Hypercalcemia in Neoplastic Disease

Myers, William G.

doi:10.1001/archsurg.1960.01290190128024

Cited by 113 publications

(18 citation statements)

References 19 publications

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“…There have been several studies of calcium metabolism in malignant disease in which fecal calcium excretion has not been reported (27)(28)(29). Meyers (17) has stated that "decreases in serum and urinary calcium are not the result of increases in fecal calcium."…”

Section: Calcium't and Metabolic Balance Studies In Multiple Myelomamentioning

confidence: 99%

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Studies of Calcium Metabolism in Multiple Myeloma With Calcium47 and Metabolic-Balance Techniques

Lazor¹,

Rosenberg²,

Carbone³

1963

J. Clin. Invest.

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Despite the fact that approximately 90% of patients with multiple myeloma present themselves with skeletal complaints (1, 2), few studies of bone mineral metabolism in this disease have been reported. Stable calcium studies in multiple myeloma were first reported in the literature by Blatherwick (3) in 1916. Since that time there have been only infrequent reports using balance techniques, or isotopic-tracer methods, or both. Adams, Mason, and Bassett (4) used metabolicbalance techniques to investigate the influence of ACTH on mineral metabolism in three patients with multiple myeloma. Case studies of one or two patients using tracer methods and balance techniques have been reported by Anderson, Emery, McAllister, and Osborn (5), after a therapeutic dose of Ca45; by Spencer, Li, Samachson, and Laszlo (6), who have studied the comparative excretion and retention of Sr85 and Ca45; and recently, by Skoog, Adams, and MacDonald (7), who have reported balance and Sr85-tracer studies in a patient with multiple myeloma treated with various combination of hormones.The study of calcium metabolism in multiple myeloma is of great interest, since diffuse osteoporosis, or osteolytic lesions, or both, are most always present, and hypercalcemia is a frequent (8) cium turnover rates can be estimated. The present report describes studies of calcium metabolism using Ca47 and balance techniques in six patients with multiple myeloma. These studies indicate that the gut is an important source of calcium loss in multiple myeloma, and that the endogenous fecal calcium contributes significantly to the negative calcium balance uniformly found in our patients. MATERIALS AND METHODSPatients. Three men and three women with multiple myeloma were studied. Their ages ranged from 44 to 65 years. All patients were ambulatory during the entire study. The diagnosis of multiple myeloma was established by abnormalities in serum-protein pattern, bonemarrow examination, and skeletal X rays consistent with that disease. Serum calcium, phosphorus, and alkaline phosphatase were within normal limits in each patient (Table I). The term "untreated," as used in this patient population, refers to the absence of systemic treatment during the 3 months before study.Metabolic balance. All patients were studied in a metabolic-balance ward while they were maintained on fixed metabolic-balance diets, analyzed in triplicate. Four patients received approximately 200 mg Ca and 800 mg P daily, and two received approximately 500 mg Ca and 1,000 mg P daily. All patients were maintained on the specified diets for 8 to 10 days before the balance studies to allow for equilibration to the low-calcium diet and to the metabolic routine. Refused food and emeses were saved, analyzed, and substracted from the daily intake for that period. Fluid intake was kept constant by providing a fixed quantity of distilled water daily. Voided urine specimens were immediately pooled in a refrigerated jar containing 10 ml of concentrated HCl. Stools were separated at intervals of 4 days with ca...

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Section: Calcium't and Metabolic Balance Studies In Multiple Myelomamentioning

confidence: 99%

“…Meyers (17) has stated that "decreases in serum and urinary calcium are not the result of increases in fecal calcium." Our results with patient NS contradict this observation.…”

Section: Calcium't and Metabolic Balance Studies In Multiple Myelomamentioning

confidence: 99%

Studies of Calcium Metabolism in Multiple Myeloma With Calcium47 and Metabolic-Balance Techniques

Lazor¹,

Rosenberg²,

Carbone³

1963

J. Clin. Invest.

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“…Hypercalcemia occurs frequently in advanced malignancies and often severely compromises management ofthe underlying neoplasm (1)(2)(3). Accelerated net bone resorption is believed to be the source of the hypercalcemia in such patients (1,4,5), although understanding of the mechanisms whereby malignant cells alter the functions of normal bone cells remains incomplete.…”

Section: Introductionmentioning

confidence: 99%

Humoral hypercalcemia of malignancy. Release of a prostaglandin-stimulating bone-resorbing factor in vitro by human transitional-cell carcinoma cells.

