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

Hypercalcemia occurs rarely at the time of diagnosis in patients found to have epidermoid carcinoma of the head and neck. It is particularly unlike in those patients who present with potentially curable lesions. Only 2 of our 307 patients who presented with potentially curable lesions were hypercalcemic at the time of diagnosis. Two hundred thirty-eight of these patients were followed up for two years or until death. Of the 139 who did not remain free of disease, hypercalcemia of clinical significance developed in ten (7.2 per cent). Pseudohyperparathyroidism was the suspected cause in seven of twelve patients. Debilitating symptoms were present in all patients with serum calcium levels greater thn 12.0 mg/100 ml. Treatment, when given, was effective in alleviating gastrointestinal and central nervous system problems. Although usually temporary, symptomatic improvement was appreciated by most patients and family members.
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PMID:Hypercalcemia in epidermoid carcinoma of the head and neck. 6 32

Four patients with thyrotoxicosis, hypercalcaemia and metabolic bone disease are described. One of them had a 'hot nodule', T3 toxicosis and a parathyroid tumour and another had thin bones, subperiosteal cortical bone erosions and complete dysphagia. Hypercalcaemia persisted during treatment with antithyroid drugs in two patients, both of whom had hyperparathyroidism. The administration of salmon calcitonin to these two patients before starting antithyroid treatment produced an immediate and sustained fall in serum calcium and urinary hydroxyproline levels. Calcitonin administration should be of value in the early management of hypercalcaemic patients.
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PMID:Thyrotoxicosis and hypercalcaemia: response to antithyroid drugs and salmon calcitonin. 6 11

Hypercalcaemia is often associated with malignant disease. Causes of elevated serum-calcium levels in the absence of bony metastases include parathyroid-hormone production by the tumour, osteolytic factors made by the tumour, and coexistent primary hyperparathyroidism. By measuring nephrogenous cyclic-A.M.P. excretion to assess parathyroid-hormone function, we have determined the mechanism of such hypercalcaemia in 15 patients. Nephrogenous cyclic A.M.P. ranges from 0.05 to 2.40 mumol/g of creatinine in normal subjects, from 2.27 to 8.45 mumol/g in patients with primary hyperparathyroidism, and from 0.50 to 1.30 mumol/g in patients with proven non-hyperparathyroid hypercalcaemia without malignancy. 9 patients (60%) with hypercalcaemia and malignancy had normal levels of nephrogenous cyclic A.M.P. (range 0.35-2.07 mumol/g creatinine). The other 6 (40%) had elevated nephrogenous cyclic A.M.P. (range 2.70-5.55 mumol/g) consistent with increased parathyroid-hormone secretion. Surgical exploration of the neck in these patients showed that the increased parathyroid-hormone secretion was secondary to primary hyperparathyroidism, not ectopic hyperparathyroidism. Thus, the data indicate that coexistent hyperparathyroidism may be common in patients with hypercalcaemia and malignancy and that the measurement of nephrogenous cyclic A.M.P. is very useful in identifying patients at risk for hyperparathyroidism.
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PMID:Primary hyperparathyroidism in paraneoplastic hypercalcaemia. 7 31

A controlled study of the effects of the potent vitamin-D metabolite, 1, 25-dihydroxycholecalciferol (1,25[OH]2D3), and vitamin D3 was done in 18 non-dialysed patients with chronic renal failure (C.R.F.). Patients with a creatinine clearance below 35 ml/min and mild renal osteodystrophy were selected. After 6 months' observation of the spontaneous course the patients were randomly allocated to 6 months' oral treatment with either 1, 25 (OH)2D3 or vitamin D3 in initial daily doses of 1microgram and 4000 I.U., respectively, combined with 0.5 g calcium. 1,25(OH)2D3 quickly corrected hypocalcaemia, reduced serum-alkaline-phosphatases and serum-immunoreactive-parathyroid-hormone, and more than doubled the urinary excretion rate of calcium. D3 had similar, but less pronounced effects. 7 out of 8 patients on 1,25(OH)2D3, developed hypercalcaemia which necessitated a reduction in dosage. None of the patients on D3 treatment developed hypercalcaemia. The percentage fall in creatinine clearance was greater during treatment than before treatment in all patients on 1, 25 (OH)2D3 (P less than 0.01) and in 7 of 9 patients on vitamin D3 treatment (though the group change here was not significant). Deterioration of renal function is a major limitation of the clinical use of 1, 25(OH)2D3 and D3 in non-dialysed patients with C.R.F. In fact, the decrased formation of 1, 25(OH)2D3 seen in C.R.F. might protect renal function at the expense of abnormalities in mineral metabolism.
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PMID:Deterioration of renal function during treatment of chronic renal failure with 1,25-dihydroxycholecalciferol. 8 Jun 33

