Serum and urinary profile of bone turn-over markers in a patient with tamoxifen-induced hypercalcaemia submitted to pamidronate therapy

Serum parathyroid hormone (PTH), plasma parathyroid hormone related protein (PTHrP) and markers of bone turn-over in serum and urine were monitored monthly, from the start of pamidronate administration, in a breast cancer patient who developed tamoxifen-induced hypercalcaemia (TamIH). At the onset of the hypercalcaemic episode the PTHrP level was three times normal and showed a subsequent decrease until values were below the dection limit by 2 months. A transient rise in bone formation markers appeared during the first month, predicting the subsequent radiological response of bone metastases. Serum and urinary calcium levels significantly decreased but, unexpectedly, an increase in bone collagen resorption indices was observed. Also, serum PTH levels rose considerably, persisting at supranormal levels even after 3 months. This case report indicates that PTHrP could be involved in TamIH. The pamidronate mediated hypocalcaemia is responsible for the PTH rise during the first month, but the elevated PTH level at 3 months was probably due to increased calcium demand as a consequence of calcification occuring in bone. Pamidronate administration is not recommended in the treatment of TamIH; it is short lived and easily controlled by supportive measures