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

A review is given of the literature concerning the so-called plant induced calcinosis in animals (tabel I), i.e. diseases which in their patological-anatomical appearance show great similarities with vit. D-intoxication. The etiology of the diseases are discussed in view of the last 5--10 years rapid development of knowledge concerning vit. D3 metabolism. It is pointed out that the most recent results indicate that enzootic calcinosis is caused by a 1,25-dihydrocholecalciferol-glycoside, which is hydrolysed in the intestinal tract. By this reaction 1.25 (OH) 2 cholecalciferol--the biological active metabolite of vit. D3 -- is set free, and thus able to act directly on the intestinal absorption mechanism. By this reaction the point of calcium metabolism regulation is essentially by-passed and calcium and phosphate absorption proceeds essentially out of control, causing hypercalcaemia, hyperphosphataemia, hypersecretion of calcitonin and calcinosis.
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PMID:[Enzootic calcinosis and other plant induced calcinoses (author's transl)]. 19 May 89

Hypercalcemia may have various causes. I should nevertheless be rapidly treated. Among recent treatmens, we may quote diuresis with furosemide, calcitonin, mithramycin, which are the most effective. More recently indomethacin has been used and may be more specific for neoplastic hypercalcemia. These various treatments should be proposed depending on the level of serum calcium, the rapidity of onset and the presumed cause.
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PMID:[Treatment of hypercalcemia]. 19 28

3 cases of hypercalcemia are reported, among 14 tetraplegic patients with porphyria. The calciuria, the estimations of parathormone, calcitonin and the isotopic calcium balance studies, suggested in the two most serious cases, hypercalcemia due to immobilisation. The main factor seems to be the duration of the immobilisation. The predisposing role of renal failure and catecholamines is discussed.
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PMID:[Hypercalcemia during acute intermittent porphyria. Apropos of 3 cases]. 19 80

Hypercalcaemia always results in serious clinical sequalae and, if not treated, carries a most unfavourable prognosis. The clinician will gain major diagnostic help from an evaluation of the calcitonin and parathyroid hormone blood levels. With regard to parathyroid hormone we have developed, for the first time, a radioimmunoassay which is specific for the estimation of biologically active hormone in the circulation. We are dealing here with an unusual radioimmunological situation as the immunochemical sites are generally quite distinct from those associated with hormonal activity. We are presenting in this first paper the normal values and also the variations that occur in different types of hypercalcaemia. The comparison of these results with those obtained by the usual methods of estimation for parathyroid hormone assay lacking in biological activity shows the value of this new technique.
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PMID:[Hypercalcemia and biologically active parathyroid hormone]. 21 91

We have discussed in an earlier paper the value of estimating the circulating levels of biologically active parathyroid hormone. We consider here the importance of an evaluation of circulating calcitonin by showing the frequency of raised calcitonin secretion in hypercalcaemia of different origins. These results lead one to attribute to calcitonin a role which goes beyond the regulation of phospho-calcium metabolism and which in fact is that of a particularly sensitive indicator of tumours.
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PMID:[Calcitonin and hypercalcaemia (author's transl)]. 21 80

Renal handling of phosphorus was studied in the following groups of parathyroidectomized rats with maleate-induced Fanconi syndrome: 1) 6 rats receiving intravenous parathyroid hormone, 2) 6 rats receiving intravenous dibutyryl cyclic AMP (DBcAMP), 3) 6 rats undergoing volume expansion with saline, 4) 12 rats receiving intravenous 25 (OH)vitamin D3, 5) 12 rats with acute hypercalcemia induced by intravenous CaCl2, 6) 6 rats with phosphate deprivation, and 7) 6 rats receiving intravenous calcitonin. Parathyroid hormone and calcitonin failed to increase the urinary excretion of both cAMP and phosphorus. Likewise, DBcAMP failed to increase the urinary excretion of phosphorus. Extracellular volume expansion and hypercalcemia (serum calcium 12.9 +/- 0.7 mg/100 ml) did not alter the tubular reabsorption of phosphorus. In phosphate-deprived animals, the fractional excretion 0.16 +/- 0.05 (mean +/- SE) was lower than that in the control animals (maleate-treated without phosphate depletion), 0.46 +/- 0.04 (P less than 0.001). 25 (OH)vitamin D3 decreased the fractional excretion of phosphorus from 0.39 +/- 0.03 in the control (maleate-treated not receiving 25 (OH)vitamin D3) to 0.23 +/- 0.02 (P less than 0.001) in the experimental animals. The present study demonstrated an antiphosphaturic effect of 25(OH)vitamin D3 in experimental Fanconi syndrome; the mechanism of this action is not well understood.
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PMID:Antiphosphaturic action of 25 (OH) vitamin D3 in experimental Fanconi syndrome. 21 76

