HYPERCALCEMIA IN BREAST-CANCER

Hypercalcemia is relatively frequent in malignancy with or without ost eolytic bone metastases. It is thought that neoplastic cells may secre te substances which not only stimulate osteoclastic activity but are a lso capable of modifying the absorption, excretion, and resorption of calcium and phosphate ions. Since 1987, we have studied 24 breast canc er patients with hypercalcemia (22 with bone metastases and two withou t). The group of 22 patients with bone metastases were divided into tw o subgroups. The first consisted of 10 patients with high serum levels of humoral factors, such as parathyroid hormone-related protein (PTHr P), and/or prostaglandin E2 (PGE2) and/or interleukin 1 (IL-1), and hi gh levels of bone markers, such as alkaline phosphatase, bone Gla prot ein and urinary hydroxyproline. The second subgroup consisted of 12 pa tients with high levels of bone markers alone. Bone histologic analysi s showed an osteoclastic activation surrounding metastatic tumor tissu e in six out of 10 patients of the first subgroup, while an evident os teolysis caused by the tumor cells was noted in seven out of 12 patien ts of the second subgroup. The two patients without bone metastases sh owed normal biochemistry and bone histologic examination. The authors, having tried to explain the pathogenesis of hypercalcemia, emphasize the importance of humoral factors secreted by tumor cells as a direct or indirect cause of hypercalcemia. The origin of hypercalcemia remain s unclear in two patients without bone metastases.