TY - JOUR
T1 - Hypercalcemia in breast cancer. Reassessment of the mechanism
AU - Isales, Carlos
AU - Carcangiu, Maria L.
AU - Stewart, Andrew F.
N1 - Funding Information:
From the Division of Endocrinology and Metabolism, West Haven Veterans Administration Medical Center, West Haven, Connecticut, and the Departments of Endocrinology and Pathology, Yale University School of Medicine, New Haven, Connecticut. This work was supported by the Veterans Administration, West Haven, Connecticut, Grants AM-30102 and RR-125 from the National institutes of Health, and the General Clinical Research Center of the Yale-New Haven Hospital. Requests for reprints should be addressed to Dr. Andrew F. Stewart, Endocrinology and Metabolism, Research1 15 1, West Haven Veterans Administration Medical Center, West Spring Street, West Haven, Connecticut 065 16. Manuscript submitted September 26, 1986, and accepted December 16, 1986.
PY - 1987/6
Y1 - 1987/6
N2 - 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.
AB - 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.
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U2 - 10.1016/0002-9343(87)90216-6
DO - 10.1016/0002-9343(87)90216-6
M3 - Article
C2 - 3037897
AN - SCOPUS:0023615106
SN - 0002-9343
VL - 82
SP - 1143
EP - 1147
JO - The American Journal of Medicine
JF - The American Journal of Medicine
IS - 6
ER -