism. 1982;131:1247-1277.Crossref 3. Suki WN, Yium JJ, Von Minden M, et al. Acute treatment of hypercalcemia with furosemide . N Engl J Med. 1970;283:836-840.Crossref 4. Hosking DJ, Cowley A, Bucknall CA. Rehydration in the treatment of severe hypercalcemia . Q J Med. 1981;200:473-481. 5. Mundy GR, Ibbotson KJ, D'Souza SM, Simpson EL, Jacobs JW, Martin TJ. The hypercalcemia of cancer: clinical implications and pathogenic mechanisms . N Engl J Med. 1984;310:1718-1727.Crossref 6. Broadus AE, Mangin M, Ikeda K, et al. Humoral hypercalcemia of cancer: identification of a novel parathyroid hormone— like peptide . N Engl J Med. 1988;319:556-563.Crossref 7. Carano A, Teitelbaum SL, Konsek JD, Schlesinger PH, Blair HC. Bisphosphonates directly inhibit the bone resorption activity of isolated avian osteoclasts in vitro . J Clin Invest. 1990;85:456-461.Crossref 8. Kanis JA, Urwin GH, Gray RES, et al. Effects of intravenous etidronate disodium on skeletal and calcium metabolism . Am J Med. 1987;82( (suppl 2A) ):55-70.Crossref 9. Jacobs TP, Gordon AC, Solverberg AJ, et al. Neoplastic hypercalcemia: physiologic response to intravenous etidronate disodium . Am J Med. 1987;82( (suppl 2A) ):42-50.Crossref 10. Schiller JH, Rasmussen P, Benson AB, et al. Maintenance etidronate in the prevention of malignancy-associated hypercalcemia . Arch Intern Med. 1987;147:963-966.Crossref 11. Ryzen ER, Martodam RR, Troxell M, et al. Intravenous etidronate in the management of malignant hypercalcemia . Arch Intern Med. 1985;145:449-452.Crossref 12. Singer FR, Ritch PS, Lad TE, et al. Treatment of hypercalcemia of malignancy with intravenous etidronate: a controlled, multicenter study . Arch Intern Med. 1991;151:471-476.Crossref 13. Ralston SH, Dryburgh FJ, Cowan RA, Gardner MD, Jenkins AS, Boyle IT. Comparison of aminohydroxypropylidene diphosphonate, mithramycin, and corticosteroids/calcitonin in treatment of cancer-associated hypercalcemia . Lancet. 1985;2:907-910.Crossref 14. Ringenberg QS, Ritch PS. Efficacy of oral administration of etidronate disodium in maintaining normal serum calcium levels in previously hypercalcemic cancer patients . Clin Ther. 1987;9:318-325. 15. Kimura S, Sato Y, Matsubara H, et al. A retrospective evaluation of the medical treatment of malignancy-associated hypercalcemia . Jpn J Cancer Res. 1986;77:85-91. 16. Ralston SH, Gallacher SJ, Patel U, Campbell J, Boyle IT. Cancer-associated hypercalcemia: morbidity and mortality: clinical experience in 126 treated patients . Ann Intern Med. 1990;112:499-504.Crossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Internal Medicine American Medical Association

Malignant Hypercalcemia: The Choice of Therapy

Archives of Internal Medicine , Volume 151 (3) – Mar 1, 1991

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Publisher
American Medical Association
Copyright
Copyright © 1991 American Medical Association. All Rights Reserved.
ISSN
0003-9926
eISSN
1538-3679
DOI
10.1001/archinte.1991.00400030007001
Publisher site
See Article on Publisher Site

