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

The relationship between the concentration of phosphate in plasma and parotid saliva was studied in six conscious sheep and a goat, either intact or thyroparathyroidectomized (t.x.p.t.x.), under conditions designed to minimize marked fluctuations in flow rate of saliva. A linear relationship between acutely induced changes in plasma phosphate concentration and the phosphate level in saliva has been demonstrated in both intact and t.x.p.t.x. animals. Dietary phosphorus depletion caused adaptation of salivary phosphate concentration so that less was secreted at a given concentration of plasma phosphate. Attention is drawn to the similarity between this phenomenon and that already described for the proximal renal tubule. Parathyroid hormone (PTH) was shown to reduce the salivary phosphate concentration with little or no effect on phosphataemia. The administration of 1,25-dihydroxycholecalciferol (1,25(OH)2CC) also caused a reduction in salivary phosphate concentration despite hyperphosphataemia and hypercalcaemia. It is suggested that salivary phosphate concentration can be influenced directly by the concurrent level of plasma phosphate but that this relationship can be modified by the circulating concentration of 1,25(OH)2CC and indirectly by PTH via increased production of 1,25(OH)2CC.
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PMID:Factors affecting the secretion of phosphate in parotid saliva in the sheep and goat. 689 39

Eleven subjects aged four to 76 years with primary hypoparathyroidism have been treated with 1,25-dihydroxycholecalciferol (1,25-D3). Five subjects were not on vitamin D analogues before starting this drug. 1,25-D3 was found to be an effective treatment and a rapid biochemical response to dose adjustments was observed. In two subjects hypercalcaemia and reversible renal failure occurred. Thiazide-type diuretics necessitated dose reductions in a further two subjects. A scheme for starting hypoparathyroid subjects on this treatment is suggested. The need for regular biochemical assessment and awareness of possible drug interactions is emphasised. It is felt that 1,25-vitamin D3 has practical advantages over traditional forms of vitamin D in the treatment of hypoparathyroidism.
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PMID:1,25-dihydroxy-vitamin D3: a new treatment for hypoparathyroidism. 693 21

A controlled therapeutic trial on seventy-four 70-year-old women was carried out with the purpose of finding the optimal treatment for post menopausal osteoporosis. The bone mineral content (BMC) was measured by I-photonabsorptiometry at two sites in the distal part of the forearms, where the trabecular/cortical ratio is 0.25 and 1.5, respectively. Radiographs were done on the right hand to measure the metacarpal bone mass (cortical area/total area=CA/TA. After observing the spontaneous course of bone loss for 6 months the participants were allocated at random to 12 months' treatment with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and oestrogen/gestagen, alone or in combination, and calcium. The groups treated with oestrogen/gestagen [with or without 1,25(OH)2D3] showed a highly significant increase in BMC. In contrast bone mineral remained unchanged or decreased in both the calcium and the 1,25(OH)2D3 groups with a tendency towards more pronounced negative bone balance in the 1,25-(OH)2D3 group. Seven out of nineteen patients of 1,25(OH)2D3 developed hypercalcaemia, which necessitated a reduction in dosage. It is concluded that the new vitamin D metabolite, 1,25(OH)2D3, given in clinically acceptable doses, is without value in the treatment of post menopausal osteoporosis.
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PMID:Treatment of post menopausal osteoporosis. A controlled therapeutic trial comparing oestrogen/gestagen, 1,25-dihydroxy-vitamin D3 and calcium. 704 20

1 alpha-hydroxycholecalciferol [1 alpha (OH)D3], the synthetic analogue of 1,25-dihydroxycholecalciferol, the active metabolite of vitamin D, was administered for a period of 18 to 24 mo to an unselected group of 12 hemodialysis patients and to 2 patients after kidney transplantation. All patients responded with a significant rise in serum Ca and Mg. The whole-body 47Ca retention, used as an index of Ca absorption, rose in eight patients and decreased or remained unchanged in four, but its overall change was not significant. Serum immunoreactive parathormone showed a general tendency to decrease. From the clinical point of view, symptomatic relief of bone pain was seen in most dialysis patients, but no significant change occurred in transplant patients. The main side effects of 1 alpha (OH)D3 treatment were hypercalcemia and pruritus, which generally subsided after the dosage was tapered off.
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PMID:Long-term effects of 1 alpha-hydroxycholecalciferol therapy in chronic hemodialysis patients. 717 69