Bringhurst¹,

Bierer²,

Godeau³

et al. 1986

J. Clin. Invest.

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Secretion by tumor cells of circulating bone-resorbing factors may frequently underlie the hypercalcemia that occurs in patients with malignancy. Efforts to identify the responsible mediators have been hampered by a lack of available human tumor cell systems suitable for study of the pathogenesis of the humoral hypercalcemia syndrome. We have established a transitionalcell carcinoma (TCC) line in vitro from a patient with humoral hypercalcemia. These cells are tumorigenic and cause hypercalcemia in athymic nude mice. Culture medium conditioned by TCC cells contains potent bone-resorbing activity in vitro, the physical and biological properties of which are similar to those of bone-resorbing activity present in the original patient's urine. The bone-resorbing activity of the TCC factor is accompanied by increased prostaglandin release from bone and is blocked by indomethacin and calcitonin. The TCC-derived bone-resorbing activity coelutes with prostaglandin-stimulating activity during gel filtration with an approximate molecular weight of 15,000. This activity is nondialyzable, stable to concentrated urea and reducing agents, and destroyed by boiling. The TCC factor does not increase cyclic AMP production in bone or kidney bioassays and does not exhibit transforming growth factor activity. We conclude that a unique macromolecular factor released by TCC cells causes bone resorption by a mechanism dependent upon stimulation of bone cell cyclooxygenase, and that this factor is the probable cause of the hypercalcemia in vivo. The TCC cell line provides a new model for study of the human humoral hypercalcemia syndrome.

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“…11 Hypercalcemia is caused by localized or generalized resorption of bone, due to synthesis of substance/substances having parathormone like activity, osteoclast activating factor, a group of cytokines, growth factors,1, 25-dihydroxy vitamin D -secreted by tumor cells which stimulate the production of cyclic adenosine monophosphate and causes increased resorption of bone, probably by reacting with receptors for parathormone. 12 Elevated Alkaline Phosphatase in cancer patients usually signifies metastasis to bones or livers. Malignancies of the prostate, colon, breast, lung, thyroid and other organs can metastasize to bone or liver.…”

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confidence: 99%

Correlation of Serum Lipid Profile, Serum Calcium, Alkaline Phosphatase and Serum Protein With Histopathological Grading and Staging in Head and Neck Cancer

Banseria¹,

Malik²,

Nigam³

et al. 2014

jemds

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Lipids have a key role in the maintenance of cell integrity. Hypolipidemia is related with increased risk of cancer and mortality. Elevated calcium and alkaline phosphatase has also been seen in cancer patients having metastasis. Alteration in serum proteins also has been reported. Hence present study was undertaken in 100 histopathologically confirmed head and neck cancer patients, in Department of Pathology Gandhi Medical College Bhopal, after taking informed written consent and ethical clearance. Lipid Profile, Serum Calcium, Alkaline Phosphatase, Serum Protein with Albumin were estimated and compared with age and sex matched healthy controls. Statistical analysis was done using chi square test. Total cholesterol (TC), high density lipoprotein-cholesterol (HDLC), low density lipoprotein-cholesterol (LDLC), Very low density lipoprotein-cholesterol (VLDLC) all decreased in head & neck cancer patients. Hypercalcemia was seen in 35% of patients. Raised Alkaline phosphatase (ALP) was seen in 8 % cancer patients. Serum calcium was found to be increasing with advancing stage. Further studies should be carried out in large number of patients to confirm the role of these parameters with special attention to modifiable ones and their relation with staging and grading of cancer, which can be used as prognostic markers.

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Hypercalcemia in Neoplastic Disease

Cited by 113 publications

References 19 publications

Studies of Calcium Metabolism in Multiple Myeloma With Calcium47 and Metabolic-Balance Techniques

Studies of Calcium Metabolism in Multiple Myeloma With Calcium47 and Metabolic-Balance Techniques

Humoral hypercalcemia of malignancy. Release of a prostaglandin-stimulating bone-resorbing factor in vitro by human transitional-cell carcinoma cells.

Correlation of Serum Lipid Profile, Serum Calcium, Alkaline Phosphatase and Serum Protein With Histopathological Grading and Staging in Head and Neck Cancer

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