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: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Predictive value of plasma levels of bone Gla-protein (BGP) for bone histology was evaluated in 30 chronically dialyzed patients. All patients underwent bone biopsies and serum biochemical parameters, including BGP, parathyroid hormone, and alkaline phosphatase; calcium and phosphate were measured at the time of biopsy. Bone histology showed renal osteodystrophy with low bone turnover and osteomalacia (LT-ROD) in 13 patients, and renal osteodystrophy with high bone turnover and prevailing hyperparathyroid bone disease (HT-ROD) in 17 patients. Values for BGP were above normal in LT-ROD (47.3 +/- 7.9 vs. 6.8 +/- 0.2 ng/ml) and extremely elevated in HT-ROD (831 +/- 170 ng/ml). Similar differences were not found with the other serum biochemical parameters, even though BGP correlated with parathyroid hormone (r = 0.64) and alkaline phosphatase (r = 0.85). There were significant correlations between BGP and cellular and non-cellular parameters of bone formation (r = 0.73 to 0.91). Weaker or no correlations were found between BGP and histologic parameters of bone, reflecting mainly mineralization or resorption. These correlations and the finding of significant differences in plasma BGP between LT-ROD and HT-ROD indicate that plasma levels of BGP reflect bone formation in uremia and predict underlying bone histology.
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PMID:Plasma levels of bone Gla-protein reflect bone formation in patients on chronic maintenance dialysis. 633 5

Seventy-six patients receiving regular haemodialysis, without biochemical or radiological evidence of renal osteodystrophy, entered a five-year double-blind placebo-controlled trial of calcitriol (1,25-dihydroxycholecalciferol) in the prevention of bone disease. Significantly more patients on placebo developed bone disease as judged by a sustained elevation of plasma alkaline phosphatase or the development of sub-periosteal erosions on hand radiographs. Serum parathyroid hormone fell significantly in the patients receiving calcitriol and was significantly lower than in patients receiving placebo. It is concluded that calcitriol delays and may prevent the development of metabolic bone disease in patients receiving regular haemodialysis therapy.
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PMID:Controlled trial of calcitriol in the prevention of bone disease in haemodialysed patients. 634 40

This paper describes a retrospective evaluation of the course of renal bone disease in 14 children undergoing treatment with continuous ambulatory peritoneal dialysis (CAPD) for an average of 11.9 +/- 1.5 months (mean +/- SE). The patients were divided in two groups according to the changes in serum alkaline phosphatase activity during the period of observation: five patients had alkaline phosphatase activity that decreased or was relatively stable (group I), and nine patients exhibited a rising serum alkaline phosphatase activity (group II). Serial radiological examinations showed adequate control of renal osteodystrophy in the patients of group I, whereas the patients of group II had no improvement or worsening of their bone disease. Group I had higher serum calcium and lower parathyroid hormone levels than group II at the end of period of observation despite similar dosage of vitamin D metabolite. The progression of bone disease was not related to the duration of CAPD or type of previous treatment for end stage renal disease. The observation that the radiological manifestations of secondary hyperparathyroidism were prevented in patients whose serum calcium levels were frequently above 2.62 mmol/liter (group I) while serum calcium levels between 2.25 and 2.50 mmol/liter in group II patients failed to lead to regression of secondary hyperparathyroidism is consistent with the existence of altered "set-point" regulation of the parathyroid gland in children undergoing CAPD.
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PMID:Renal osteodystrophy in children undergoing continuous ambulatory peritoneal dialysis. 647 46

