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Hypercalcemia in breast cancer. Reassessment of the mechanism

  • ,
  • Maria L. Carcangiu
    ,
  • Andrew F. Stewart(corresponding author)
*Corresponding author for this work
  • Unknown
Scholary Output:
Contribution to journal
Article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

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.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1143-1147 (5 pages)

Journal (Volume, Issue Number)

The American Journal of Medicine (Volume 82, Issue 6)

Publication milestones

  • Published - 06/1987

Publication status

Published - 06/1987

ISSN

0002-9343

Publication IDs

  • Scopus: 0023615106
  • PubMed: 3037897

Publication metrics

Metrics

Fractional count
1
Fractional count
0.33
Fractional count
2
Fractional count
0.67
Fractional count
1
Fractional count
1
Scopus
citations

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Citation count
60
Captures
4

Funding Details

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.
FundersFunding numbers
Vet. Administration Medical Center
RR-125, AM-30102
Yale New Haven Hospital
-
NIH
-