The clinical spectrum of hypocalcaemia associated with bone metastases

Abstract

Malignancy-related hypocalcaemia has received less attention in the literature than the opposite perturbation, hypercalcaemia. Only, scarce and contradictory data exist about hypocalcaemia associated with bone metastases (BMH). We have reviewed the clinical records of 155 patients with bone metastases of solid tumours, 122 of which were followed during the whole course of the disease until death. The frequency of hypocalcaemia ranged from 5 to 13%, depending on the formula used to correct calcium values for protein concentration. BMH was almost exclusively limited to patients with osteoblastic metastases. The frequency of BMH among patients with prostate carcinoma was 13-27%, depending on the formula used. Only two of 60 patients with lytic bone lesions presented hypocalcaemia, and in both cases it was rather mild. The development of hypocalcaemia did not seem to imply a worse prognosis, at least in patients with carcinoma of the prostate. Thus, the prevalence of BMH appears to be higher than is usually considered. Adequate attention should be given to this disorder because of the potentially deleterious effects on several organ systems.

Alternation of Hypo- and Hypercalcemia in a Parathyroidectomized Patient with Breast Cancer

“…However, we cannot exclude the possibility of osteogenic metastases on the basis of X-ray findings of mixed densifying bone lesions. In fact, the association of severe forms of hypocal cemia with neoplasia with extensive osteoblastic metas tases is well documented in patients with normal [6] and reduced [7] parathyroid function. The tumors frequently associated with this phenomenon are prostate, lung and breast cancer [4], In patients with osteoblastic metastases and hypocalcemia, an increased uptake of radioactive cal cium has been demonstrated [4],…”

“…For hypocalcemia in neoplastic disease, the following mechanisms have been proposed: ( 1 ) secondary effects of chemotherapy and antibacterial agents; (2) tumoral lysis with consequent hyperphosphatemia and precipitation of calcium and phosphorus [4]; (3) production of calcitonin-like sub stances [5]; (4) removal of serum calcium for bone repair during remission of neoplasia ('hungry bone'), and (5) cal cium capture in osteoblastic metastasis [6]. The feedback mechanism with regulation of PTH and CT release by serum concentrations of calcium was not possible in our patient because of total thyroidectomy with accidental parathyroidectomy.…”

Hypocalcaemia in patients with prostate cancer treated with a bisphosphonate or denosumab: prevention supports treatment completion

“…It is rare for patients with cancer to develop hypocalcaemia as a direct result of the primary tumour [ 23 ]. However, low calcium concentrations are quite frequently observed in individuals with osteoblastic bone metastases, in whom rapid mineralization of newly formed bone sequesters calcium from the bloodstream [ 24 , 25 ]. In retrospective analyses, conducted before the introduction of bisphosphonate or denosumab treatment, hypocalcaemia was reported in 5–13% of patients with bone metastases, depending on the formula used to correct for albumin levels.…”

“…In retrospective analyses, conducted before the introduction of bisphosphonate or denosumab treatment, hypocalcaemia was reported in 5–13% of patients with bone metastases, depending on the formula used to correct for albumin levels. Among these patients, 35% had hypocalcaemia of grade 1, 60% grade 2, and 5% grade 3 or higher [ 25 ]. Prevalence was highest among individuals with prostate cancer and bone metastases; 13–27% of these patients developed hypocalcaemia [ 25 ].…”

The potential role of bisphosphonates in prostate cancer

“…Hypocalcaemia is believed to be caused by calcium entrapment in bone as a consequence of excessive osteoblast activity in sclerotic metastasis. There have been a number of reports of low serum calcium levels 77,78 and high PTH levels in patients with advanced prostate cancer. 79 Secondary hyperparathyroidism may occur frequently and may contribute to the generalised osteoclastic activity in patients with osteoblastic metastasis.…”