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

In a review of a hundred and nineteen patients with primary hyperparathyroidism an unexpectedly high number (17.5%) were found to have evidence of associated endocrine disease and were deemed to have multiple endocrine adenomatosis (M.E.A.). The clinical pattern of hypercalcaemia in no way distinguished these patients from other hyperparathyroid patients. M.E.A. was most commonly found in patients with several diseased parathyroid glands.
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PMID:Occurrence of other endocrine tumours in primary hyperparathyroidism. 7 51

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

A specific receptor for 1,25-dihydroxyvitamin D has been demonstrated in a cultured human breast cancer cell line. This is the first such demonstration in any cancer cell. It may explain the high incidence of metastatic bone destruction and hypercalcaemia in this common malignancy, and the limited success of other steroid-receptor assays in predicting the response of breast cancer to therapy.
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PMID:1,25-dihydroxyvitamin-D-receptor in breast cancer cells. 9 76

The urinary output of beta 2-microglobulin was measured in ten hypercalcemic patients undergoing surgery because of hyperparathyroidism. In three subjects the beta 2-microglobulin excretion was abnormally increased and in seven patients it was normal before surgery. Three of these seven patients displayed markedly impaired distal tubular function with a reduced urinary concentration capacity. After surgery all patients became normocalcemic and the urinary concentrating capacities improved. The beta 2-microglobulin excretion, on the other hand, remained unchanged. Thus, hypercalcemia per se does not readily affect the proximal tubular function of reabsorbing low molecular weight proteins. "Tubular proteinuria", if found in patients with hypercalcemia, should be suspected to reflect damage to the kidney by additional mechanisms.
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PMID:Hyperparathyroidism associated with distal tubular dysfunction but intact reabsorption of protein in the proximal tubules. 9 49

Acexamic acid is currently used to avoid pulmonary fibrosis in patients treated with bleomycim. It seems to be equally effective to prevent pulmonary fibrosis in adult respiratory distress syndrome. The complications of this therapy are hypercalcemia and hypernatremia.
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PMID:[So-called refractory hypoxemia: treatment with acexamic acid]. 9 46

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

The hypercalcemia observed during the acute calcitonin test reflects the size and the activity of the osteoclastic population throughout the entire skeleton. Several calcitonins of animal origin (pork, salmon) have already been used for this test in human pathology, but the results can be flawed by the presence of anti-calcitonin antibodies. The authors demonstrate that human synthetic anti-calcitonin in man has a hypocalcemia effect identical to salmon synthetic calcitonin, with an equipotential dose for the rat. The systematic study of acute salmon calcitonin in various osteopathies makes it possible to note a certain number of paradoxical responses with prolonged hypercalcemia in the hours following injection. This is observed especially in the "hyperosteoidosis states" and the authors attempt to give it a physiopathological explanation. Finally, the acute salmon calcitonin test can be used as a mean of surveillance of the anti-osteoclastic activity of the disphosphonates in the treatment of Paget's disease.
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PMID:[The hypocalcemia test, using human and salmon synthetic calcitonins. Paradoxical hypercalcemic responses. Responses in patients with Paget's disease treated with EHDP]. 11 60


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