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 purpose of the present investigation was to study various aspects of renal bone disease in patients treated at a centre with a low general incidence of symptomatic renal osteodystrophy. In a study of signs of progressive secondary hyperparathyroidism (HPT) in a random sample of patients with chronic renal disease, symptomatic bone disease occurred only in transplanted patients with osteonecroses of major joints. Biochemical and radiographic signs of severe progressive HPT were comparatively infrequent. Hypercalcaemia was the major indication for parathyroid surgery. Normocalcaemic patients on haemodialysis (HD) investigated with dynamic bone histomorphometry showed normal mean bone formation rates. Serum PTH was a major determinant of bone remodelling activity. Histochemical evidence of bone aluminium accumulation was found in the majority, and the trabecular surface extent of aluminium was directly related to indices of defective mineralization. Long-term continuous ambulatory peritoneal dialysis (CAPD) was associated with normocalcaemia and acceptable control of hyperphosphataemia. Serum PTH remained high and radiographic evidence of progressive HPT developed in some patients. Histomorphometrical findings, including signs of aluminium accumulation, were similar to those in HD, indicating that CAPD has no specific effect on renal bone disease. Low serum 25-hydroxycholecalciferol in CAPD could not be related to specific findings regarding histomorphometry. Chronic haemofiltration (HF) was associated with a high risk of calcium loss and hypocalcaemia. Despite decreasing serum calcium serum PTH decreased, and bone biopsy findings indicated decreased skeletal effects of PTH as a further cause of hypocalcaemia. Bone histomorphometry also showed the development of a progressive mineralization defect probably related to calcium deficiency, while trabecular bone aluminium decreased in all patients during HF.
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PMID:Bone disease in renal failure. Clinical and histomorphometric studies. 639 22

Because calcitonin administration has been shown to decrease the serum calcium level in certain hypercalcemic conditions, 10 patients on maintenance dialysis with renal osteodystrophy and persistent hypercalcemia were treated with salmon calcitonin for 3 months. While plasma calcium concentrations were reduced by calcitonin therapy in four patients, therapy was ceased in two patients due to a worsening of their hypercalcemia, although in another two patients the initial worsening of the hypercalcemia settled with continued therapy. No significant changes in calcium levels occurred in the remaining two patients. Analysis of the data suggests that a hypocalcemic effect of calcitonin was most likely in the presence of osteomalacia, while predominant osteitis fibrosa favored a hypercalcemic response. Calcitonin administration caused a mean increase in parathyroid hormone (PTH) secretion 3.6 +/- 1.5 to 6.5 +/- 1.7 ng/ml; p less than 0.05) after 6 weeks of therapy. Three patients reported improvement in their bone pain. These studies show that despite possible symptomatic and morphological effects of calcitonin, its hypocalcemic effect in patients with renal osteodystrophy and hypercalcemia is inconsistent.
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PMID:Effect of calcitonin on hemodialysis patients with hypercalcemia and renal osteodystrophy. 653 90

We treated 24 patients who had chronic renal insufficiency and renal osteodystrophy with either calcitriol (1,25-dihydroxyvitamin D3) or dihydrotachysterol. Renal function was evaluated before and during treatment to determine if these vitamin D analogues caused an accelerated rate of renal function deterioration. An accelerated rate of increase in the serum creatinine level was found in three of 12 patients in each treatment group after therapy was started, but the mean rate of increase during treatment did not differ significantly from the rate during the pretreatment control period in either group. The occurrence of hypercalcemia or an excessive serum calcium x phosphorus-product did not correlate with the rate of change in renal function during treatment with either drug. We concluded that children receiving calcitriol are not at greater risk for an accelerated rate of renal function deterioration than are children treated with dihydrotachysterol. Furthermore, neither vitamin D analogue could be directly implicated as a cause of an accelerated rate of renal function deterioration when episodes of hypercalcemia were transient and occurred infrequently.
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PMID:Vitamin D replacement therapy and renal function. Calcitriol v dihydrotachysterol. 654 70

Patients with predialysis chronic renal failure and bone disease were treated with 1 alpha-hydroxy-derivatives of vitamin D. The observation period consisted of 22 patient years. All patients showed histological improvement of renal osteodystrophy after the initial 6 months of treatment. Bone resorption indices improved most strongly. There was also a considerable decrease of non-mineralized osteoid and no change in the total trabecular bone volume. Hypercalcemia occurred 24 times in 9 patients. Although in general the 1,25-(OH)2-vitamin D serum levels were increased at the time of hypercalcemia, as compared to the preceding non-hypercalcemic period, no elevation above the normal range occurred. In cases of hypercalcemia two different groups of patients, with suppressed and non-suppressed levels of iPTH respectively, could be distinguished. In both groups different significant correlations between serum 1,25-(OH)2-vitamin D and serum calcium levels were found. If serum iPTH was not suppressed hypercalcemia was more severe. It is concluded that the occurrence and severity of hypercalcemia in patients with chronic renal failure during treatment with 1 alpha-hydroxy-derivatives of vitamin D is related to the presence of parathyroid hormone.
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PMID:Follow-up of long-term treatment of predialysis renal bone disease with 1-alpha-hydroxy-derivatives of vitamin D. 668 50

