Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.
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PMID:[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis]. 131 65

Calcitonin has been used clinically to treat hypercalcemia, Vitamin D intoxication, osteolytic bone metastases and increased skeletal remodeling in Paget's disease. In general calcitonin is given every 6 to 12 hrs intramuscularly or subcutaneously. It has been found in this study that the same results can be achieved by giving calcitonin through eyes as ophthalmic solutions. When 25 microliters of 0.05% calcitonin was given as eyedrops to New Zealand white rabbits, it did not reach the concentration achieved by i.v. administration at the same dose level. The systemic absorption of calcitonin did not reach the level achieved by i.v. administration even though the eyedrop concentrations were increased 2-fold (0.1%) to 10-fold (0.5%). When absorption enhancers such as BL-9 and Brij-78 were added to calcitonin eyedrops, however, the systemic absorption of calcitonin was enhanced markedly. BL-9 (0.5%) increased calcitonin (0.5%) absorption 16-20 fold and raised blood concentration of calcitonin above levels achieved by i.v. injection (25 microliters, 0.05%) with 0.5% calcitonin eyedrops instillation. Effects of Brij-78 (0.5%) were even more impressive. It increases calcitonin absorption 22-24 fold and raised the blood concentration of calcitonin above the levels achieved by i.v. injection (25 microliters 0.05%) with 0.15% and 0.5% calcitonin eyedrops instillation. These results indicate that the therapeutic level of calcitonin can be reached through the ocular route.
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PMID:Systemic administration of calcitonin through ocular route. 173 6

The appropriate use of phosphate binders, calcium supplements and especially calcitriol therapy has significantly decreased the incidence of overt secondary hyperparathyroidism in dialysis patients. Nevertheless some patients may still need parathyroidectomy, especially in the event of severe clinical signs and symptoms such as persistent hypercalcemia, pruritus, calcifilaxis, or extensive extra-skeletal calcification. Since aluminum-induced bone disease may resemble hyperparathyroidism in dialysis patients, whenever parathyroidectomy is contemplated the diagnosis of secondary hyperparathyroidism must be firmly established. Thus, a bone biopsy is mandatory prior to parathyroidectomy. It is our experience that once the patient goes to surgery the most important factor in the surgical approach is the presence of a skilled surgeon who has extensive experience in parathyroid gland surgery. The data comparing subtotal parathyroidectomy with total parathyroidectomy and autotransplantation are similar. The most important shortcoming is the lack of long-term follow-up. Recently, new data by several investigators has been advanced reintroducing total parathyroidectomy. Long-term observations in patients who despite total parathyroidectomy still have normal PTH levels are of special interest. In addition, long-term follow-up of these patients has shown that normal plasma calcium and phosphorus levels may be maintained without the use of Vitamin D; this occurred in the presence of active mineralization. However, our major objection to this procedure is the risk of aluminum-induced bone disease. At the present time we feel that the relative high incidence of recurrent hyperparathyroidism following subtotal parathyroidectomy is a reasonable trade off for the risk of aluminum bone disease which may develop in absence of PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroidectomy in chronic renal failure: indications, surgical approach and the use of calcitriol. 221 49

Vitamin D in large doses is a proper therapy in hypoparathyroidism, osteomalacia, vitamin D-resistant rickets and also in chronic renal failure although in those cases the active metabolite of vitamin D is preferred because of the much shorter biologic halflife. Apart from these disorders there are no good reasons for using megadoses of vitamin D. Pseudo-vitamin D intoxication is caused by granulomatous diseases as a so-called inappropriate calcitriol secretion. In cases of vitamin D intoxication the 25-OHD3 content in the serum is much too high, the parathyroid hormone concentration is suppressed and the I,25-(OH)2D3 level is low, whereas in pseudo-vitamin D intoxication the 25-OHD3 content in the serum is normal and the I,25-(OH)2D3 is seriously elevated. Cultured alveolar macrophages of patients with sarcoidosis can produce I,25-(OH)2D3 as can sarcoid lymph node homogenate. I,25-(OH)2D3 proved to promote the fusion of alveolar macrophages to form polykaryons. Local concentrations of I,25-(OH)2D3 may be higher at sites of granulomatous tissue and can act in a paracrine or autocrine fashion to enhance granuloma formation. The action of glucocorticoids and chloroquine in patients with sarcoidosis and hypercalcaemia is presumably an interruption of the described vicious circle.
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PMID:[Vitamin D poisoning; real and spurious]. 223 47

