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

In 12 uraemic patients with symptomatic secondary hyperparathyroidism, 13 parathyroid hyperplasias, detected by sonography and confirmed by fine-needle aspiration biopsy, were treated by ultrasonically-guided percutaneous injection of absolute ethanol, in order to reduce the gland mass. Only in the larger glands were significant volume reductions recorded, whereas in the smaller ones evident structural changes were observed. In most cases with single lesions, a reduced incidence of vitamin D hypercalcaemia and a permanent improvement in bone alkaline phosphatase and PTH were documented. This technique can be usefully employed either as an alternative to surgery in selected cases, or as support to medical therapy in single lesions.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Ultrasonically guided fine-needle alcohol injection as an adjunct to medical treatment in secondary hyperparathyroidism. 399 88

Vitamin D3 metabolites and iPTH were measured in 26 patients at various times after renal transplantation. Hypercalcaemia (serum Ca greater than 2.62 mmol/L, 14 patients) was associated with hyperparathyroidism (p less than 0.02) and raised 1,25(OH)2D3 (p less than 0.05) but raised 1,25(OH)2D3 was also found in most patients in the normocalcaemic group. Lower 25(OH)D3 concentrations were found in the group with normal 1,25(OH)2D3 compared to the group with elevated 1,25(OH)2D3 (p less than 0.05). Low values of 24,25(OH)2D3 were found in both the normocalcaemic and hypercalcaemic patients (p less than 0.002). Impaired creatinine clearance (less than or equal to 55 ml/min, mean: 38 ml/min) was not associated with reduced 1,25(OH)2D3. No difference in D3 metabolites was found between hypophosphataemic and normophosphataemic patients.
Proc Eur Dial Transplant Assoc 1983
PMID:Vitamin D3 metabolites in hypercalcaemic adults after kidney transplantation. 631 19

Three women on different forms of maintenance dialysis developed persistent steroid-responsive idiopathic hypercalcaemia, with low calcium absorption, severe skeletal decalcification, multiple fractures, and severe clinical problems. Bone histology showed osteomalacia with suppression of osteoblast activity and no hyperparathyroidism. The disease persists at least six months after transplantation. The features are compatible with poisoning by a toxin with many similar properties to aluminium: we only found significant aluminium overload in one of these cases.
Proc Eur Dial Transplant Assoc 1983
PMID:Idiopathic hypercalcaemia of chronic dialysis. 634 38

Osteonecrosis is a frequently disabling complication of renal transplantation. Thirty-one of 244 patients (12.7%), who received cadaver renal transplants from 1968 to 1978 developed an osteonecrosis. An analysis of 14 possible risk factors suggested that only the following were significantly more frequent in the osteonecrosis group: greater than 3 pulse doses of 1.2 g prednisolone, serum creatinine greater than 133 mumol/L, steroid-induced diabetes mellitus and second and subsequent transplantation. An important decline in the incidence of osteonecrosis (26.7 per cent to 6.5 per cent) was seen with prophylactic vitamin D2 treatment and the onset of osteonecrosis was on average one year later. Dangerous side effects of the large doses of vitamin D2 were minimal. Hypercalcaemia due to overdosage with vitamin D2 during simultaneous prednisolone therapy was usually mild and returned to normal in a few days by dose reduction.
Proc Eur Dial Transplant Assoc 1983
PMID:Prevention of osteonecrosis following renal transplantation by using vitamin D2 (ergocalciferol). 636 47

A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.
Clin Exp Dial Apheresis 1983
PMID:Hypophosphatemia-induced hypercalcemia during acute renal failure. 667 51

Al(OH)3 was discontinued in 26 patients on chronic haemodialysis as well as vitamin D metabolites in eight. Oral CaCO3 was progressively increased from 4 +/- 3 to 10 +/- 5g/d to keep plasma PO4 less than 6.0mg/dl and P Ca less than 10.5mg/dl. This treatment had to be discontinued in three cases because of diarrhoea and/or uncontrolled hyperphosphataemia. In the remaining patients the control of hyperphosphataemia and of PTH values was as good or even better. Hyperaluminaemia disappeared in most patients demonstrating the role of oral Al(OH)3 in the induction of hyperaluminaemia. Because of frequent transient hypercalcaemia and of the occurrence of vascular calcification in two patients, high doses of CaCO3 after discontinuation of Al(OH)3 are advised only in cases of hyperaluminaemia.
Proc Eur Dial Transplant Assoc 1983
PMID:Substitution of aluminium hydroxide by high doses of calcium carbonate in patients on chronic haemodialysis: disappearance of hyperaluminaemia and equal control of hyperparathyroidism. 687 65

