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

Male rats weighing 220-250 g were injected i.m. daily with 0.1 mg commercial human growth hormone for 3 days or 12 days. The serum concentration of total calcium phosphorus and alkaline phosphatase were significantly elevated for some days and returned to normal values at the end of the test period. The parathyroid glands, as studied by light and electron microscopical morphometry showed signs of reduced activity at the 4th day and also at the 13th day: a lowered nucleo-cytoplasmic ratio and a decrease of rough endoplasmic reticulum, of Golgi apparatus and of plasmalemmal tortuosity. The findings suggest a hypercalcemic effect of growth hormone involving peripheral organs of calcium metabolism, especially kidney and bone, and a secondary suppression of parathyroid glands by hypercalcemia.20
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PMID:Parathyroid function in rats treated with growth hormone. A morphometric study. 82 5

The effect of ingestion of dried leaves of Cestrum diurnum, a plant shown to contain a 1,25-dihydroxycholecalciferol-like principle, was tested in normal pigs fed 1.2% calcium and 1.0% phosphorus for 10 weeks from weaning and in hyperparathyroid pigs fed 0.8% calcium and 1.6% phosphorus for the same periods of time. Addition of 3% Cestrum diurnum leaf meal rapidly resulted in decreased feed consumption and weight gain, hypercalcemia and hypophosphatasemia. In normal pigs, plasma calcium rose to 16 mg/100 ml within one week and remained high for the 4 week experimental period. In hyperparathyroid pigs with hypocalcemia, plasma calcium rose to 12.75 mg/100 ml within one week and later approached 15 mg/100 ml. Ingestion of Cestrum diurnum retarded cell differentiation of growth cartilages. Arrested osteocytic osteolysis was observed within one week with osteopetrosis of epiphyses and metaphyses. The negative effect on the resorbing osteocytes then caused osteonecrosis which, in combination with lack of bone formation because of atrophy of osteoblasts, resulted in osteopenia within 4 weeks. Dystrophic calcinosis occurred within 2 weeks and was widespread after 4 weeks in lungs, kidneys, heart and vessels. Atrophy of parathyroid cells was severe after one week. Hyperparathyroid pigs responded with skeletal lesions, dystrophic calcinosis and parathyroid atrophy more rapidly and severely than normal pigs. The biochemical and anatomical changes in Cestrum diurnum ingestion are closely similar to those in vitamin D3 intoxication in pigs. Whereas pigs can tolerate large amounts of vitamin D3 because of feed-back control of 1 alpha-hydroxylation in the kidney, this control point is by-passed in Cestrum diurnum ingestion and intoxication occurs promptly.
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PMID:Cestrum diurnum intoxication in normal and hyperparathyroid pigs. 87 Feb 84

Fourteen patients with renal osteodystrophy were treated for at least one year with 1-alpha-hydroxycholecalciferol (1-alpha-OHD3) in a dose varying from 1 microgram/week to 3 microgram/day. Plasma calcium and inorganic phosphorus concentrations increased significantly. The plasma alkaline phosphatase concentration fell in 11 of the 12 patients in whom it was initially raised and returned to normal in seven. Serum parathyroid hormone concentrations were initially raised in all patients, but they decreased significantly with treatment and became normal in eight patients within one year. The 10 patients with radiological abnormalities showed some improvement. Hypercalcaemia occurred in 11 patients, and necessitated a reduction in the dose of 1-alpha-OHD3 in some. 1-alpha-OHD3 was effective in reducing the biochemical and radiological abnormalities of renal osteodystrophy, but it should be used wtih care, and plasma calcium concentrations should be monitored.
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PMID:1-alpha-hydroxycholecalciferol for renal osteodystrophy. 91 69

Hypocalcemia is a frequent accompaniment of acute renal failure, but paradoxically hypercalcemia also has been described in association with acute renal failure. In this paper we describe two patients who provide some insights into both the potential clinical importance and mechanism of the hypercalcemia associated with acute renal failure. The clinical significance is emphasized by the presence of diffuse metastatic calcification observed at postmortem examination in one patient. In both patients the increase in serum calcium concentration was not coincident with a decrease in serum phosphorus concentration; when measured in one patient, serum levels of parathyroid hormone were undetectable. These findings, along with the consistent association with rhabdomyolosis, support the proposal that the hypercalcemia of acute renal failure is caused by dissolution of dystrophic calcifications in traumatized muscle and may lead to severe metastatic calcifications.
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PMID:Hypercalcemia of acute renal failure. Clinical significance and pathogenesis. 93 62