The development of accurate methods for measuring bone density has made it possible to evaluate more effectively methods for the prevention and treatment of osteoporosis. Calcium supplements are not required in early life for people with a normal dietary intake of the substance, but may reduce the risk of fractures in postmenopausal women. The role of oestrogens in the reduction of postmenopausal bone loss is well established. Vitamin D and its metabolites are of doubtful efficacy in this situation and carry the risk of side effects associated with hypercalcaemia. Treatment with sodium fluoride increases bone density, but its effect on the incidence of fractures remains uncertain. Bone rarefaction can be reduced with calcitonin but administration remains a problem. Elderly patients can be effectively treated with anabolic steroids with relatively small risk of long term side effects. Coherence therapy is a promising new approach which has yet to be fully evaluated. There is no doubt that physical exercise reduces bone loss and increases skeletal density.
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PMID:Osteoporosis. 240 51

Squamous cell carcinoma with hypercalcemia and leukocytosis arising from burn scars in a 45-year-old man is reported. Hypercalcemia and leukocytosis improved with pepleomycin treatment and worsened with recurrence of the tumor. Serum levels of parathyroid hormone, prostaglandin E and 25-OH-Vitamin D were within normal limits. Autopsy did not disclose any bone metastases or abnormalities of the parathyroid glands. It is suggested that hypercalcemia and leukocytosis were due to factors produced by the squamous cell carcinoma. This is the fifth reported case of cutaneous squamous cell carcinoma associated with hypercalcemia in the absence of bone metastasis or parathyroid gland abnormalities.
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PMID:Squamous cell carcinoma with hypercalcemia and leukocytosis. 242 67

Vitamin D has complex effects in bone: it stimulates matrix formation and bone maturation but also enhances osteoclastic activity and may influence differentiation of bone cell precursors. Calcitonin inhibits the function of osteoclasts, reducing bone resorption, thus, the combination of vitamin D and calcitonin could result in a positive bone balance. We tested the hypothesis that chronic treatment with high doses of vitamin D (150,000 U/week), moderate doses of salmon calcitonin (120 MRC U/week), and adequate Ca supplementation (1 g/day) could be beneficial in osteoporosis. Thirteen women with postmenopausal osteoporosis received this treatment for 2-6 years (mean 3.5 years). No side effects, hypercalcemia, or hypercalciuria occurred. There was marked reduction in bone pain. The fracture rate in 11 patients with vertebral compression fracture was 240/1,000 patient years, threefold lower than the reported 834 fractures for untreated patients of similar age. Single photon bone densitometry of the radius did not change. Iliac crest bone biopsies obtained at the initiation and conclusion of the study showed a 43% increment in trabecular bone volume (P = 0.0003), without changes of the normal osteoid thickness, surface, and volume. Because single photon densitometry reflects mostly cortical bone, the data suggest that the combination of vitamin D and calcitonin increases trabecular bone mass and prevents the fall of cortical bone mass in osteoporosis. Previous reports suggest that calcitonin alone or with small doses of vitamin D increased bone mass for about 2 years. The present study suggests a prolonged beneficial effect of the combination of high doses of vitamin D with rather moderate (less than 150 MRC U/week) doses of calcitonin in postmenopausal osteoporosis.
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PMID:Effect of calcitonin and vitamin D in osteoporosis. 250 3

