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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and forty-seven patients with hypercalcaemia and advanced breast cancer have been reviewed. One hundred and twenty-five (85%) had definite bone metastases but in 22 (15%) there was no radiographic evidence of skeletal involvement. Sixty-eight (46%) patients also had liver metastases. These were present in 15/22 (68%) without definite skeletal involvement and 53/125 (42%) with bone metastases (P = less than 0.05). In a series of 498 patients with first relapse in bone after primary treatment hypercalcaemia was more common after the development of liver metastases than in patients with disease remaining confined to the skeleton (31% v 15%; P = less than 0.001). A subsequent prospective biochemical study of 35 patients with hypercalcaemia suggested that a humoral factor was more pronounced in 18 with liver metastases. In this group renal tubular reabsorption of calcium was higher, serum phosphate and tubular reabsorption of phosphate lower, and cyclic AMP excretion was increased. The data suggest that there is an association between the presence of liver metastases and the development of hypercalcaemia in patients with breast cancer. The mechanisms by which liver involvement may contribute to the pathogenesis of hypercalcaemia are not known but could arise from either increased production or decreased clearance of a humoral factor.
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PMID:Hypercalcaemia and breast cancer--an increased humoral component in patients with liver metastases. 284 66

Hypercalcemia as a complication of carcinoma of the colon is uncommon (1). It usually occurs in the presence of anorectal or rectal carcinoma that metastasizes to the lumbosacral vertebrae (2-4). Hypercalcemia complicating colon carcinoma in the absence of bone metastases--so-called humoral hypercalcemia of malignancy or paraneoplastic hypercalcemia--is rare. Only two such cases associated with adenocarcinoma of the colon (5,6) and two cases associated with adenosquamous carcinoma of the distal colon (rectum and sigmoid) (7) have been reported. We describe the first reported case of an adenosquamous carcinoma of the cecum and ascending colon that was accompanied by severe humoral hypercalcemia. The hypercalcemia was associated with a parathyroid hormone (PTH)-like substance.
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PMID:Humoral hypercalcemia complicating adenosquamous carcinoma of the proximal colon. 291 Jun 74

Humoral hypercalcemic syndrome associated with tumors of the female reproductive system is believed to be uncommon, and only 27 such cases have been identified prior to 1980. We describe 2 patients with humoral hypercalcemia in clear cell adenocarcinoma of the uterus, and review the literature on previously published cases. Both our patients fulfilled the criteria for humoral hypercalcemic syndrome, namely: hypercalcemia without bone metastases ranging from 12.8 to 14.1 mg/dl in the presence of normal serum parathyroid hormone levels, reduced tubular reabsorption of phosphate, and reduced serum albumin. We propose that humoral hypercalcemia is perhaps not a rare complication of uterine malignancy and, that increased awareness may result in early diagnosis of this important metabolic problem.
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PMID:Paraneoplastic hypercalcemia in endometrial carcinoma. 291 93

Bone metastases are frequently one of the first signs of disseminated disease in cancer patients. In the majority of patients, the primary tumour originates from the breast, prostate or lungs. Even although the prognosis is serious, a proportion of the patients will survive for several years and will thus require active treatment. More than 25% of the patients have no symptoms whereas pain dominates in the remainder. Frequent complications are pathological fractures, hypercalcaemia and spinal cord compression. Normally, the diagnosis can be established from the clinical picture compared with a series of laboratory analyses, x-ray investigations of the skeleton and bone scintigraphy. As treatment is mainly palliative, the purpose is primarily relief of pain, prevention of fractures and ensuring a reasonable functional level. The therapeutic possibilities comprise local treatment in the form of surgery and irradiation and also systemic treatment in the form of chemotherapy, endocrine therapy and possibly diphosphonates. of these, irradiation still plays the most important role. About 80% of the patients respond to treatment and, after 12 months, 50-70% of the surviving patients will still be free from pain. Only few randomized investigations are found in the literature available and the criteria of response are, in general, difficult to interpret. There is, therefore, a great requirement for more clinically controlled investigations which assess the efficacy of the numerous therapeutic possibilities.
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PMID:[Bone metastasis]. 291 54

In this review different aspects of osteolytic bone metastasis of breast carcinoma including morbidity, pathogenesis, accompanying hypercalcaemia and treatment, are discussed. Bone metastases occur in many patients with breast cancer (percentages of up to 85% have been reported); although patients seldom die of bone metastases morbidity is pronounced. Literature data point out that humoral factors, such as prostaglandins and the recently described growth factors are of importance beside cell interactions between monocytes, lymphocytes, osteoclasts and tumour cells. Nowadays, no significance is attributed to parathyroid hormone (PTH) overproduction in this respect. The differential diagnosis between primary hyperparathyroidism and tumour-induced hypercalcaemia is not always easy biochemically; combinations of both do occur less frequently than has been assumed in the past. A new and promising line of investigations involves the growth factors, which can increase osteolytic bone resorption and may bind to epidermal growth factor (EGF) or PTH receptors, thus inducing some of the biological effects of PTH (including hypercalcaemia). Until recently it was exceedingly difficult to treat tumour-induced hypercalcaemia (TIH) (the acute condition). Since the availability of the bisphosphonates dichloromethylidene bisphosphonate (Cl2MDP) and 3-amino-1-hydroxypropylidene-1, l-bisphosphonate (APD) this treatment has become very simple. Preliminary results, derived from the literature, point out that bisphosphonate treatment might also be effective in providing long-term control.
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PMID:Osteolytic bone metastases in breast carcinoma pathogenesis, morbidity and bisphosphonate treatment. 294 9