Sheep treated with a single dose of an extract of the dried leaves of Solanum malacoxylon (SM) at the rate of 0-2 g of leaves per kg liveweight produced a pronounced hypercalcaemia (49 per cent, P less than 0-005) after 24 h, which persisted for at least six days. The ultra-filtrable fraction of the serum calcium rose to approximately the same extent as the protein-bound calcium. This finding is consistent with osteosclerosis and parathyroid atrophy found to occur in cases of experimental SM intoxication. At the dose level given serum inorganic phosphorus was not significantly increased and packed cell volume, serum proteins and ceruloplasmin concentrations remained constant.
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PMID:Serum calcium fractions in sheep treated with Solanum malacoxylon. 95 23

Sham-operated and parathyroidectomized (PTX) rats were divided into two pair-fed groups, one on a normal mineral intake (0.5% Ca, 0.3% P), the other on a regimen low in phosphorus (0.5% Ca, 0.03% P). P depletion led to a drop in plasma P and urine P, a rise in plasma Ca and a marked rise in urine Ca, a drop in serum magnesium and a rise in urine Mg. The changes were more pronounced in the PTX animals, but final values were the same in both groups. Parallel bone-seeking isotope (85Sr, 177Lu, 237Np) studies in nonablated animals revealed an increase in the urinary nuclide output and in the urine/tibia ratio in P-deficient animals. Normal and primary bone osteocytes decreased and enlarged osteocytes increased as a result of P deficiency; osteoclasts and osteoblasts also increased. Bone composition showed a drop in ash content and a rise in water, with a light decrease in both Ca and P, and a corresponding rise in hydroxyproline and nitrogen in the P-deficient animals. The results are interpreted to mean that P-deficiency in the young growing rat leads to an increase in bone resorption which occurs also in the absence of parathyroid hormone (PTH). The fact that final values were similar in the control and PTX P-deficient animals suggests that steady-state regulation can also occur without PTH. Because P-deficiency leads to rapid hypercalcemia and rapid marked hypercalciuria, there may exist a mechanism for phosphate regulation which would then supersede Ca homeostasis. The change in serum and urine Mg levels may reflect a decrease in tubular Ca and Mg reabsorption associated with P-deficiency.
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PMID:Phosphorus deficiency, parathyroid hormone and bone resorption in the growing rat. 95 82

Lactating rats were compared with nonlactating controls, with regard to the intake and absorption of calcium, serum calcium level, and te protective effect of thyroacalcitonin (TC) against hypercalcemia and hyperphosphatemia. While consuming a commercial diet, intact, nonfasted lactating rats maintained a serum calcium level of approximately 9 mg/100 ml, which was 1 mg/100 ml lower than that of nonlactating controls. The level rose to that of the controls within one day after removal of the litters from the mother. Compared with nonlactating rats, lactating rats had a three-fold higher calcium intake and a six-fold higher rate of net absorption of calcium. After intragastric calcium (10 mg/100 g body wt) the increase in serum calcium was small (1 mg/100 ml) 2 h later in both groups of sham-operated rats but was markedly increased in thyroparathyroidectomized groups, with the lactating rats showing a significantly greater increase than the nonlactating rats. The injection of a small dose of porcine thyrocalcitonin completely counteracted this hypercalcemia in lactating rats, but did not have any effect on nonlactating controls. Protection by the thyroid gland against hyperphosphatemia after intragastric calcium also was significant in both lactating and nonlactating rats. The results show that TC is much more effective in lactating than in nonlactating rats, suggesting that TC may be of particular importance in lactation by restricting elevations of serum calcium and phosphorus levels after eating, thereby aiding in conservation of these ions.
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PMID:Calcium metabolism during lactation: enhanced effects of thyrocalcitonin. 95 38

