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

A case of an elderly female patient, presented with a rare association of primary hyperparathyroidism and renal cell carcinoma, is reported. As a common finding in the elderly, the patient had mild hypercalcaemia for many years but she developed several complications from untreated hyperparathyroidism. The mechanisms of malignant hypercalcaemia are discussed and the importance of properly investigating and managing symptomatic primary hyperparathyroidism in the elderly is emphasised.
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PMID:Primary hyperparathyroidism and renal cell carcinoma in an elderly patient: a rare association. 145 2

This retrospective study was conducted to evaluate the incidence and prognostic significance of humoral hypercalcemia in 218 renal cell carcinoma patients during the last 20 years. Of 218 patients 20 (9.2%) were hypercalcemic, with serum calcium levels ranging from 10.7 to 16.0 mg./dl. The respective incidence of humoral hypercalcemia was 3% in patients with stage I, 5.9% with stage II, 14.1% with stage III and 18.9% with stage IV disease without bone metastasis. The survival curves between the hypercalcemic and eucalcemic groups among stages I to III cancer patients showed no statistical significance (p greater than 0.05). The survival curve deteriorated significantly in stage IV cancer patients with humoral hypercalcemia (p less than 0.005), with a median survival of 45.0 +/- 39.7 days versus 286.4 +/- 27.6 days in eucalcemic patients. No specific correlation was found between pathological cell type and humoral hypercalcemia.
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PMID:The incidence and prognostic significance of humoral hypercalcemia in renal cell carcinoma. 198 11

Hypercalcemia is one of the most serious metabolic disorders associated with cancer. The incidence and clinical circumstances associated with hypercalcemia vary in different types of cancer. Hypercalcemia is the most frequent metabolic complication of breast cancer and is usually related to widespread osteolytic metastases; however, local and systemic humoral factors mediating bone resorption have been described. In some patients with breast cancer, hypercalcemia results from treatment with estrogens, antiestrogens, androgens, or progestins. Coexisting primary hyperparathyroidism rarely confounds the diagnosis. In patients with lung cancer, the incidence of hypercalcemia varies with histology and is often unrelated to bone metastases. Hypercalcemia may occur either late or early in the disease but is seldom a presenting symptom. In patients with cancers of the head and neck region, hypercalcemia is most often associated with advanced recurrent and terminal disease, presumably humorally mediated. In renal cell carcinoma, hypercalcemia is also an adverse prognostic indicator, commonly mediated by humoral factors. On the other hand, almost all patients with multiple myeloma have extensive osteolytic bone destruction and hypercalcemia is frequently a presenting symptom. Hypercalcemia is uncommon in most lymphomas; however, it is usually a prominent feature of adult T-cell lymphomas and also occurs in some large cell, diffuse B-cell lymphomas. Awareness of the setting in which hypercalcemia of malignancy occurs will lead to its prompt diagnosis and institution of appropriate therapy.
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PMID:Overview of cancer-related hypercalcemia: epidemiology and etiology. 218 51

In recent years, diagnostic imaging techniques, especially ultrasonography (US) and CT scanning, have been widely adopted in clinical practice, making early accurate diagnosis of renal tumors possible. A total of 452 cases of renal tumors have been admitted to the institute since 1951, of which 220 were seen from 1951 to 1979 and 232 in the past 9 years (1980-1988). The frequency of renal parenchymal tumors was obviously higher in the latter group, including asymptomatic renal carcinoma in 20.2% and hamartoma in 38.1%. All these were discovered on routine physical check-up by ultrasonography and/or CT scanning and would otherwise have gone undiagnosed on conventional urography. Ultrasonography and CT can also reveal the nature and the extent of the tumor. The idea that "a renal tumor should be considered malignant unless pathologically proven otherwise" is no longer valid. However, general manifestations of renal carcinoma, such as elevated erythrocyte sedimentation rate (ESR), hypertension, malaise, anemia, fever and hypercalcemia, still deserve proper attention. We suggest that ultrasonography of both kidneys should be mandatory in routine physical check-up, as far as the urinary system is concerned, in order to discover asymptomatic renal tumors.
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PMID:Imaging techniques for the diagnosis of renal tumors. 224 36