The distribution of 14C-labeled clodronate (dichloromethylene bisphosphonate), a new bisphosphonate for the treatment of osteolytic bone metastases and hypercalcemia, was studied in mice by whole-body autoradiography and by measuring the 14C activities in various tissues [14C]Clodronate was administered into the tail vein, and its distribution was followed from 5 min to 90 days after the injection. The drug disappeared promptly from the plasma and accumulated intensively in the bone and moderately in the spleen. In both tissues, relatively high radioactivities were measured as late as 90 days after the [14C]clodronate administration. Small amounts of 14C activity were also detected in the liver for 90 days. The results agree well with the previous observations that bisphosphonates deposit rapidly in the bone. Our findings indicate further that clodronate accumulates in the bone and the spleen for several months.
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PMID:Distribution of [14C]clodronate (dichloromethylene bisphosphonate) disodium in mice. 295 50

Normocalcaemic breast cancer patients with progressive osteolytic bone metastases were treated with clodronate 1.6 g/day (17) or placebo (17) for 12 months. Bone pain, extension of bone metastases and formation of new osteolytic foci were reduced by clodronate, and development of severe hypercalcaemia was prevented. After withdrawal of treatment the patients were followed-up for at at least 12 months. New bone metastases developed in both groups. There were, however, less fractures and less hypercalcaemia in the clodronate than in the placebo group. The survival rate was higher in the clodronate group than in the placebo group. No haematological toxicity was observed in the clodronate group.
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PMID:Treatment of skeletal disease in breast cancer: a controlled clodronate trial. 296 55

Breast-cancer patients with multiple osteolytic bone metastases were treated with clodronate (Cl2MDP) 1.6 g/day (17 patients) or placebo (17 patients) for 12 months. Bone pain, extension of bone metastases and formation of new osteolytic foci were reduced by Cl2MDP, and development of severe hypercalcaemia was prevented. After withdrawal of treatment, the patients were followed up for at least 12 months. New bone metastases developed in both groups. There were, however, less fractures and less hypercalcaemia in the Cl2MDP than in the placebo group. The survival rate was higher in the Cl2MDP group than in the placebo group. No side-effects were observed in the Cl2MDP group.
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PMID:Clodronate for osteolytic metastases due to breast cancer. 297 3

The pathophysiological mechanisms of hypercalcaemia were assessed in 50 rehydrated patients with cancer-associated hypercalcaemia. Surprisingly, renal tubular calcium reabsorption appeared to increase progressively as serum calcium rose, suggesting that the nomogram used for the calculation may have been inaccurate, in absolute terms, probably due to its failure to take account of the levels of urinary sodium excretion. There were significant differences in the mechanisms of hypercalcaemia in different patient subgroups, however, independent of differences in urinary sodium excretion. In those with few or no bone metastases, increased renal tubular calcium reabsorption was the principal cause of hypercalcaemia, often in association with increased bone resorption. These abnormalities were thought to reflect the renal and skeletal actions of a tumour-associated humoral mediator. The main cause of hypercalcaemia in those with extensive metastatic bone disease was increased bone resorption, with contributions from impairment of glomerular filtration rate and, to a minor extent, increased renal tubular calcium reabsorption. These abnormalities were thought to reflect a mainly local-osteolytic mechanism of hypercalcaemia with secondary impairment of GFR. Of all the biochemical variables assessed pre-treatment, the renal tubular component of hypercalcaemia correlated most strongly with post-treatment serum calcium values (r = 0.61, P less than 0.001). Because of their generally lower levels of renal tubular calcium reabsorption, patients with extensive skeletal metastases also had significantly lower post treatment calcium values than patients with few or no metastases (P less than 0.05). These data indicate that the pathophysiological mechanisms of hypercalcaemia are a major determinant of the calcium lowering response after antihypercalcaemic treatment. This should be taken into account during comparative studies of antihypercalcaemic therapy in patients with malignancy.
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PMID:Malignancy-associated hypercalcaemia: relationship between mechanisms of hypercalcaemia and response to antihypercalcaemic therapy. 297 9

Forty patients with hypercalcaemia (2.75 to 3.5 mmoles/l) due to bone metastases or to a neoplastic syndrome were treated with synthetic human calcitonin after previous hyperhydration. On entering the study, the patients were allocated at random to either an 0.5 mg dose or a 1 mg dose of the compound administered 6-hourly by the intravenous route. Calcemia was measured every 6 hours: if it became normal, treatment was discontinued 12 hours later, but if after 3 injections the blood calcium level had not been reduced by more than 0.4 mmoles/l, incremental doses of calcitonin were given. Synthetic human calcitonin reduced calcemia by more than 0.4 mmoles/l in 22 patients (group 1) and brought it down to normal value in 18 of these 8 hours on average after the first injection. A new rise in calcemia was observed in 12/18 cases 44 hours on average after treatment was discontinued. Reduction of calcemia by less than 0.4 mmoles/l was observed in 11 patients (group 2). Treatment was ineffective in 7 patients (group 3). There were no significant differences between the 3 groups in mean values and variances of the initial blood calcium levels. Whatever the initial dose of calcitonin, the therapeutic effect was obtained within the first 24 hours of treatment. In patients with incomplete results increasing the dosage did not result in a further reduction of calcemia. No hypocalcaemia was observed. This study confirms that synthetic human calcitonin has a normalizing effect on calcemia. This effect is not dose-dependent, and blood calcium levels rise again after treatment is discontinued.
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PMID:[Human calcitonin in neoplastic hypercalcemia. Results of a prospective randomized trial]. 297 78


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