Thirty-seven osteodystrophic and chronically haemodialyzed patients have been treated for 1-22 months by means of 1,25(OH)2D3. Under treatment a marked improvement of symptomatology and radiographic findings has been observed in the majority of cases; from the haematochemical viewpoint a rise of calcemia and phosphoremia, a fall in alkaline phosphatase and a variable course of PTH have been observed. Several episodes of asymptomatic hypercalcemia ceased with posology reduction; only 3 cases needed stopping the treatment for this reason, one of them definitively; 12/37 cases needed hypophosphoric diets and increase in oral aluminium hydroxide doses to control hyperphosphoremia. The Authors conclude that, to achieve a correct management of a 1,25(OH)2D3 therapy for renal osteodystrophy, is mandatory a strict and accurate biochemical control: in this way is possible to obtain an effective modulation of the posology avoiding the appearance of side-effects as hypercalcemia and ectopic calcifications.
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PMID:[Course and significance of various biochemical parameters in 1,25-dihydroxyvitamin D3 therapy of uremic osteodystrophy]. 668 45

Twenty-three patients with end-stage renal failure on maintenance haemodialysis were treated with 1,25-dihydroxy vitamin D3 or 24-25-dihydroxy vitamin D3 for 3-32 months (total 232 patient months). Treatment with 1,25-dihydroxy vitamin D3 was marked by symptomatic, biochemical and histological improvements in the majority of patients. In contrast, treatment with 24,25-dihydroxy vitamin D3 produced no biochemical or histological improvements and such patients developed severe symptomatic bone disease. Successful renal transplantation resulted in rapid improvement in symptoms, biochemistry and bone histology in nine of 10 patients irrespective of whether prior treatment was with 1,25-dihydroxy vitamin D3, 24,25-dihydroxy vitamin D3 or both. During treatment with 1,25-dihydroxy vitamin D3 progressive reduction in dosage was required in the majority of patients because of hypercalcaemia, which was rapidly corrected by stopping treatment for a few days. Hypercalcaemia did not occur until serum alkaline phosphatase (AP) and amino terminal parathyroid hormone (N-PTH) had fallen towards normal. Treatment failure was uncommon in 1,25-dihydroxy vitamin D3-treated patients and was characterized by the early development of hypercalcaemia. Addition of 24,25-dihydroxy vitamin D3 in such patients rendered the hypercalcaemia more manageable but did not lead to any further improvement in biochemistry or bone histology. Treatment with 24,25-dihydroxy vitamin D3 was accompanied by the development of severe symptomatic bone disease in the majority of patients and a characteristic pattern of biochemical abnormalities with hypocalcaemia and rises in AP and N-PTH. Substitution of 1,25-dihydroxy vitamin D3 treatment for 24,25-dihydroxy vitamin D3 in these patients resulted in prompt improvement in clinical, biochemical and histological abnormalities. Successful renal transplantation was accompanied by rapid resolution of clinical, biochemical and histological features of renal osteodystrophy irrespective of whether previous treatment was with 1,25-dihydroxy vitamin D3 or 24,25-dihydroxy vitamin D3. Hypophosphataemia was common in the early months after renal transplantation without evidence of continuing hyperparathyroidism. The studies have confirmed that 1,25-dihydroxy vitamin D3 is effective in controlling clinical, biochemical and histological features of renal osteodystrophy while 24,25-dihydroxy vitamin D3 did not have a useful therapeutic effect in the dose used.
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PMID:Long-term effects of 1,25-dihydroxy vitamin D3 and 24,25-dihydroxy vitamin D3 in renal osteodystrophy. 676 Feb 36

Bone Gla protein (BGP) was measured in the plasma by radioimmunoassay (RIA) during treatment of 59 patients with bone diseases including Paget's disease (N = 9), primary hyperparathyroidism (N = 25), chronic renal failure (N = 20), and cancer involving bone (N = 5). Plasma BGP was increased above normal in all patients. BGP decreased in the patients with Paget's disease following the acute and chronic administration of salmon calcitonin. Plasma BGP was higher in women then in men with primary hyperparathyroidism. Following parathyroidectomy, BGP decreased in both sexes but the decrease was significant in women only. Plasma BGP was increased in patients with renal osteodystrophy and did not change after hemodialysis. In the patients with bone cancer, plasma BGP decreased during treatment of the attendant hypercalcemia with salmon calcitonin. Although plasma BGP and serum alkaline phosphatase (AP) levels were generally correlated in these studies, there were examples of dissociation between the two. The measurement of plasma BGP appears to provide a specific index of bone metabolism that may in some circumstances be more sensitive than serum alkaline phosphatase measurement. However, further studies are necessary to establish the clinical value of plasma BGP measurement by RIA in the management of patients with bone diseases.
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PMID:Changes in plasma bone GLA protein during treatment of bone disease. 680 17

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.
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PMID:Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol. 689 3

We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1 alpha, 25-dihydroxycholecalciferol) lad to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.
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PMID:Vitamin-D-resistant osteomalacia in hemodialysis patients lacking secondary hyperparathyroidism. 689 20

A case of renal osteodystrophy treated with high doses of vitamin D is presented. The treatment, carried out when the patient was between 3 1/4 and 6 years of age, induced hypercalcemia (up to 13.9 mg./dl.) which resulted in dentinal bridging corresponding chronologically to the part of the root developing at this age. Dentinal bridging associated with iatrogenic hypercalcemia has not been reported previously.
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PMID:Calcific bridging of dental pulp caused by iatrogenic hypercalcemia. Report of a case. 693 91


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