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

Six long-term hemodialysis patients with progressive skeletal deterioration during long-term pharmacologic vitamin D2 therapy were treated for six to 12 months with oral 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) to determine its therapeutic effectiveness in vitamin D2-unresponsive osteodystrophy. On bone biopsy, three of the patients had severe osteomalacia and three showed predominant osteitis fibrosa. Previous therapies, including phosphate binders and dialysis schedules, were maintained. The three patients with osteomalacia and the two with osteitis fibrosa showed clinical deterioration. There was no significant change in serum calcium, phosphate, alkaline phosphatase, bone densitometry, immunoreactive parathyroid hormone levels or bone histology. Roentgenograms showed multiple new fractures of ribs and femoral necks in the patients with osteomalacia and increased bone resorption in two of three patients with osteitis fibrosa. 1,25-(OH)2D3 dosage had to be decreased in all patients because of hypercalcemia with a mean tolerated dose of 0.22 microgram/day. In these patients, 1,25-(OH)2D3 was not effective therapy for progressive osteodystrophy unresponsive to pharmacologic vitamin D2.
 ...
PMID:Experience with 1,25-dihydroxycholecalciferol therapy in undergoing hemodialysis patients with progressive vitamin D2-treated osteodystrophy. 38 92

Maximal tubular phosphate reabsorption capacity corrected for changes in glomerular filtration rate (TmP/GFR) was taken as a measure of renal phosphate handling in patients with good and stable functioning kidney allografts. TmP/GFR values were within the normal range in only one-fifth of the patients. Eighty per cent had an abnormally low renal phosphate threshold concentration. Persistent hyperparathyroidism was the causative factor of this diminished tubular reabsorption in less than half of these patients, the majority of them showing an iPTH independent phosphate leak. Although glucocorticoids, azathioprine and tubular damage of the graft in the perioperative phase may contribute to this iPTH independent phosphate wasting, no single causative factor could be identified. Cases with hypophosphataemia should be treated in order to avoid symptoms of phosphate depletion. Active Vitamin D metabolites would be the therapy of choice by suppressing the parathyroid glands ("chemical PTX") and by directly enhancing tubular phosphate reabsorption. In persistent hyperpathyroidism with hypercalcaemia, surgical parathyroidectomy must be considered. Therapy with phosphate salts is only symptomatic and should be used only as an adjunct.
 ...
PMID:Handling of phosphate by the transplanted kidney. 39 23

Disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) is known to inhibit the crystallization of calcium phosphate salts in vitro. Large doses of EHDP administered in vivo inhibit skeletal mineralization, decrease intestinal calcium absorption, and produce hypercalcemia. In the present study, EHDP or one of 13 other phosphonates were given to rats at 10 mg P/kg-day sc for 7 days in order to better define the nature of the relationship between bone mineralization, intestinal absorption, and plasma calcium in the regulation of calcium homeostasis. Each of the phosphonates which inhibited skeletal mineralization in vivo also inhibited crystallization in vitro, but the converse was not true. A very close correlation was found between inhibition of skeletal mineralization, decreased intestinal calcium absorption, and slight hypercalcemia. A dose-response study with two compounds also revealed the same close correlation. It is argued that the impairment of intestinal calcium absorption in phosphonate-treated rats may represent a secondary homeostatic response to the primary effect of the drugs on bone mineralization. This response may be mediated by an elevation of a fraction of plasma calcium.
 ...
PMID:Relation between bone mineralization, Ca absorption, and plasma Ca in phosphonate-treated rats. 40 23

There are conflicting reports on the effect of insulin on plasma Ca concentration in rats. Low doses appear to decrease and higher doses to increase plasma Ca. Since birds are known to be very sensitive to parathyroid hormone and have resistance to the hypoglycemic effects of insulin, the effect of commercial and highly purified insulin on plasma Ca concentration was studied in 10-day-old chicks 60 min after the administration of the hormone. Both commerical bovine and purified porcine insulin provoked a dose-related elevation of plasma Ca. Although hypophosphatemia was observed with the highest dose of insulin used (0.4U), hypercalcemia was observed with 0.05 U insulin, a dose that did not modify plasma phosphate concentration. The slopes of the dose-response curves of insulin and parathyroid hormone were indistinguishable and different from that of 1 alpha-hydroxyvitamin D3. Neither propranolol nor deprivation of vitamin D altered the hypercalcemic response to insulin. Unexpectedly, propranolol (40 microgram/chick) provoked elevation of plasma Ca. It is concluded that insulin raises plasma Ca concentration in the chick by a mechanism(s) not yet elucidated.
 ...
PMID:Hypercalcemic effect of insulin in the chick. 44 96

We studied weanling rats fed 0.06% (group 1) and 0.10% (group II) magnesium (Mg) during phosphate depletion (PD) in order to evaluate the role of Mg in the bone, soft tissue, and serum changes of PD. The following results were obtained: 1) serum Mg remained stable in the face of a negative Mg balance; 2) the hypercalcemic and hypercalciuric response to PD was the same in both groups; 3) bone Mg content was decreased with PD in both groups and was associated with a significant decrease in bone calcium and phosphorus. We conclude that: 1) the hypomagnesemia of PD is dependent mainly on the dietary intake of Mg; 2) the hypercalcemia and hypercalciuria of PD are not caused by primary changes in Mg homeostasis; 3) low-dietary Mg during PD may cause a defect in soft tissue utilization of P in the growing rat.
 ...
PMID:Influence of dietary magnesium in experimental phosphate depletion: bone and soft tissue mineral changes. 46 91