A 36-year-old man with sarcoidosis had four episodes of hypercalcaemia in seven years, all of them during the summer months. Measurement over three years showed that hypercalcaemia was associated with small seasonal increases in serum-25-hydroxycholecalciferol within the normal range. These changes could be mimicked by the administration of 3000 units of vitamin D3 daily. Serum 1, 25-dihydroxycholecalciferol concentrations ranged between 26--62 pg/ml when serum calcium was normal, but were strikingly high, up to 137 pg/ml, when the patient was hypercalcaemic. These studies show for the first time that hypercalcaemia in sarcoidosis is associated with abnormally high circulating concentrations of 1, 25-dihydroxycholecalciferol, probably as a result of overproduction of this, the hormonal form of vitamin D.
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PMID:1, 25-dihydroxycholecalciferol in the pathogenesis of the hypercalcaemia of sarcoidosis. 8 69

14 patients with osteolytic bone disease due to breast cancer or myeloma, 7 of whom had hypercalcaemia, received oral treatment with (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.). Serum-calcium dropped to low normal values in all 14 patients, accompanied by a decrease in urine calcium and hydroxyproline excretion-rate. The results show that A.P.D. may inhibit tumour-induced osteolysis.
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PMID:Inhibition of osteolytic bone lesions by (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.). 8 43

The effects of the intravenous administration of atropine or magnesium on pancreatic secretion which has been stimulated by secretin and induced hypercalcaemia have been studied in man. In the presence of secretin (0.5 CU/kg.h) the infusion of Ca2+ (0.3 mmol/kg.105 min) resulted in an increase in secretion of enzymes by 100-200%, and in that of Ca2+ and Mg2+ by 50-100% without affecting fluid and bicarbonate secretion. The additional injection of atropine (0.5 mg i.v. and 0.5 mg s.c.) were followed by a prompt fall in enzymes but not in Ca2+ and Mg2+ to the secretin-stimulated values. The additional infusion of Mg2+ (0.12 mmol/kg.45 min) to the Ca2+-infusion did not alter the secretion of enzymes, Ca2+ or Mg2+ compared with the calcium infusion alone. It is suggested that the hypercalcaemic stimulus depends on an intact innervation of the acinar cells. In these experiments the secretion of Ca2+ and Mg2+ seem to originate mainly from extracellular fluxes.
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PMID:Interactions of calcium, magnesium and atropine on exocrine pancreatic secretion in man. 10 22

We describe a patient with immunoglobulin G (IgG)-kappa myeloma and severe, long-standing, asymptomatic hypercalcemia. Serum nonprotein-bound calcium concentration was 5.2 mg/dl (normal 4.2 to 5.0 mg/dl) at a time when total serum calcium concentration was 17.8 mg/dl. The patient's myeloma protein, IgGCAB, and Fab fragments of IgGCAB migrated more anodally when agarose gel electrophoresis was performed in the absence of calcium ion than when electrophoresis was performed in the presence of calcium ion; 60 other myeloma proteins did not demonstrate such behavior. Purified IgGCAB bound 1.5 calcium ions with a single dissociation constant of 1.2 X 10(-4) M. We speculate that the rare syndrome of myeloma and high protein-bound calcium is due to binding of calcium to variable regions of the myeloma antibody molecules.
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PMID:Calcium binding by a myeloma protein. 11 50

Rhesus monkey (Macaca mulatta) were subjected to hypercalcaemia by daily intramuscular injections of vitamin D2 (100,000 IU) and by providing them gram soaked in 1% CaCl2 solution for eating and 1% CaCl2 solution (prepared in tap water) for drinking. After 10, 15, 20 and 30 days of such treatment the serum calcium level recorded a rise (18.24 +/- 0.56, 26.20 +/- 1.30, 17.25 +/- 0.25 and 20.50 +/- 0.55 mg/dl respectively) as compared to those of control animals (12.80 +/- 1.00, 12.30 +/- 0.50, 12.70 +/- 0.20 and 12.30 +/- 0.30 mg/dl). Serial sections of thyroid parathyroid complex and isthmus were subjected to selective staining for lcalising the C cells. The structure and behaviour of these cells both under normal and experimental conditions has been studied. Hypercalcaemia resulted in the increase of these cells. Mitotic figures of the C cells were also encountered after 10 days of hypercalcaemia. The specimens subjected to 30 days treatment showed complete degranulation of these cells. Chronic hypercalcaemia inhibits the activity of parathyroid cells which display degenerative changes. The anterior and posterior poles, the peripheral regions of thyroid and isthmus are completely devoid of calcitonin cells.
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PMID:Thyroid calcitonin cells and parathyroid gland of the Indian rhesus monkey Macaca mulatta in response to experimental hypercalcaemia. 11 36

Twenty-nine patients with acute hypercalcemia secondary to carcinoma, myeloma and parathyroid adenoma have been treated with large doses of furosemide, mithramycin, or salmon calcitonin perfusion. With furosemide administration the treatment was successful in 6 of 10 patients. Furosemide was injected intravenously at the rate of 125 mg every 3 hours. With mithramycin perfusion only 2 of 8 patients have a return of the serum calcium levels to normal. With salmon thyrocalcitonin 3 of 10 patients obtained a good result. It can be interesting to suggest the association of furosemide and salmon calcitonin infusion to treat hypercalcemia of myeloma.
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PMID:Furosemide, mithramycin, and salmon calcitonin in hypercalcemia. 13 Feb 39


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