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Breast Cancer-Associated Hypercalcaemia: A Reassessment of Renal Calcium and Phosphate Handling

1990; SAGE Publishing; Volume: 27; Issue: 6 Linguagem: Inglês

10.1177/000456329002700605

1758-1001

Stephen Gallacher, William D. Fraser, Uday Patel, F.C. Logue, M. Soukop, Iain T. Boyle, Stuart H. Ralston,

Parathyroid Disorders and Treatments

The mechanisms of hypercalcaemia were assessed in 20 hypercalcaemic patients with breast cancer. Abnormalities suggestive of a PTH-related peptide (PTHrP) mechanism were observed in up to 60% of cases; urinary cyclic adenosine monophosphate (UcAMP) was elevated in nine patients (45%), renal tubular reabsorption of calcium (RTRCa) was elevated in nine (45%) and the renal tubular threshold for phosphate reabsorption (TmPO4) depressed in 12 (60%). While TmPO4 was lower in patients with high UcAMP, there was no consistent relationship between RTRCa and UcAMP or UcAMP and the extent of bone metastases. In a control group of nine normocalcaemic breast cancer patients, bone resorption as assessed by urinary calcium/creatinine ratio was slightly increased but UcAMP, RTRCa and TmPO4 were generally normal. These observations indicate that a PTHrP-mediated mechanism of hypercalcaemia may be operative in up to 60% of patients with breast cancer, irrespective of the presence or extent of bone metastases.