Fifty-nine patients with end-stage renal disease undergoing long-term dialysis were studied prospectively for joint disease. Radiographic assessment allowed division of patients into 3 groups: group 1 included 12 patients with renal osteodystrophy and erosions of the metacarpophalangeal, proximal interphalangeal, distal interphalangeal, shoulder, wrist, and knee joints; group 2 had 11 patients with renal osteodystrophy without articular erosions; group 3 included 36 patients without osteodystrophy or erosions. Clinical manifestations were frequent in patients of group 1 and included episodes of arthralgias of the metacarpophalangeal, wrist, proximal interphalangeal, and knee joints. Patients of groups 1 and 2, particularly those of group 1, had a longer mean duration of dialysis and a higher mean serum alkaline phosphatase level compared with group 3 patients. The study indicates that there is a relatively high incidence (20%) of erosive arthropathy in dialysis patients. Renal osteodystrophy, more specifically, secondary hyperparathyroidism, and duration of dialysis are important factors in the development of this articular disorder.
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PMID:Erosive azotemic osteoarthropathy. 648 93

At present, only a few data are available on the effects of continuous ambulatory peritoneal dialysis (CAPD) on renal osteodystrophy. Twelve patients on CAPD were studied for one year, in order to evaluate the progress of renal osteodystrophy. Our results showed a downward trend of plasma calcium, a good control of phosphatemia, a significant increase of alkaline phosphatase and parathyroid hormone. We also found an important decrease of plasma vitamin D metabolites (25(OH)D3 and 1,25 (OH)2D3) and bone mineral content. Bone biopsy showed a general worsening of both secondary hyperparathyroidism and osteomalacia. Thus, we can conclude that CAPD alone is not able to control the evolution of renal osteodystrophy.
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PMID:Progress of renal osteodystrophy during continuous ambulatory peritoneal dialysis. 652 71

Fifteen children undergoing continuous ambulatory peritoneal dialysis for 0.3 to 2.4 years were evaluated longitudinally for renal osteodystrophy. Immunoreactive parathyroid hormone, 25-OHD, total and ionized calcium, inorganic phosphate, and alkaline phosphatase levels were measured regularly. Skeletal radiographic studies were performed at the onset and conclusion of CAPD and at six-month intervals during therapy. All children received 1,25(OH)2D3 and aluminum hydroxide, and nine received supplemental calcium. Plasma 25-OHD concentrations were normal to elevated, and calcium increased steadily to high normal levels despite a trend to persistent hyperphosphatemia. The increased calcium levels suppressed parathyroid hormone overactivity in only one patient. At the onset of CAPD, nine patients had hyperparathyroid bone disease seen radiographically, three of whom also had rachitic lesions. At the end of CAPD, the hyperparathyroid lesions had improved in four patients, completely resolved in three, and deteriorated in two. Rachitic lesions had completely healed in two patients and improved in the third. However, among the six children without radiographically evident lesions at onset of CAPD, hyperparathyroid bone lesions developed in two and rachitic lesions in two others during CAPD. Although CAPD and appropriate therapy benefited most patients with renal osteodystrophy, the benefits were not uniform, and bone lesions deteriorated in some.
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PMID:Renal osteodystrophy in children undergoing continuous ambulatory peritoneal dialysis. 663 99

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

Many hemodialysis patients undergo subtotal parathyroidectomy (sPTx) because of the complications of severe secondary hyperparathyroidism. In some patients, however, renal osteodystrophy fails to regress. In uremia, the high levels of circulating immunoreactive parathyroid hormone (iPTH) which accompany osteitis fibrosa are associated with accelerated bone formation. After sPTx, the fall in iPTH may decrease mineralization and increase osteoid formation. Bone histomorphometry, densitometry, and serum biochemical determinations were done in 20 patients on regular maintenance hemodialysis and after sPTx in 3 additional patients. Densitometry at the radial diaphysis was inversely related to osteoid volume so that low bone mineral content indicated excess osteoid. Elevated serum alkaline phosphatase activity was associated with osteitis fibrosa. Tetracycline double labels identified 5 patients with an increased rate of mineralization. Levels of iPTH and serum phosphorus were positively correlated to the mineralization rate. The fall in iPTH after sPTx was accompanied by a reduction in osteitis fibrosa and decreased mineralization. The nonosteoblastic osteoid became more abundant. After sPTx some hemodialysis patients may convert the osteitis fibrosa to a poorly treatable low turnover osteomalacia.
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PMID:Decreased mineralization in hemodialysis patients after subtotal parathyroidectomy. 680 55

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


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