Malignancy is the most common cause of hypercalcemia, which may result from direct involvement of bone or from local or distant production of substances that enhance bone resorption. The recognized incidence of primary hyperparathyroidism has increased greatly since the advent of automated biochemical screening. A single parathyroid adenoma is most frequently the cause. Sarcoidosis commonly results in hypercalciuria but seldom causes sustained hypercalcemia. Increased production of 1,25-dihydroxycholecalciferol leads to hyperabsorption of calcium and enhanced bone resorption.
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PMID:Evaluation of the hypercalcemic patient. 721 54

Powdered Cestrum diurnum leaves, mixed with two diets differing in calcium and phosphorus contents, produced nephrocalcinosis in young chicks regardless of serum calcium elevation. The calcific deposits, found in both proximal and distal portions of cortical tubules, began either in the cytoplasm or in lysosomal bodies as a unilaminar spheroid structure containing apatite crystals. The ultrastructural characteristics of intraluminal concretions suggested that they were formed intracellularly but later were extruded into the lumen. The extent of calcific deposits increased with duration and with hypercalcemia. Although Cestrum contains an analog of 1,25-dihydroxycholecalciferol, neither mitochondria nor basal lamina contained calcific deposits described in nephrocalcinosis secondary to hypervitaminosis D.
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PMID:The ultrastructure of nephrocalcinosis induced in chicks by Cestrum diurnum leaves. 746 73

Vitamin D preparations [1-alpha-hydroxycholecalcifol (1-alpha OHD3) or 1,25-dihydroxycholecalciferol (1,25(OH)2D3)] may be administered orally, subcutaneously, intraperitoneally or intravenously. They may be given daily, sometimes in divided doses, or intermittently in large bolus doses, usually three times per week. A further variable is the timing of administration, which may be at night when the gut calcium load is at a minimum. In at least some studies high dose intermittent bolus administration of vitamin D can reduce parathyroid hormone (PTH) secretion by a mechanism separated in time from an increase in ionized calcium (iCa2+). In addition, some but not all studies have shown an improvement in calcium set point and in parathyroid gland sensitivity to calcium. It is also clear from a number of studies that this treatment can succeed where conventional daily administration has failed. Bolus intravenous therapy is most conveniently given after haemodialysis treatment sessions. Bolus oral therapy, perhaps administered prior to sleep, may achieve a similar objective (PTH suppression without hypercalcaemia) in patients on continuous ambulatory peritoneal dialysis (CAPD). It is also becoming apparent that the parathyroid gland may yet again escape following bolus therapy. The success of bolus therapy may lie in several not mutually exclusive mechanisms: high peak concentrations of 1,25(OH)2D3 directly affecting the parathyroid gland, improved compliance, and a small but significant increase in plasma iCa2+. Further long-term controlled trials are needed before bolus therapy can be generally recommended.
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PMID:Optimum route of administration of vitamin D in renal failure. 747 47

