Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the clinical characteristics of primary and post-operative hypoparathyroidism in 39 patients. Laboratory follow-up data were compared under two different treatment programs using either AT 10 or 25 Hydroxycholecalciferol (25 OHCC). Clinical analysis revealed the atypical characteristics of primary hypoparathyroidism. From a therapeutic standpoint, AT 10 and 25 OHCC were equally effective in provoking a return to normal plasma calcium levels, except in complex cases of vitamin D resistance. 25 OHCC proved much easier to manipulate than at 10 and offered a higher security with respect tothe risk of hypercalcemia. The biological activity of 25 OHCC seems to differ from that of AT 10, especially regarding phosphorus metabolism.
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PMID:[Hypoparathyroidism in adults (author's transl)]. 74 36

The purpose of this study was to test the effectiveness of various doses of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) in an experimental rabbit model of athero-arteriosclerosis designed by Hass et al. (Amer. J. Pathol., 49 (1966) 739). This model, which involves the feeding of a hypercholesterolemic diet in conjunction with the administration of moderately high doses of vitamin D and nicotine, results in an extensive arterial disease with complicated lesions. EHDP was administered daily by subcutaneous injection at levels of 0.25, 1.0 and 2.5 mg/kg body weight beginning with the initiation of the atherogenic regimen. Results of chemical and histopathological analyses after 8 and 12 weeks of treatment indicate the following: (1) There was a dose-related inhibition of arterial calcification at 8 weeks. At 12 weeks, only the 2.5 mg/kg dose of EHDP resulted in reduced calcification. (2) EHDP administration appeared to influence arterial lipid-containing plaque formation in medium sized arteries at 12 weeks. There was no apparent effect of EHDP administration on serum cholesterol and triglyceride levels. (3) EHDP, at a dose of 2.5 mg/kg/day, inhibited the vitamin D induced hypercalcemia. (4) EHDP administration at 2.5 mg/kg/day almost totally inhibited the thromboarteritis accompanying this disease. (5) The data thus indicate that if arterial calcification is inhibited, the other morphological effects of this treatment regime are also inhibited. This effect occurred even though serum lipid levels were unaffected. The data therefore emphasize the role of calcification in the pathogenesis of this type of experimental atherosclerosis and perhaps in human disease as well.
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PMID:The effect of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) on a rabbit model of athero-arteriosclerosis. 81 8

The rate of reversal of hypercalcaemia or hypercalciuria induced by calciferol, dihydrotachysterol, 1-alpha-hydroxycholecalciferol (1-alpha-OHD3), or 1-alpha, 25-dihydroxycholecalciferol (1-alpha, 25-(OH)2D3) was measured in three normal subjects, two patients with osteoporosis, and 14 patients with disorders resistant to vitamin D. The half time for reversal after stopping 1-alpha, 25 (OH)2D3 was less than that after stopping 1-alpha-OHD3, calciferol, or dihydrotachysterol. The differences observed were independent of the dose given or length of treatment. When 1-alpha-OHD3 or 1-alpha-25-(OH)2D3 was stopped patients with vitamin D resistant states (hypoparathyroidism, renal tubular hypophosphataemia, or chronic renal failure) showed less rapid reversal of hypercalcaemia and hypercalciuria than did normal subjects. These studies show one potential advantage of 1-alpha-25-(OH)2D3 over vitamin D, and possibly over 1-alpha-OHD3, in the management of vitamin D resistant states.
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PMID:Rate of reversal of hypercalcaemia and hypercalciuria induced by vitamin D and its 1alpha-hydroxylated derivatives. 83 19

Hypercalcemia was induced in 5/6 nephrectomized rats fed a low calcium diet by administering pharmacologic doses of vitamin D. The degree of hypercalcemia was greater in uremic rats than in sham-operated rats both of which were given vitamin D. Bone resorption was marked in both groups but differed in distribution. Increased osteoclasis in uremic rats was limited to diaphyseal cortical bone while metaphyseal trabeculae were relatively unaffected compared to sham-operated rats administered vitamin D. Ultrastructurally thyroid C cells were degranulated and in an active stage in both groups of rats receiving vitamin D. Urinary calcium excretion was greater in sham-operated rats given vitamin D than in uremic rats. The greater renal retention of calcium in uremic rats given vitamin D was felt to contribute to the development of hypercalcemia. These studies suggest that although trabecular bone was resistant to pharmacologic levels of vitamin D in renal failure, hypercalcemia developed due to selective resorption of cortical bone and impairment of renal calcium excretion.
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PMID:Vitamin D-induced hypercalcemia in experimental renal failure. 84 25

Synthetic 1alpha-hydroxycholecalciferol, a potent vitamin D analogue, was given daily together with calcium to seven patients with senile osteoporosis and to three patients with prednisone-induced bone loss. Quantitative bone histology indicated increased formation and mineralization after three months of treatment. The bone resorption was reduced, a finding supported by a decrease in the urinary hydroxyproline excretion. Photon absorptiometry of the forearm showed a significant rise in the bone mineral content, in accordance with the histological findings. Serum calcium rose in all patients and severe hypercalcemia developed in one case. Urinary excretion of calcium and magnesium increased significantly. The findings indicate that treatment with 1alpha-hydroxycholecalciferol may be useful in osteoporosis due to aging or following corticosteroid administration. The patients must be carefully followed up because of the risk of hypercalcemia.
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PMID:Effect of 1alpha-hydroxycholecalciferol in senile osteoporosis and in bone loss following prednisone treatment. 85 74