Parathyroid (PT) glands from 20-day-old embryonic chicks cultured in a chemically defined medium secreted a stimulator of in vitro bone resorption. This stimulator was presumed to be parathyroid hormone (PTH) because: 1) the in vitro dose response curve was parallel to that obtained with bovine PTH; 2) the activity was eluted on Sephadex G-1--chromatography at a postition similar to that for PTH; and 3) the material produced hypercalcemia in vivo in chicks. The amount of PTH-activity secreted was inversely proportional to the calcium concentration of the medium over the range of 0.75-2.25 mM. The chick PT glands also secreted an inhibitor of PTH-stimulated bone resorption in vitro. This inhibitor was presumed to be calcitonin (CT) because: 1) the in vitro dose-response curve was parallel to that obtained with synthetic salmon CT; 2) the activity was eluted on Sephadex G-50 chromatography at a position similar to that for salmon CT; and 3) the material produced hypocalcemia in vivo in rats. In contrast to what would be expected for CT secretion, the CT-activity was secreted by the PT glands in response to a low, not high calcium concentration. The data suggest that the secretion of avian PTH is similar to that of the mammalian hormone, and that the ultimobranchialectomized chick with an intact parathyroid gland may not be deficient in CT.
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PMID:The detection of transmissible gastroenteritis viral antigens by immunodiffusion. 23 83

1 Agents known to delay absorption from a subcutaneous site were tested in chicks for their ability to prolong the hypercalcaemic response to parathyroid hormone (PTH). 2 Polyvinylpyrrolidone was found to enhance the response but gelatine greatly reduced the 2 h hypercalcaemia. 3 The reduction by gelatine was reversed when the protease inhibitor aprotinin was added to the injection vehicle, and hypercalcaemia then persisted for more than 8 h. 4 Of other protease inhibitors studied, epsilon-aminocaproic acid was also found to enhance the hypercalcaemic response to subcutaneous PTH and its fragments but, unlike aprotinin, it was ineffective in the presence of gelatine. 5 By radioimmunoassay and bioassay respectively, it was confirmed that aprotinin raised circulating levels of PTH and also of another peptide hormone, calcitonin, injected subcutaneously. 6 Addition of calcium to the solutions injected subcutaneously abolished the hypercalcaemic response to PTH while injection of calcium and PTH simultaneously but at separate sites left the response unaltered. 7 The two protease inhibitors, epsilon-aminocaproic acid and aprotinin, each restored the response to subcutaneous PTH despite the presence of calcium at the injection site. 8 It was concluded that protease inhibitors injected subcutaneously with PTH and calcitonin in the chick reduced the rate of degradation of these hormones and that the proteases responsible for hormone degradation at the subcutaneous injection site may be released or activated by calcium ions.
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PMID:Evidence that protease inhibitors reduce the degradation of parathyroid hormone and calcitonin injected subcutaneously. 31 28

Long term hypercalcaemia was induced in F. pennanti by alternate day intramuscular injections of 50,000 IU of vitamin D2 and by giving them 1% CaCl2 solution prepared in tap water to drink. The controls were not injected with vitamin D2 and were given tap water. The serum calcium levels at various stages of the experiment (1-29 days) show increased values as compared with those of control animals. The calcitonin cells in the treated animals generally exhibit an increase in their number up to the 15th day. Mitotic figures are also encountered between the 7th and the 15th day of treatment. This exhibits the increase in the number of C cells. Constant calcium challenge results in increased quantities of secretory granules among these cells up to the 15th day and in degranulation from the 17th day onwards. It also causes degenerative changes in a certain number of C cells. The parathyroids exhibit atrophic changes (25 days onwards) due to chronic hypercalcaemia. For short term hypercalcaemia, animals were injected intravenously with 1 ml of 10% solution of calcium gluconate. The calcitonin cells do not exhibit any change during the first half hour but thereafter they exhibit progressive degranulation, resulting in marked degranulation after 5 hours of the injection. The parathyroids remain unaffected throughout the experiment and show no histological change.
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PMID:Studies of calcitonin cells and parathyroid glands of the Indian palm squirrel, Funambulus pennanti in response to experimental hypercalcaemia. 31 55

The effect of i.v. infusions with salmon calcitonin was evaluated in the treatment of acute hypercalcemia in 12 patients. Clinical improvement and a less critical level of serum calcium were achieved within 24 hours for eight of the patients, for another two after treatment for 48 hours. In malignant conditions (six patients) calcitonin was less effective, which could be evaluated within 24 hours. In addition to rehydration, the rapid onset of action and the lack of side-effects make calcitonin a drug of first choice in the treatment of acute hypercalcemia.
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PMID:Salmon calcitonin in the acute treatment of moderate and severe hypercalcemia in man. 35 62


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