Abstract

Abstract Malignant hypercalcemia is the leading cause of hypercalcemia in hospital practice and is the most common life-threatening metabolic disorder associated with cancer.1,2 Left unattended, clinical deterioration is often rapid, resulting in profound volume depletion, azotemia, neuromuscular irritability, and progressive obtundation. When it is properly managed, however, responses may be gratifying, with symptomatic improvement achieved within days of initiation of treatment. The ideal treatment of patients with cancer-related hypercalcemia is cytoreductive therapy directed against the underlying malignancy. For the vast majority of patients, however, this is an unrealistic option, since most have advanced disease and have failed primary cytotoxic therapy. In the acute setting, measures to restore plasma volume and enhance calciuresis with vigorous intravenous hydration remain the cornerstone of therapy. Although this treatment is effective in the short term, fewer than 30% of patients can be expected to achieve normocalcemia with hydration alone,3,4 and most will require additional References 1. Fisken RA, Heath DA, Bold AM. Hypercalcemia: a hospital survey . Q J Med. 1980;49:405-418. 2. Mundy GR, Martin TJ. The hypercalcemia of malignancy: pathogenesis and management . Metabolism. 1982;131:1247-1277.Crossref 3. Suki WN, Yium JJ, Von Minden M, et al. Acute treatment of hypercalcemia with furosemide . N Engl J Med. 1970;283:836-840.Crossref 4. Hosking DJ, Cowley A, Bucknall CA. Rehydration in the treatment of severe hypercalcemia . Q J Med. 1981;200:473-481. 5. Mundy GR, Ibbotson KJ, D'Souza SM, Simpson EL, Jacobs JW, Martin TJ. The hypercalcemia of cancer: clinical implications and pathogenic mechanisms . N Engl J Med. 1984;310:1718-1727.Crossref 6. Broadus AE, Mangin M, Ikeda K, et al. Humoral hypercalcemia of cancer: identification of a novel parathyroid hormone— like peptide . N Engl J Med. 1988;319:556-563.Crossref 7. Carano A, Teitelbaum SL, Konsek JD, Schlesinger PH, Blair HC. Bisphosphonates directly inhibit the bone resorption activity of isolated avian osteoclasts in vitro . J Clin Invest. 1990;85:456-461.Crossref 8. Kanis JA, Urwin GH, Gray RES, et al. Effects of intravenous etidronate disodium on skeletal and calcium metabolism . Am J Med. 1987;82( (suppl 2A) ):55-70.Crossref 9. Jacobs TP, Gordon AC, Solverberg AJ, et al. Neoplastic hypercalcemia: physiologic response to intravenous etidronate disodium . Am J Med. 1987;82( (suppl 2A) ):42-50.Crossref 10. Schiller JH, Rasmussen P, Benson AB, et al. Maintenance etidronate in the prevention of malignancy-associated hypercalcemia . Arch Intern Med. 1987;147:963-966.Crossref 11. Ryzen ER, Martodam RR, Troxell M, et al. Intravenous etidronate in the management of malignant hypercalcemia . Arch Intern Med. 1985;145:449-452.Crossref 12. Singer FR, Ritch PS, Lad TE, et al. Treatment of hypercalcemia of malignancy with intravenous etidronate: a controlled, multicenter study . Arch Intern Med. 1991;151:471-476.Crossref 13. Ralston SH, Dryburgh FJ, Cowan RA, Gardner MD, Jenkins AS, Boyle IT. Comparison of aminohydroxypropylidene diphosphonate, mithramycin, and corticosteroids/calcitonin in treatment of cancer-associated hypercalcemia . Lancet. 1985;2:907-910.Crossref 14. Ringenberg QS, Ritch PS. Efficacy of oral administration of etidronate disodium in maintaining normal serum calcium levels in previously hypercalcemic cancer patients . Clin Ther. 1987;9:318-325. 15. Kimura S, Sato Y, Matsubara H, et al. A retrospective evaluation of the medical treatment of malignancy-associated hypercalcemia . Jpn J Cancer Res. 1986;77:85-91. 16. Ralston SH, Gallacher SJ, Patel U, Campbell J, Boyle IT. Cancer-associated hypercalcemia: morbidity and mortality: clinical experience in 126 treated patients . Ann Intern Med. 1990;112:499-504.Crossref

Journal

Archives of Internal MedicineAmerican Medical Association

Published: Mar 1, 1991

References