The effects of phosphate restriction and of 1 alpha OH D3 administration were investigated in patients with advanced chronic renal failure. Few modifications of the various biochemical parameters in the patients were achieved with the restriction of dietary phosphate while better results were obtained with 1 alpha OH D3 administration. In dialyzed patients the treatment with this drug resulted in a normalization in serum calcium and alkaline phosphatase levels and in a remarkable significant decline in plasma parathyroid hormone and a reduction in the bone disease associated with uremia. This treatment in dialyzed uremic patients could avoid the employment of higher dialysate calcium concentration potentially dangerous for postdialysis hypercalcemia with the risk of metastatic calcifications.
 ...
PMID:Effects of 1-alpha OH D3 therapy in uremic patients in conservative or dialytic treatment. 47 81

Malignant disease and primary hyperparathyroidism are the most common causes of hypercalcemia, but there are many minor causes. Mechanical or humoral factors, or both, may underlie the increase in bone resorption. Parathyroid hormone (PTH) is a major mediator of bone resorption, but many other humoral agents have the same effect, eg, prostaglandin, osteoclast-activating factor, and thyroid hormone. Serial determination of total calcium concentration is the most important laboratory test in hypercalcemia. Other useful tests include the determination of serum and urinary phosphorus concentration, chloride/phosphate ratio, urinary cyclic adenosine 3',5'-monophosphate (cAMP) level; carboxyl-terminal PTH assay; corticosteroid challenge; and appropriate radiologic studies. Nephrogenous cAMP and urinary prostaglandin determinations are research tools that hold great promise in the future. Differentiation between PTH- and non-PTH-mediated hypercalcemia determines subsequent steps in diagnosis and treatment.
 ...
PMID:Differential diagnosis of hypercalcemia: a mechanistic approach. 48 78

Serum chloride and phosphate concentrations were measured in 79 hypercalcemic patients. The chloride values were higher (mean 106.7 mEq/l) and phosphate lower (mean 2.08 mg/100 ml) in the 53 hyperparathyroid patients, where as the chloride concentrations were lower (mean 99.3 mEq/l) and phosphate higher (mean 4.07 mg/100 ml) in the 26 patients with hypercalcemia from other causes. The chloride phosphate ratio ranged from 19 to 32 in the subjects with hypercalcemia from other causes with 90 per cent of values less than 30. In patients with primary hyperparathyroidism we found 96 per cent of the values more than 34. From our experience with chloride phosphate ratio it seems to us that this ratio is a very useful and simple preliminary test for distinguishing patients with primary hyperparathyroidism from patients with hypercalcemia from other causes, with normal renal functions.
 ...
PMID:The chloride phosphate ratio as the screening test for primary hyperparathyroidism. 52 Oct 12

In male Wistar rats, 1 alpha-HCC and 1 alpha, 25-DHCC induced diuretic effects in doses of 2.5 and 25 micrograms/kg p.o., while no such effects of 1 alpha-HCC were seen with a dose of 0.25 microgram/kg p.o. Effect of 1 alpha-HCC appeared later than that of 1 alpha, 25-DHCC, but at 24 hr, the difference disappeared. Similar results were obtained with urinary concentrations of calcium (increase) and phosphorus (decrease). Glomerular filtration rate (GFR) and tubular reabsorption of phosphate (TRP) were remarkably elevated by 1 alpha, 25-DHCC, and effects of 1 alpha-HCC were rather weak and apparently not dose dependent. In light of these results and the finding that there was no difference between the effects of 1 alpha-HCC and 1 alpha, 25-DHCC on serum calcium and phosphorus at 24 hr, the mechanism of action of these sterols on the renal function seems to differ. In male Beagle dogs, 0.25 microgram/kg/day p.o. of 1 alpha-HCC or 1 alpha, 25-DHCC induced a severe hypercalcemia and GFR was decreased in the 1 alpha, 25-DHCC treated group. A gradual recovery occurred with cessation of the administration. Thus decrease in GFR was considered to be due to calcification of the kidney.
 ...
PMID:[Studies on biopharmacological actitivy of active vitamin D3 analogues (VII) Effect of 1 alpha-hydroxycholecalciferol on renal function in rats and Beagle dogs (author's transl]. 54 Aug 87

A chronic hypercalcaemia was induced in Suncus murinus by the daily subcutaneous injections of parathormone for 15 days. Serum calcium increased 4 hours after the first injection (+ 0.88 mg/100 ml), it reached its highest value on day 10 (+ 2.18 mg/100 ml), and then decreased slightly at the end of the experiment (day 15). The serum phosphate level in treated animals showed a progressive fall throughout the experiment. Serial sections of thyroid-parathyroid complex were subjected to selective staining for C cells identification. The chronic hypercalcaemia increased the number of C cells. This was supported by the presence of mitotic figures. Degranulation of the secretory material was observed as the result of the chronic hypercalcaemia; degenerative changes were found in some C cells. The chronic hypercalcaemia also inhibited the activity of parathyroid "Chief-Cells" which ultimately degenerated.
 ...
PMID:Influence of parathormone on C cells, parathyroid glands, serum calcium and serum phosphate levels in the house shrew, Suncus murinus. 55 38


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>