Parathyroid hormone related peptide (PTHrP) has been implicated in the cause of the hypercalcemia associated with a number of malignant tumours. The data presented here suggests that PTHrP (in addition to its known role of mediating hypercalcemia) may be involved in the autocrine regulation of growth of some tumours. Polyclonal PTHrP antiserum almost totally inhibited the growth of a human renal cell carcinoma cell line, known to secrete PTHrP, in vitro and growth was significantly inhibited by the competitive PTH antagonist PTH (3-34)NH2.
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PMID:Parathyroid hormone related peptide can function as an autocrine growth factor in human renal cell carcinoma. 232 62

A retrospective study was conducted to evaluate the prognostic significance of hypercalcemia associated with renal cell carcinoma and the efficacy of different treatment modalities. Twenty-seven of 160 (16.8%) patients with renal cell carcinoma were found to have tumor-induced hypercalcemia: 24 had Stage IV disease, 1 Stage III disease, and 2 Stage I disease. There was no evidence of bone metastasis in 13 of 27 (48%) patients. A total of 89 episodes of acute hypercalcemia were treated: 36 episodes resulted in a complete response ([CR] calcium levels returning to normal), 24 partial response ([PR] calcium decrease greater than 1 mg/dL, but above normal) and 29 negligible response ([NR] calcium decrease less than 1 mg/dL) to treatment modalities used. One patient with Stage I disease and 3 with Stage IV disease underwent nephrectomies resulting in 2 CR and 1 PR. There was a complete response (CR) to mithramycin in 7 of 10 (70%) acute hypercalcemic episodes, to furosemide and mithramycin in 12 of 20 (60%), to steroids or furosemide and steroids in 3 of 7 (43%), to hydration in 4 of 13 (31%), and to furosemide in 7 of 25 (28%). The response rates to phosphates, indomethacin, and calcitonin were low but involved a small number of patients. Survival in 24 patients with Stage IV disease was 5-239 days (av 87.3 days). There was essentially no survival difference between patients who had an initial calcium elevation less than or greater than 13 mg/dL. We conclude that mithramycin is more effective in controlling acute hypercalcemia secondary to renal cell carcinoma than furosemide or hydration. Steroids appear to be effective but our experience was limited. Surprisingly, the degree of calcium elevation did not show a significant correlation with survival.
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PMID:Management and prognostic significance of hypercalcemia in renal cell carcinoma. 252 66

An in vivo model of humoral hypercalcaemia of malignancy has been used to examine the role of circulating PTH-like bioactivity in the development of bone resorption and hypercalcaemia. After inoculation of cells from a renal carcinoma cell line into nude mice, circulating PTH-like bioactivity as measured by the sensitive renal and metatarsal cytochemical bioassays for PTH was elevated in only 18% and 53% of the mice respectively. Bone resorption was elevated in all the mice investigated irrespective of the level of PTH-like bioactivity. Thus, in this model, while the circulating PTH-like moiety is more potent when acting on bone, it did not correlate with the degree of bone resorption suggesting that it may not be the sole cause of the hypercalcaemia.
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PMID:Bone resorption and circulating PTH-like bioactivity in an animal model of hypercalcaemia of malignancy. 274 81

Carbetimer (carbethimer, N-137, NED-137, carboxyimamidate) is a low molecular weight polyelectrolyte with antitumor activity in a variety of tumor models. This phase I trial evaluated a single dose of carbetimer infused over 1-2 h every 28 days. Forty-three patients received 71 courses of the drug at doses ranging from 180 to 8500 mg/m2. The dose-limiting toxicity was hypercalcemia (serum calcium greater than 12.5 mg/dl) noted in two of three patients at a dose of 8500 mg/m2. Serum calcium levels between 10.5 and 12.5 mg/dl were noted in an additional three patients treated at doses greater than or equal to 1600 mg/m2. Calcium balance studies in three patients treated at 6500 mg/m2 revealed an increase in urinary cyclic AMP and phosphate excretion after treatment accompanied by a mild elevation of serum parathyroid hormone. Immunological studies in these patients revealed a statistically significant increase in the percentage of peripheral T-helper cells. An increase in the T-helper/suppressor cell ratio was observed in two of the three patients studied. Interleukin 2 production by phytohemagglutinin-stimulated peripheral mononuclear cells was increased in two of three patients. One patient with a renal cell carcinoma showed a mixed response. The recommended dose for phase II trials as assessed from this study is 6500 mg/m2 as a single dose every 28 days.
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PMID:Phase I clinical trial of carbetimer. 284 47

