Hypercalcemia in breast cancer. Reassessment of the mechanism.
Hypercalcemia in patients with breast cancer is usually attributed to osteolytic bone metastases. Seventeen patients with biopsy-proved breast cancer and hypercalcemia were identified in a prospective, unselected manner. Biochemical and clinical evaluation included measurements of parathyroid hormone, nephrogenous cAMP, vitamin D metabolites, fasting calcium excretion, and maximal tubular phosphate reabsorption, and bone radionuclide scanning. Tumor histologic findings were also reviewed. Four of the 17 patients (23.5 percent) had no evidence of bone involvement by bone scanning or radiography. Two additional patients (a total of 35 percent) appeared to have a humoral component to their hypercalcemia as determined by the presence of elevated nephrogenous cAMP excretion. These observations suggest that humoral, tumor-derived products may play a more important role in the hypercalcemia of breast cancer than has been previously recognized.
D000368:Aged; D001859:Bone Neoplasms / Q000378:metabolism / Q000556:secondary; D001943:Breast Neoplasms / Q000150:complications* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology*; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000378:metabolism; D011446:Prospective Studies; D014807:Vitamin D / Q000378:metabolism
D010281:Parathyroid Hormone; D014807:Vitamin D; D000242:Cyclic AMP; D002118:Calcium