1. Two experiments were performed to compare the relative effectiveness of feeding 1,25-dihydroxycholecalciferol (1,25-DHCC) in minimising leg abnormalities in broilers with other methods and to investigate interactions between dietary 1,25-DHCC and calcium. 2. Adding 5 micrograms 1,25-DHCC/kg to a diet containing 12 g calcium/kg was more effective than early food restriction or meal feeding in preventing leg abnormalities but was found to cause a growth depression. 3. The second experiment, which had a factorial design, with diets containing 7.5, 10.0 and 12.5 g calcium and 0, 2.0, 3.5 and 5.0 micrograms 1,25-DHCC/kg, showed linear and quadratic interactions between these dietary factors. Diets with higher concentrations of both 1,25-DHCC and calcium resulted in growth depression associated with hypercalcaemia. 4. The incidence of tibial dyschondroplasia (TD) at 3 weeks of age was highest with the basal diet containing 7.5 g calcium/kg and was markedly reduced by addition of 1,25-DHCC and/or calcium. The incidence was very low or non-existent when 1,25-DHCC was fed at 3.5 micrograms/kg or greater. 5. Feeding 5 micrograms/kg 1,25-DHCC had no effect on plasma 1,25-DHCC concentrations, although at the higher dietary calcium contents plasma concentrations of 25-hydroxy- and 24,25-dihydroxy-cholecalciferol were lower in those birds fed 1,25-DHCC. 6. It is concluded that 1,25-DHCC is most effective in preventing TD without accompanying growth depression when it is fed in conjunction with diets containing less than 10 g calcium/kg.
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PMID:Interaction between dietary 1,25-dihydroxycholecalciferol and calcium and effects of management on the occurrence of tibial dyschondroplasia, leg abnormalities and performance in broiler chickens. 758 77

Secondary hyperparathyroidism is found in a large proportion, but not all patients on dialysis. Calcitriol controls moderate hyperparathyroidism in most patients but only in a proportion of those with advanced hyperparathyroidism. Patients with nodular parathyroid hyperplasia respond less frequently, presumably because of monoclonal growth and diminished calcitriol-receptor expression by parathyroid cells. In patients with nodular parathyroid hyperplasia, parathyroidectomy is an important alternative to calcitriol treatment. A priori reasoning indicates that prophylactic administration of calcitriol (to prevent parathyroid hyperplasia) is a reasonable option, but currently no controlled evidence for long-term efficacy of this approach without side effects is available. Intermittent administration of calcitriol by intravenous or oral routes is effective and, at least in experimental studies, superior to continuous calcitriol. However, in clinical comparisons, no superiority of intravenous versus oral or daily versus intermittent calcitriol has been documented. Calcitriol treatment must be closely supervised to prevent hypercalcemia, hyperphosphatemia, and excessive suppression of parathyroid hormone. Because of an altered dose response relationship, parathyroid hormone levels should not be completely normalized so as to prevent low bone turnover (adynamic bone lesion).
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PMID:Vitamin D therapy in patients receiving dialysis. 761 32

We prospectively studied the long-term effects of intravenous calcitriol in 17 hemodialysis patients with severe secondary hyperparathyroidism (HPT) for 25.7 +/- 3.4 (+/- SE) months. Calcitriol was given thrice weekly after dialysis. Subsequently, changes were made every 3-4 weeks based upon serum chemistries. Total calcium and inorganic phosphorus were measured weekly; alkaline phosphatase (AP) and IRMA-PTH were measured monthly. Inorganic phosphate was controlled with calcium supplements. With calcitriol therapy both IRMA-PTH and AP decreased from 876 +/- 113 to 65 +/- 13 pg/ml (p < or = 0.001) and 432 +/- 106 to 103 +/- 15 U/ml (p < or = 0.001), respectively. Each patient had a reduction in IRMA-PTH and AP. Nadir IRMA-PTH occurred at 55.4 +/- 7.3 weeks. The maximum and mean maximum doses of calcitriol were 8.0 and 4.1 +/- 0.4 micrograms thrice weekly, respectively. Hypercalcemia tended to occur in those patients who were hypercalcemic prior to the initiation of intravenous calcitriol therapy. All hypercalcemic episodes were asymptomatic and reversed either by temporary withdrawal or lowering of the calcitriol dose. Hyperphosphatemia developed in those patients with a history of elevated serum phosphates and was mostly related to dietary and medication noncompliance. We conclude that intravenous calcitriol was uniformly effective and safe for the long-term therapy of severe HPT in ESRD. Careful attention to serum phosphate control is required.
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PMID:Long-term high dose intravenous calcitriol therapy in end-stage renal disease patients with severe secondary hyperparathyroidism. 763 48


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