Hypercalcemia of malignancy: a review of advances in pathophysiology
Kaplan, M.
Oncology Nursing Forum 21(6) 1039-1046; Quiz: 1047-1048
1994
ISSN/ISBN: 0190-535X PMID: 7971410 Document Number: 429960
To review normal calcium homeostasis, recent advances in understanding the pathologic mechanisms responsible for precipitating hypercalcemia of malignancy, the role of the kidneys in potentiating hypercalcemia, and the principles of antihypercalcemic treatment. Journal articles, edited reference works, and selected texts. A complex set of changes in calcium processing in the intestine, kidney, and bone, mediated by humoral factors released from or induced by malignant cells, is responsible for development of humoral hypercalcemia of malignancy (HHM). A minor cause of cancer-induced hypercalcemia is bone destruction resulting from direct tumor invasion. Synergistic interactions between humoral factors stimulated by the presence of malignant cells enhance bone resorption of calcium and impair renal excretion of calcium ions resulting in HHM. Essential facets of antihypercalcemic treatment include controlling the precipitating malignancy, reversing dehydration, and inhibiting bone resorption. The signs and symptoms of increasing serum calcium are difficult to distinguish from disease-related or cytotoxic treatment-related side effects. Oncology nurses must have an understanding of which malignancies pose increased risk and how pathophysiologic mechanisms precipitate or contribute to hypercalcemia of malignancy. Knowledge of the rationales for the various treatment modalities will assist nurses in implementing antihypercalcemic treatments, evaluating treatment effectiveness and side effects, instituting pain management programs, and providing comfort measures and emotional support.