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

Development of experimental chronic renal insufficiency in rats was accompanied by an increase in concentration of residual nitrogen and phosphorus in blood and also by a decrease in intestinal absorption of Ca2+, however, no hypocalcemia was observed and the alkaline phosphatase activity was unaltered in blood serum. At the same time the renal insufficiency caused in some animals metastatic calcification of aorta and kidney, which was manifested by increased calcium concentration in these tissues. Administration of dihydrotachysterol increased the active transport of Ca2+ in rat intestine at the later steps of the impairment and led to development of moderate hypercalcemia and particularly to an increase in the degree of calcinosis of aorta and kidney. Administration of thyrocalcitonine did not prevent the hypercalcemia and calcinosis of internal tissues.
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PMID:[Changes in phosphorus-calcium metabolism in experimental renal insufficiency and after administration of dihydrotachysterol and thyrocalcitonin]. 103 Aug 98

Effects of NaF, CaCl2, NaCl and mammalian calcitonin on the histology of ultimo-branchial (UTB) and corpuscle of Stannius (CS) and plasma levels of calcium and phosphorus in the teleost Heteropneustes fossilis are recorded. Administration of NaF, NaCl, and mammalian calcitonin resulted in varying degree of hypolcalcaemia and hyperphosphataemia, whereas hypercalcaemia and hypophosphataemia developed during CaCl2 treatment. These treatments also produced various histological changes in UTB and CS. It is suggested that CS and UTB are involved in metabolisms of Ca and P, and in osmoregulation. Moreover, it is an important hypocalcaemic mechanism in this fish in combating hypercalcaemia.
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PMID:Role of ultimobranchial body and corpuscle of Stannius in regulation of the plasma calcium and phosphorus levels in the teleost Heteropneustes fossilis. 103 54

Five patients with hypoparathyroidism (three post thyroidectomy and two idiopathic) were treated with synthetic 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) for up to 6 months. In each case daily oral administration of 1 microgram 1,25-(OH)2-D3, either alone or with additional calcium, raised ther serum calcium into the normal range. The serum phosphorus and the renal tubular reabsorption of phosphorus fell during treatment. None of these patients developed hypercalcaemia and no other complications of treatment have been recorded. 1,25-(OH)2D3 seems to represent a significant improvement over conventional methods for treating hypoparathyroidism.
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PMID:Treatment of hypoparathyroidism with 1,25-dihydroxycholecalciferol. 105 76

Five patients who had gross abnormalities of calcium and phosphorus metabolism due to long standing renal failure are described to illustrate the difficulties with the term "tertiary hyperparathyroidism". One patient who had unequivocal biochemical tertiary hyperparathyroidism was found histologically to have nodular hyperplasia of all four glands even though one gland weighed twice as much (12g) as the combined weight of the other three. Another patient was not hypercalcaemic but had all the other features of the condition including rapid onset of osteitis fibrosa, vascular calcification and a probable parathyroid adenoma, with hyperplasia of the three glands. The other three had hypercalcaemia only after a reduction in the plasma inorganic phosphorus due either to renal transplantation or aluminum hydroxide therapy. The bone histology of the five patients varied from severe osteomalacia to severe osteitis fibrosa. A consideration of the factors involved in causing hypercalcaemia in these patients and a review of the literature leads to the conclusion that the term tertiary hyperparathyroidism is often misleading and best avoided.
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PMID:What is tertiary hyperparathyroidism? 106 86

Using rats previously labeled with 45Ca, the effects of a severely phosphate deficient diet on calcium mobilization from bone into serum were examined in both intact and thyroparathyroidectomized (TPTX) RATS. With the TPTX animals, increased calcium mobilization from bone was evident 12 hr after the rats had been placed on the low phosphorus diet. At that time period, both TPTX and intact rats had become severely hypophosphatemic. However, in intact rats, calcium mobilization was not observed until 48 hr had elapsed. Both intact and TPTX hypophosphatemic rats developed hypercalcemia. To determine if inhibition of calcium deposition into bone contributed to this change, the course of 45Ca movement from blood into bone was followed in an experiment where rats received a single injection of the isotope at the time the low phosphorus diet was given. The animals on the low phosphorus diet showed a significantly lower bone specific activity and a higher serum specific activity compared to the control group, indicating calcium deposition into bone was inhibited. We conclude that the acute response to hypophosphatemia, resulting from the low phosphorus dietary regimen, was an increase in bone resorption and an inhibition of bone mineralization. The increase in bone resorption occurred more rapidly in TPTX rats than in the intact animals.
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PMID:Acute inhibition of mineralization and stimulation of bone resorption mediated by hypophosphatemia. 111 57