Human renal carcinoma cell line 786-0 elaborates a protein that is structurally and immunochemically distinct from parathyroid hormone (PTH) and that activates renal cortical adenylate cyclase via an interaction with the PTH receptor. Because of the high frequency of excessive bone resorption and resultant hypercalcemia in patients with malignant disease we evaluated the ability of this 786-0 cell factor to reproduce PTH action in bone-derived cells. The 786-0 factor as well as bovine PTH (BPTH) (1-34) and prostaglandin E1 produced marked increases in cyclic adenosine 3':5'-monophosphate (cAMP) accumulation in the clonal rat osteosarcoma cell line UMR-106. A competitive antagonist of PTH action, [norleucine8, norleucine18, tyrosine34] BPTH(3-34)amide, blocked the cAMP stimulation produced by 786-0 factor and BPTH(1-34) but not that produced by prostaglandin E1. In the presence of forskolin (0.1 microM) UMR-106 cells were extremely sensitive to 786-0 factor, showing significant increases in cAMP production at a concentration 10-fold less than that required to activate adenylate cyclase in renal membranes. In contrast UMR-106 cells were less sensitive to BPTH(1-34) than were renal membranes. This preferential increase in sensitivity to 786-0 factor was not seen in membranes prepared from UMR-106 cells suggesting the importance of cytosolic components. Six additional human genitourinary carcinoma cell lines were found to produce factors that increased cAMP levels in UMR-106 cells. We conclude that 786-0 factor is a potent activator of the PTH receptor-adenylate cyclase system in these bone-derived cells. These findings are consistent with the view that cancer-associated hypercalcemia may frequently be attributable to tumor secretion of proteins (such as 786-0 factor) that are distinct from PTH but are capable of activating skeletal PTH receptors.
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PMID:Activation of the parathyroid hormone receptor-adenylate cyclase system in osteosarcoma cells by a human renal carcinoma factor. 299 59

When grown as sc tumors in the nude (nu/nu) mouse, cells of the established human renal carcinoma cell line 786-0 produce hypercalcemia; this has an apparent humoral basis because it is reversed by resection of the primary tumor. We have investigated the pathogenesis of hypercalcemia in this model. Tumor-bearing mice were hypercalcemic (13.4 +/- 0.9 vs. 9.52 +/- 0.13 mg/dl in control mice) and hypophosphatemic (10.0 +/- 0.8 vs. 13.8 +/- 1.5 mg/dl in control mice; all values are mean +/- SEM). The serum concentration of 1,25-dihydroxyvitamin D was increased in tumor-bearing animals (70.0 +/- 9.3 vs. 43.8 +/- 4.8 pg/ml in control animals). Urinary excretion of cAMP was similar in control (33.7 +/- 1.4 nmol/mg creatinine) and tumor-bearing mice (38.2 +/- 4.7 nmol/mg creatinine). However, in the latter, the acute response of urinary cAMP to PTH was blunted. Although intestinal calcium transport in everted duodenal sacs in vitro was increased in tumor-bearing mice, hypercalcemia was unaffected by feeding the animals for 8 days a diet containing less than 0.02% calcium. Hence, absorption of dietary calcium did not play a significant role in maintenance of hypercalcemia. In hypercalcemic animals, the calcium content of the humerus was decreased (2.95 +/- 0.08 vs. 3.29 +/- 0.13 mg in controls; P less than 0.05). Quantitative histomorphometric analysis of the distal femoral metaphysis disclosed a significant reduction in trabecular bone volume in tumor-bearing mice (12.0 +/- 1.1% vs. 16.1 +/- 1.1% in controls; P less than 0.02). A strong trend for increased osteoclast surface and number was observed, suggesting that bone resorption was increased. Osteoblast surface and number were also somewhat increased, as was the rate of mineral apposition (2.55 +/- 0.14 vs. 1.91 +/- 0.04 micron/day in controls; P less than 0.01). Thus, the decrease in trabecular bone volume was associated with high turnover of bone, with an apparent net increase in bone resorption. We conclude that hypercalcemia in the nude mouse bearing human renal carcinoma cells is associated with increased bone resorption, high bone turnover, hypophosphatemia, and increased serum levels of 1,25-dihydroxyvitamin D.
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PMID:Pathogenesis of hypercalcemia in nude mice bearing a human renal carcinoma. 301 91


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