Vitamin D ingested in excess results in hypercalcemia, which is caused by excessive absorption of massive quantities of calcium by the intestine and enhanced bone resorption. The symptoms of this intoxication include feeding difficulties, polydypsia, polyuria, irritability, lassitude and poor weight gain. Because daily intakes of 400 IU (10 microg) of vitamin D2 or D3 are completely safe, and because as low as 100 IU (2.5 microg) daily may prevent rickets, it is difficult to justify recent studies that attempt to firmly establish an upper limit of daily vitamin D intake in the normal neonate. Thus, despite efforts to better understand the upper limits of daily vitamin D intake, a concentration of 100 IU (2.5 g) of vitamin D per 100 kcal ingested, as is currently recommended by the Committee on Nutrition of the American Academy of Pediatrics, seems entirely appropriate.
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PMID:Vitamin D: can an upper limit be defined? 269 42

The mammalian fetus is maintained hypercalcaemic relative to its mother by the action of a calcium pump believed to be located at the basement membranes of the epithelial cells of the fetal chorion. It has recently been demonstrated that the activity of this putative pump is stimulated by a new fetal hormone, parathyroid hormone-related protein, described originally as the product of a human BEN cell line which was derived from a lung tumour associated with hypercalcaemia of malignancy. Whereas the circulating level of immunoreactive parathyroid hormone in the fetus is very low, in keeping with the hypercalcaemia, the plasma concentrations of bioactive parathyroid hormone and parathyroid hormone-related protein can be measured using a sensitive cytochemical bioassay and the separate concentrations assessed by pre-incubation with appropriate antisera. The total plasma concentration of both hormones is inversely related to the prevailing calcium ion concentration but the set point of parathyroid hormone-related protein is probably higher than that for parathyroid hormone. Probably as a result of the hypercalcaemia, the circulating concentration of calcitonin is also higher than in maternal plasma and may serve to limit bone resorption to favour net bone accretion as part of the overall growth of the fetus. Vitamin D and its most active metabolite, 1,25(OH)2D, can pass across the placenta in either direction, in contrast to most peptide hormones. In addition to the supply of some 1,25(OH)2D by the mother to her fetus, the fetal placenta and fetal kidneys can all synthesize 1,25(OH)2D. The relative concentrations circulating in maternal and fetal plasma pools vary with the species, presumably as a result of differing importance of the three sources of supply to the fetus and the relative concentrations of vitamin D-binding protein circulating in mother and fetus. The importance of parathyroid hormone-related protein derived from fetal parathyroid glands has been clearly demonstrated in the fetal sheep. Such animals develop rickets following the removal of their parathyroid glands, despite the demonstration of this substance in fetal placental membranes. However, the relative importance of the parathyroid glands versus the placenta and its membranes as the principal source of parathyroid hormone-related protein remains to be elucidated and may vary with species.
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PMID:Development of endocrine pathways in the regulation of calcium homeostasis. 269 50

The effects of WR-2721 [S-2-(3-aminopropylaminoethyl)phosphorothioic acid] in two in vivo and in vitro models of experimental hypercalcemia in the rat were examined. Chronic WR-2721 administration by osmotic minipump (250 mg/kg/24 hr) reduced serum calcium from 12.0 +/- 0.1 to 9.5 +/- 1.0 mg/dl (P less than .01) in rats receiving 1,25-(OH)2 Vitamin D3. Control rats receiving Vitamin D without WR-2721 had a rise in serum calcium to 13.4 +/- 0.2 mg/dl over the same 5-day period. In an experimental form of humoral hypercalcemia of malignancy, the Walker carcinosarcoma tumor-implanted rat, WR-2721 reduced serum calcium from 13.6 +/- 0.3 to 8.4 +/- 0.6 mg/dl by 5 to 6 days (P less than .001). In vitro bone resorption assays utilizing fetal rat long bones in organ culture showed complementary results. WR-2721 (10(-4) M) blocked bone resorption (assayed as percentage of 45Ca release) induced by both conditioned medium derived from cell lines of Walker carcinosarcoma (7.6 +/- 1.4 vs. 24.0 +/- 1.8%, P less than .01) and by addition of 1,25-(OH)2 Vitamin D3 (10(-8) M) (9.8 +/- 0.8 vs. 17.3 +/- 1.0%, P less than .01). These results suggest that WR-2721 may be effective in controlling clinical hypercalcemia due to excess bone resorption.
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PMID:In vivo and in vitro effects of WR-2721 in experimental hypercalcemia in the rat. 301 29


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