Fine structural alterations of thyroid C cells and parathyroid chief cells were evaluated after feeding dried leaves of the calcinogenic plant, Solanum malacoxylon, to cattle for 1, 6 and 32 days. Thyroid C cells initially were degranulated in response to the hypercalcemia, and parathyroid chief cells accumulated secretory granules. There was hypertrophy of thyroid C cells with well-developed secretory organelles but few secretory granules in the cytoplasm after 6 days of feeding S. malacoxylon. Inactive chief cells with dispersed profiles of endoplasmic reticulum and increased lysosomal bodies predominated in the parathyroid glands. Multiple foci of soft tissue mineralization were present in the heart, lung, and kidney. Thyroid C cells underwent hypertrophy and hyperplasia after 32 days of S. malacoxylon, and parathyroid chief cells were inactive or atrophic in response to the long-term hypercalcemia. Severe soft tissue mineralization was present throughout the cardiovascular system, lung, kidney, and spleen. These ultrastructural changes in thyroid C cells and parathyroid chief cells plus the widespread soft tissue mineralization observed after feeding cattle small amounts of S. malacoxylon are consistent with the recent evidence that leaves of this plant are a potent source of the active metabolite, 1,25-dihydroxycholecalciferol, of vitamin D.
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PMID:Ultrastructural evaluation of parathyroid glands and thyroid C cells of cattle fed Solanum malacoxylon. 86 16

The effects of small oral doses (1-2 microgram/day) of 1alpha-hydroxycholecalciferol, given for 1 to 2 years, have been examined in four nondialysed adolescents with chronic renal failure and bone disease. Treatment increased calcium retention and plasma calcium, and decreased plasma levels of alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone. X-ray abnormalities of bone regressed, and 2 patients underwent successful surgical correction of knock-knees; bone histology in these 2 was normal at the time of operation. 2 patients developed hypercalcaemia which promptly reversed when 1alpha-hydroxycholecalciferol was withdrawn. In one patient treatment was initially successful, but later there was biochemical, radiographic, and histological evidence of relapse. Long-term treatment of such patients with 1alpha-hydroxycholecalciferol may be effective and facilitate the surgical correction of deformities, but this is not invariable. Toxic effects are similar to those of vitamin D itself, but are more readily reversible.
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PMID:Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol. 87 33

The incidence of cytoplasmic metachromasia has been studied in cultures of skin fibroblasts derived from 6 cases of the syndrome of supravalvular aortic stenosis, characteristic facies, and mental retardation which in many instances represents the late normocalcaemic stage of the severe form of infantile hypercalcaemia. The percentage of metachromatic cells (mean positivity 7.3%) was significantly higher than in control cultures. The addition of vitamin D2 and calcium to culture media caused a highly significant increase in metachromatic cells (mean positivity in supplemented media 16.1%) compared with a lesser increase in controls. These findings strengthen previous suggestions that there is a genetically determined hypersensitivity to vitamin D in some cases of the syndrome. A multifactorial aetiology is proposed, dependent on a variable genetic susceptibility of fetal connective tissues to a non-physiological effect of D vitamins and a variable level of maternal vitamin D nutrition.
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PMID:Supravalvular aortic stenosis-infantile hypercalcaemia syndrome: in vitro hypersensitivity to vitamin D2 and calcium. 93 23

Five adult patients with chronic renal failure and associated renal osteodystrophy have been treated for 6 months with 1-alpha-hydroxycholecalciferol (1 alpha-OH-D3), a synthetic vitamin D analogue. All 5 patients had severe metabolic bone changes as estimated by bone scintigraphy. Three patients were hypocalcemic, 4 had elevated serum alkaline phosphatases, 5 had elevated serum immunoreactive parathyroid hormone (i-PTH) concentration and 3 had bone pains. During treatment serum calcium increased in all patients (mean 11.4%) and 3 originally hypocalcemic patients became normocalcemic. Serum alkaline phosphatases decreased (mean 27.3%) and became normal in 4 patients, who initially had elevated values. A pronounced decline in the serum concentration of i-PTH (mean 53%) was seen in all patients and 1 patient obtained normal i-PTH levels after 4 months of treatment. The intestinal calcium absorption, which was low initially, even when calcium intake was considered, rose almost threefold (mean 273%) and reached normal values in all cases. The bone mineral content increased in all patients, but the changes were small (mean 4.9%) and insignificant. Finally, bone pain disappeared in 2 patients and improved in 1 of 3 patients exhibiting this symptom. A linear correlation (r = 0.48, p less than 0.001) was found between the dose of 1 alpha-OH-D3 and serum calcium. But in spite of this and the frequent control, all patients developed one episode of hypercalcemia. This disappeared within 48 hours after discontinuing the drug. It is concluded that treatment with 1 alpha-OH-D3 appears to be of therapeutic value in metabolic bone disease associated with chronic renal failure, but frequent control of blood biochemistry seems mandatory.
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PMID:L-alpha-hydroxycholecalciferol treatment of adults with chronic renal failure. 96 64

Combined calcium balance and 47Ca turnover studies in sarcoidosis (4 patients) and vitamin D intoxication (1 patient) disclosed three different patterns of calcium metabolism. On patient with sarcoidosis had a normal metabolism of calcium, and two patients presented the usual pattern of intestinal hyperabsorption, hypercalcemia, and hypercalciuria. The fourth patient with sarcoidosis and the patient with vitamin D intoxication, both studied during spontaneous remissions, presented the third pattern. The main features here were hypercalcemia despite normal intestinal absorption of calcium, enlarged exchangeable calcium pool, accelerated accretion and resorption rates, hypercalciuria, and a distinctly negative calcium balance. This pattern of remission seems to represent a mobilization of extraosseous or metastatic calcifications, rather than a resorption of bone calcium.
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PMID:Observations on the different calcium metabolic patterns in sarcoidosis. A metabolic and kinetic study. 98 4


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