The relative contributions of Ca++, phosphorus, and parathyroid hormone (PTH) on insulin secretion were evaluated in three groups of dogs. Dogs were studied with glucose infusions (group I) or standard intravenous glucose tolerance tests (IVGTT) (group II) before and after the development of diet-induced hypophosphatemia. Mean serum phosphorus levels for both groups fell from 4.1 to 1.1 mg/100 ml. Animals in group I demonstrated a fall in glucose disappearance rates (Kg) from 5.3+/-0.6% min to 3.5+/-0.5% after induction of hypophosphatemia (P less than 0.001). Mean insulin response was significantly greater in the hypophosphatemic animals than in controls in this group. In group II animals, mean insulin areas obtained during the IVGTT increased from 1,426+/-223 to 2,561+/-141 muU/ml/60 min after induction of hypophosphatemia, and were unaffected by Ca++ or PTH administration. Ca++ administration, but not hypophosphatemia or PTH infusion, increased significantly the mean insulin response to tolbutamide. Secondary hyperparathyroidism was induced by dietary manipulation in four dogs (group III). Mean PTH values increased from 71.4+/-2.1 to 3,012+/-372 pg/ml (P less than 0.001). Mean insulin response to an IVGTT was similar to group III animals, but increased from 1,352+/-128 to 1,894+/-360 muU/ml/60 min after the excessive dietary phosphorus was reduced for 3 mo, and plasma phosphorus fell from 3.2+/-0.1 to 2.8+/-0.3 mg/100 ml. PTH values decreased to 647+/-53 pg/ml. The insulin response to tolbutamide was comparable to that in group II animals, but increased significantly after calcium administration. Immunoreactive insulin disappearance rates were unaffected by hypophosphatemia or diet-induced secondary hyperparathyroidism. These data demonstrate that hypophosphatemia is associated with an augmented glucose-stimulated insulin release, without any effect on tolbutamide-stimulated insulin release. Hypercalcemia produces an augmented tolbutamide-stimulated insulin release with no apparent effect on glucose-stimulated insulin release. Finally, PTH does not appear to be an insulin antagonist and has no apparent effect on either glucose- or tolbutamide-stimulated insulin release in animals with dietary-induced secondary hyperparathyroidism.
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PMID:The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release. 95 71

Between 1969 and April 1975 24 patients with severe secondary hyperparathyroidism (sHPT) clinically presenting with uremic osteopathy required either total (n=5) or subtotal (n=18) parathyroidectomies, 17 patients were already supported by maintenance hemodialysis, 6 patients suffered from terminal renal insufficiency. The leading clinical symptoms consisted of general osteoporosis, spontaneous fractures, extraosseous calcifications and histologically proven dissecting fibroosteoclasia. After operation 18 patients experienced complete relief from their complaints and repair of their skeletal lesions, 2 patients required reexploration for an undetected hyperfunctioning 4th parathyroid gland, regretfully with no success. In 4 patients with subtotal parathyoidectomy a recurrence of varying intensity with increased PTH-secretion from the remnant had to be registered after months and years.-The indication for surgical treatment of sHPT due to chronic renal failure has to be based on two sets of findings: 1) inadequate longterm suppression of increased PTH secretion by conservative measures like high dialysate calcium concentration or oral calcium intake, serum phosphorus depletion by oral intake of aluminium hydroxyde and possibly also by Vit. D; 2) persistent hypercalcemia, progressive osteodystrophy and severe complaints like bone pain and pruritus.
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PMID:[Surgical aspects of secondary hyperparathyroidism (author's transl)]. 101 8

Automated laboratory procedures have made possible to "screen" a large population for specific biochemical abnormalities. Primitive hyperparathyroidism is for several respects an excellent disease model for testing "mass screening". Il is often asymptomatic, not uncommon, and is manifested by abnormalities in the levels of serum calcium and inorganic phosphorus, that can be detected cheaply with automated equipment. A computer program has been developed to screen patients with hypercalcaemia. During a period of 18 months 22720 hospitalized patients were investigated by the evaluation of serum calcium, and 80 hypercalcaemic patients were found. The diagnosis of primary hyperparathyroidism was established in 24 patients (in 19 histologically confirmed) so that the incidence of primary hyperparathyroidism (1,05%) compares favorably with that reported from some foreign Authors.
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PMID:[Serum calcium evaluation and incidence of primary hyperparathyroidism in hospitalized patients (author's transl)]. 102 89


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