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)

An oral dose of 0.5 microgram of 1,25-dihydroxycholecalciferol (1,25-[OH]2D3) and 4 g of calcium carbonate was given daily to two dialysed patients and three undialysed patients in chronic renal failure with renal osteodystrophy. Treatment was given for 4-16 months. Intestinal calcium absorption became normal in all five patients. Plasma alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone were considerably reduced in all of the patients and in four of them these values were restored to normal. Bone histology was improved in all patients after treatment with 1,25-(OH)2D3. As well as a dramatic improvement in bone mineralisation, there was remodeling of trabecular architecture and a decrease in fibrosis in patients with initial parathyroid overactivity.
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PMID:Long-term effects of small doses of 1,25-dihydroxycholecalciferol in renal osteodystrophy. 7 68

The effect of propranolol upon parathyroid hormone (P.T.H) concentrations was investigated in patients undergoing chronic haemodialysis. 9 patients receiving propranolol for the treatment of hypertension or angina pectoris were compared with 25 similar patients not taking the drug. P.T.H. and alkaline phosphatase concentrations were lower in patients receiving propranolol and there was less radiological evidence of renal osteodystrophy in these patients. Prospective studies are needed to determine whether propranolol may be helpful as an adjunct to other therapy in reversing or preventing renal osteodystrophy.
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PMID:A possible role for propranolol in the treatment of renal osteodystrophy. 7 9

Renal bone disease was assessed for an average of 5.5 years in 9 patients on maintenance haemodialysis. The investigative methods included serial biochemical estimations, radiographic skeletal surveys and quantitative bone histology. Repeated bone mineral analyses and neutron activation analyses of a hand were also performed in order to monitor changes in skeletal calcium content. Before treatment, progressive osteodystrophy was demonstrated by all techniques. Following therapy with the vitamin D analogues, all patients noted symptomatic improvement; serum alkaline phosphatase reverted to normal and serum parathyroid hormone concentrations decreased. Radiographically, subperiosteal erosions healed while the histological features of osteomalacia and osteitis fibrosa were abolished. Both bone mineral and neutron activation analyses indicated that progressive skeletal demineralisation had been halted. However, a sustained increase in the overall mineral content of bone was not demonstrated. Thus, vitamin D therapy although improving the biochemical, radiological, and histological features of renal osteodystrophy may not restore bone mass to osteopenic bone.
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PMID:Renal osteopenia - an assessment of long-term therapy with vitamin D analogues. 23 16

Two children suffering from renal osteodystrophy were treated by 1 alpha hydroxycholecalciferol (1 alpha OHD3) 1 microgr. each day, for 18 months. In both the level alkaline phosphatase decreased at the same time as endogenous immunoreactive CT increased, iPTH did not change steadily, whereas plasma creatinine rise. As plasma calcium concentration did not increase, it is suggested that the increase in endogenous CT concentration is a part of the favourable response to the treatment by 1 alpha OHD3.
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PMID:[Renal osteodystrophy in two children : a comparison of the effects of 1 alpha-hydroxycholecalciferol (author's transl)]. 47 7

The effects of 25-OHD3 on renal osteodystrophy have been studied in 6 patients on maintenance haemodialysis. Administration of 25-OHD3, 50 microgram/day, did not improve biochemical data and intestinal absorption of calcium. With a dose of 100 microgram/day in all patients an increase in blood calcium levels eventually reaching hypercalcemic values was observed. In two cases a fall in alkaline phosphatase toward normal values was noted. In the same cases the treatment-induced hyperphosphatemia, uncontrolled by AI(OH)3 supplementation and similarly high iPTH levels were observed. In two cases repeated bone biopsy following 8 months treatment and not show substantial improvement of bone lesions. In one case addition of 1,25-(OH)2D3 to the treatment with 25-OHD3 led to a more rapid improvement in biochemical parameters and iPTH serum levels. Doses of 25-OHD3 capable to correct blood calcium levels and intestinal absorption of calcium, may have minimal benefit on the osteitis fibrosa component of the bone lesion.
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PMID:25-hydroxycholecalciferol in the treatment of renal osteodystrophy in haemodialysed patients. 51 68

9 patients with advanced renal failure and renal osteodystrophy documented by iliac crest biopsy were treated with 1,25-dihydroxycholecalciferol (average dose 0.53 micrograms per day) for 6 months. Under 1,25-DHCC there was a statistically significant increase in serum calcium and decrease in serum alkaline phosphatase and immune parathyroid hormone. Histomorphometric evaluation of posttreatment bone biopsies showed reduction of osteoclastic resorption and endosteal fibrosis. Osteoid volume decreased in most cases. In 3 patients with predominant fibroosteoclasia, bone turnover practically normalized. Bone mineral content of the radius (photoabsorptiometry) did not change with treatment. Transient hypercalcemia occurred in 5 patients and was easily corrected by adjustment of 1,25-DHCC dosage.
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PMID:[Effect of 1,25-dihydroxycholecalciferol in renal osteopathy]. 53 67

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.
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PMID:Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy. 60 Sep 61

Ten patients with renal osteodystrophy were treated with 1alpha-hydroxyvitamin D3 for 18 months. The effect of treatment was measured by a number of different methods and bone mass assessed by mineral and neutron activation analysis. In the majority of patients, raised serum levels of parathyroid hormone and alkaline phosphatase, histological features and radiological changes returned to normal. These effects were inconsistent in patients with a raised serum calcium level before starting treatment. In general, in patients without evidence of severe hyperparathyroidism there was a reduction in the rate of fall or an increase in the mineral and calcium content of the bone.
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PMID:The effect of 1alpha-hydroxyvitamin D3 on calcium and mineral content of bone in renal osteodystrophy. 60 11

During treatment of renal osteodystrophy with 1alpha-hydroxyvitamin D3 in eleven patients, regional changes in the skeleton have been compared with long-term calcium balance as assessed by whole-body calcium. Radial bone changes did not correlated well with calcium balance, but spinal calcium changes were of a similar magnitude when changes were large. Bone alkaline phosphatase changes correlated well with changes in spinal calcium, but less well with changes in radial bone density.
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PMID:Spinal calcium changes with 1alpha-hydroxyvitamin D3. 60 12

Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.
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PMID:The effect of 1alpha(OH)D3 and 1alpha,25(OH)2D3 on the bone in patients with renal osteodystrophy. 62 25


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