A 56-year-old man with multiple myeloma and compromised renal function underwent peritoneal dialysis for the treatment of severe hypercalcemia. During dialysis, peritoneal clearances of total calcium, unbound calcium, urea, and creatinine were assessed. Clearances of total calcium (4.8 +/- 0.4 ml/min) and unbound calcium (7.8 +/- 0.5 ml/min) were shown to vary directly with the clearances of urea (15.5 +/- 1.3 ml/min) and creatinine (8.5 +/- 0.8 ml/min). Despite relatively low clearances of all these solutes, during the period of 42 hours, 1,638 mg of calcium was removed in the dialysate and total serum calcium decreased from 17.6 mg/dl to 10.2 mg/dl. Our data indicates that peritoneal dialysis is an effective adjunct in controlling severe hypercalcemia and should be considered when other forms of therapy are inadequate.
J Dial 1980
PMID:Peritoneal dialysis in the treatment of severe hypercalcemia. 744 Aug 44

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.
Nephrol Dial Transplant 1995
PMID:Optimum route of administration of vitamin D in renal failure. 747 47

To assess the effect of the different modes of calcitriol administration on PTH-ionized calcium relationship we conducted a prospective clinical trial in 33 patients on chronic haemodialysis with secondary hyperparathyroidism (four times upper normal limit intact PTH) who were randomly assigned, with stratification to PTH levels, to receive daily oral, intermittent oral, or intermittent intravenous calcitriol at the same dose of 0.045 micrograms/kg/weekly. PTH-iCa curves were generated by inducing hypo- or hypercalcaemia in sequential haemodialysis 1 week apart, before and after 10 weeks on treatment. All patients were dialysed against a dialysate calcium concentration of 2.5 mEq/l throughout the study period. After drop-outs, 26 patients completed the study: 11 on intravenous calcitriol (mean basal PTH +/- SD: 666 +/- 280 pg/ml), eight on intermittent oral calcitriol (mean basal PTH: 831 +/- 361), and seven on daily oral calcitriol (mean basal PTH: 719 +/- 280). Serum ionized calcium and phosphorus significantly increased in intravenous and daily oral groups after calcitriol treatment, but not in the intermittent oral group. Basal PTH did not significantly change in the three groups after 10 weeks on treatment. Maximal PTH significantly decreased in intravenous group (1449 +/- 660 versus 1122 +/- 691 pg/ml, P = 0.0085) and at the limit of statistical significance in the intermittent oral group (1701 +/- 774 versus 1445 +/- 634, P = 0.12), but it did not change in the daily oral group. Minimal PTH did not modify in the three groups. In all three groups, a shift to the right in the PTH-iCa relationships were observed, with significant changes in the set point of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1995
PMID:Effect of the mode of calcitriol administration on PTH-ionized calcium relationship in uraemic patients with secondary hyperparathyroidism. 756 80

We evaluated the effect of pulse oral calcitriol (4 micrograms three times weekly for 6 months) on parathyroid function in nine CAPD patients with hyperparathyroidism refractory to conventional low-dose oral calcitriol. Zero calcium peritoneal solutions were used to prevent the development of hypercalcaemia. The peritoneal loss of calcium increased from 168 +/- 40 to 417 +/- 48 mg/day using zero calcium solutions. Pulse oral calcitriol resulted in a significant decrease in PTH (from 617 +/- 272 to 382 +/- 299 pg/ml) by the 15th day of therapy, while serum iCa did not change from baseline. During the first month of therapy the mean PTH levels remained significantly reduced compared to baseline, thereafter PTH increased in four of nine patients. Hyperphosphataemia was not satisfactorily controlled in four patients, despite large amounts of binders used; seven of nine patients developed hypercalcaemia and required either the substitution of calcium acetate for calcium carbonate or reduction of calcitriol dose. Three patients showed a progressive increase in PTH. In conclusion our data suggest that in most CAPD patients with severe hyperparathyroidism oral calcitriol pulse therapy is not effective in maintaining a permanent suppression in PTH levels.
Nephrol Dial Transplant 1994
PMID:High-dose oral calcitriol and zero calcium peritoneal solutions in CAPD patients with refractory secondary hyperparathyroidism. 770 73


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