The development of nephrocalcinosis in the rat following intraperitoneal injections of various concentrations of neutral sodium phosphate (pH 7-4) was studied using histology, histochemistry, electron microscopy and quantitative techniques. Daily injections of 0-5 M phosphate consistently produced nephrocalcinosis after 6 days or more. Calcium deposits were at first confined to the basement membranes of proximal tubules; but a longer course of injections, up to 10 days, resulted in additional basement membrane calcification in the outer cortes, and outer medulla, together with intra-luminal casts, often calcified, in the outer medulla and papilla. Calcification was not found in other organs such as liver, lung, heart or aorta. Results from quantitative estimations of total kidney calcium and phosphorus suggested that it was the calcium content which was important to the initiation of nephrocalcinosis. Ultrastructural changes, suggestive of degeneration or alteration in function, were found in mitochondria of proximal tubules in experimental animals before the onset of histologically evident nephrocalcinosis. Later changes, especially to the basal part of proximal tubular cells and their basal laminae, were thought to be consequent upon the mitochondrial changes. It is suggested that the initial renal damage was caused both directly, by a toxic effect of the phosphate load on the kidney and, indirectly, by stimulation of the parathyroid glands as a result of the hypocalcaemia and hyperphosphataemia which followed an injection of phosphate. Daily doses of 1 M phosphate for 3 days produced a type of nephrocalcinosis which was more typical of that reported by previous investigators, who used high doses of phosphate. Twice daily injections of 0-25 M phosphate for 6 days did not induce nephrocalcinosis, whereas 0-375 M phosphate given twice daily for 6 days produced only minimal calcium deposits compared with animals given 0-5 M phosphate once daily for the same period. This may have important clinical implications, since phosphate has been used to control hypercalcaemia of various etiologies.
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PMID:The development of nephrocalcinosis in the rat following injections of neutral sodium phosphate. 113 87

Constant intravenous infusion (65 to 260 ng/min) of prostaglandin E2 (PGE2) produced an elevation of the plasma calcium concentration in unanesthetized rats in a period of 4 h. The increase in plasma calcium was related to the amount of PGE2 infused, and the hypercalcemia persisted for at least 10 h during continuous infusion. There was also a small increase in plasma inorganic phosphorus concentration. The increase in plasma calcium was not due to hemoconcentration; in fact, there was a small decrease in hematocrit during infusion of PGE2, and no change in total plasma protein concentration was detected. Infusion of PGF2, did not raise plasma calcium concentration. We conclude that under appropriate conditions, the exogenous administration of PGE2 can cause an elevation of plasma calcium in the intact rat.
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PMID:Intravenous infusion of prostaglandin E2 raises plasma calcium concentration in the rat. 114 Jan 71

The strain of Walker carcinosarcoma 256 described induces hypercalcaemia, hyperphosphataemia and hyperuraemia in tumour bearing rats. Changes in calcium and phosphorus excretion are observed as well as accompanying calcification of soft tissue organs and loss of bone calcium. These changes in calcium metabolism disappear after removal of the tumour, so that long-range action of the tumour can be stated. The results are discussed in comparison with three other animal models of tumour dependent hypercalcaemia.
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PMID:The hypercalcaemic syndrome in rats bearing the Walker carcinosarcoma 256. 117 20

Two experiments were conducted with cockerels to determine whether the presence or absence of the ultimobranchial glands would influence the relationship between dietary and plasma calcium and phosphorus. Broiler type cockerels, 16 weeks of age which had been sham operated (SHAM) or ultimobranchialectomized (UBX) 1 to 3 weeks earlier, were fed diets containing 0.8 or 2.4% calcium and 0.13 to 0.33% phosphorus. The SHAM cockerels fed diets containing 0.8% Ca and 0.13% P did not develop hypercalcemia whereas the UBX cockerels fed this diet developed slight significant hypercalcemia after 17 to 21 days. In Experiment I, SHAM cockerels fed the diet containing 2.4% Ca and 0.13% P developed mild, chronic hypercalcemia (12.7 mg./100 ml.) with a plasma phosphorus of 3.03 mg. P/100 ml., whereas the UBX cockerels fed the same diet developed severe hypercalcemia (16.0 mg./100 ml.) and hypophosphatemia, 1.68 mg. P/100 ml. In Experiment 2 the following plasma values were observed after 17 days of consuming the experimental diets: SHAM fed 2.4% Ca and 0.13% P had 10.6 mg. Ca/100 ml. and 3.59 mg. P/100 ml., whereas UBX fed the same diet had 12.8 mg. Ca/100 ml. and 2.24 mg. P/100 ml. The UBX fed 2.4% Ca and 0.33% P for 17 days had plasma values of 10.8 mg. Ca/100 ml. and 4.48 mg. P/100 ml. It is concluded that the presence of the ultimobrancial glands are essential to the regulation of plasma calcium and phosphorus in chickens which consume high calcium-low phosphorus diets.
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PMID:Relationships between dietary and plasma concentrations of calcium and phosphorus in intact and ultimobranchialectomized chickens. 117 97

Serum calcium, inorganic phosphorus and alkaline-phosphatase were determined in 3,191 women as a part of a multiphasic health testing program. A fasting sample of blood was drawn between 9 and 11 a.m. and the separated serum was applied to a Technicon Autoanalyzer SMA 12/60 and measured. In 527 women, who were found to have no abnormalities on the other laboratory tests or by the physical examination, were the results of determination studied in relation to age and menstrual status. The values obtained from 13,258 men were employed as a control. In regularly menstruating women the serum calcium level was decreased with the advance of age. Once the menstrual cycle had got irregular toward the menopause, the serum calcium level was rapidly increased, reached maximum in 2-5 years after the menopause, and was slightly decreased thereafter. The serum inorganic phosphorus level also varied in a similar attitude. On the other hand both the serum calcium and phosphorus levels in men were gradually reduced with the advance of age and no fluctuation was observed. Alkaline-phosphatase in serum was distinctly enhanced in the postmenopause. These data indicate that the decline in estrogen secretion results in hypercalcemia and hyperphosphatemia and that a prophylactic estrogen therapy may be considered at the early stage of the postmenopause for preventing the increased bone resorption.
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PMID:[The effect of menopause on serum levels of calcium and inorganic phosphorus (author's transl)]. 123 18


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