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*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*1,25-DIHYDROXYCHOLECALCIFEROL
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
*PARATHYROID HORMONE
Medline Plus Health Information
*Bone Cancer
*Breast Cancer
The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 118-122
Copyright © 1997 by The Endocrine Society

Endocrinological Oncology

Serum 1,25-Dihydroxyvitamin D May Be Related Inversely to Disease Activity in Breast Cancer Patients with Bone Metastases1

E. Barbara Mawer, Janet Walls, Anthony Howell, Michael Davies, Wendy A. Ratcliffe and Nigel J. Bundred

University of Manchester Bone Disease Research Centre, Department of Medicine, Manchester Royal Infirmary (E.B.M., M.D.), Departments of Surgery and Medical Oncology (J.W., A.H., N.J.B.), University Hospital of South Manchester, Manchester, United Kingdom; and Wolfson Research Laboratories, Queen Elizabeth Medical Centre (W.A.R.), Birmingham, United Kingdom

Address all correspondence and requests for reprints to: Nigel J. Bundred, Department of Surgery, University Hospital of South Manchester, Nell Lane, Manchester, M20 8LR, United Kingdom.

1,25-dihydroxyvitamin D (1,25-(OH)2D) stimulates differentiation and controls proliferation in breast cancer cells. The role of endogenous 1,25-(OH)2D and its relation to PTH related protein (PTHrP) during the progression of breast cancer is not known; we therefore investigated these hormones in two studies. In a cross-sectional study of patients with breast cancer at different stages of disease, serum 1,25-(OH)2D levels (mean ± SE) were highest in early disease (102 ± 3.7 pmol/L), fell in normocalemic patients with bone metastases (52 ± 5.3 pmol/L; P < 0.01), and were lowest in hypercalcemic patients (33 ± 5.6 pmol/L; P < 0.001). PTHrP was detectable in the serum of only one normocalcemic patient with progressive metastases but was present in 11 of the 12 hypercalcemic patients, thus PTHrP did not stimulate 1,25-(OH)2D synthesis.

In a 6-month longitudinal study of normocalcemic patients with bone metastases undergoing hormonal therapy, serum 1,25-(OH)2D concentrations fell in patients whose disease progressed (P = 0.0056), but remained constant in those who were stable or responded to treatment. These changes in 1,25-(OH)2D preceded clinical signs of progression and predicted disease response. In the progressive group, five of whom died during the study, 1,25-(OH)2D decreased between the initial and final samples, PTH fell significantly from 24.8 to 13.5 ng/L (P = 0.025), serum calcium rose from 2.27 to 2.39 mmol/L (P = 0.017), and the urinary calcium/creatinine ratio rose from 0.37 to 0.68 (P = 0.046). PTH and 1,25-(OH)2D were significantly correlated in the final samples from this group, Spearman’s rank correlation = 0.80, P = 0.022. The results indicate that normocalcemia in these patients is maintained, at the expense of suppressing PTH and 1,25-(OH)2D, in the face of increased calcium released from lytic lesions in bone. Loss of the antiproliferative effects of 1,25-(OH)2D may then permit more rapid secondary growth of the tumor.




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