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)

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.
Proc Eur Dial Transplant Assoc 1979
PMID:Renal osteopenia - an assessment of long-term therapy with vitamin D analogues. 23 16

Ten patients with renal bone disease have been treated with 1 alpha-hydroxycholecalciferol for periods of 10-18 months. Responses in bone histology, plasma alkaline phosphatase, whole body calcium, spinal calcium content and bone mineral content of the forearm were compared. Improvements in histology of bone were seen in 5 patients. These patients showed greater increases in total body calcium, and the increments in total body calcium correlated significantly with decrements in alkaline phosphatase. Changes in forearm bone mineral content or spinal calcium were less predictable and did not invariably reflect measured changes in whole body calcium. We conclude that total body calcium may provide a useful and early index of response to treatment with 1 alpha-hydroxycholecalciferol. In contrast, skeletal changes noted by regional methods of assessment should not be judged as reflecting changes occurring in the whole skeleton, and may even be misleading.
Proc Eur Dial Transplant Assoc 1977
PMID:Comparison of whole body and regional assessments of calcium balance in renal osteodystrophy in the response to 1 alpha-hydroxy vitamin D3. 60 Sep 60

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.
Proc Eur Dial Transplant Assoc 1977
PMID:Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy. 60 Sep 61

Successful treatment of osteitis fibrosa with 1alpha-hydroxycholecalciferol (1alpha-OHD3) in 9 patients with end-stage chronic renal failure was associated with a significant increase in plasma levels of immunoreactive calcitonin (iCT) independently of changes in plasma calcium, and a decrease in levels of parathyroid hormone (iPTH). In 9 further patients whose plasma alkaline phosphatase activity failed to suppress with 1alpha-OHD3, changes in iPTH were associated with proportionate changes in iCT. This suggests that a rise in endogenous calcitonin (CT) secretion contributes to the success of treatment with 1alpha-OHD3. In 13 further patients, injections of salmon CT induced a fall in plasma calcium and phosphate which was proportional to the prevailing level of plasma alkaline phosphatase. These data provide further evidence that bone resorption can be effectively inhibited when CT levels are raised either by exogenous CT or its endogenous stimulation.
Proc Eur Dial Transplant Assoc 1978
PMID:Biological activity of endogenous and exogenous calcitonin in patients with osteitis fibrosa and chronic renal failure. 74 Jun 83

Three adolescents on regular haemodialysis were treated for more than one year with 1alphaOHD3 in doses of 0.25 - 10 mug/day orally. All the patients had hypocalcaemia, a high serum level of alkaline phosphatase and signs of uraemic osteodystrophy on X-ray. Clinical signs of bone disorder were present in two cases. During the treatment serum calcium and alkaline phosphatase normalised, and there was a marked improvement in the X-ray changes. Clinical improvement also took palce but not to the same extent as indicated by the laboratory data. It seems therefore important that treatment should start before severe bone lesions are present. Careful control of the treatment is necessary to avoid hypercalcaemia.
Proc Eur Dial Transplant Assoc 1976
PMID:Long-term treatment of uraemic osteodystrophy with 1-alpha-hydroxycholecalciferol. 93 14

Four microgrammes of 1-alpha-hydroxycholecalciferol (1-alpha-OH D3) or 200 mug of 25-hydroxycholecalciferol (25-OH D3) were given orally every other day respectively to 10 uraemic patients (8 on chronic haemodialysis) for 1-12 weeks and to 3 patients on chronic haemodialysis for 4-8 weeks. A transilial bone biopsy and serial evaluation of serum immunoreactive PTH (iPTH) calcium phosphate and alkaline phosphatase were performed before and at the end of therapy. Both 1-alpha-OH D3 and 25-OH D3 (the latter at a 50 times higher dose) were able to depress hyperparathyroidism in two-thirds of the cases and to consistently improve the mineralisation defect. In no case did iPTH or the bone histomorphometric parameters return to normal, so that long term evaluation of these two drugs is warranted.
Proc Eur Dial Transplant Assoc 1976
PMID:1 alpha hydroxycholecalciferol and 25 hydroxycholecalciferol in renal bone disease. 93 15

Five patients with haemodialysis bone disease were treated with 1 to 1.5 mug of 1,25 (OH)2D3 daily for periods ranging from 6 -8 months. There was a significant improvement in calcium absorption but no troublesome hypercalcaemia was encountered. Secondary hyperparathyroidism improved, both histologically and radiologically, and there was a fall in serum PTH and return of serum alkaline phosphatase to within normal limits. There was also improvement in the patients' mineralisation status, but this change was slower and less marked. Muscle power improved significantly, both clinically and electromyographically.
Proc Eur Dial Transplant Assoc 1976
PMID:Long term therapy with 1,25(OH)2D3 in dialysis bone disease. 93 16

Intestinal-type alkaline phosphatase (IAP) is a specific and sensitive marker for alterations of the S3 segment of the human proximal tubule, the preferred part for several nephrotoxins. We studied IAP and other renal parameters in mercury-exposed workers and their controls. IAP excretion is clearly increased in the exposed workers, compared to other parameters, indicating that the determination of this enzyme can be a useful screening test of renal effects in occupational mercury exposure.
Nephrol Dial Transplant 1992
PMID:Intestinal-type alkaline phosphatase in urine as an indicator of mercury induced effects on the S3 segment of the proximal tubule. 131 94

The use of oral calcium carbonate as a phosphate binder is often complicated by hypercalcaemia, particularly with concomitant use of vitamin D analogues. We previously found that stepwise reduction of dialysate calcium effectively countered this complication in haemodialysis patients, and have now assessed the strategy in CAPD patients. Seventeen patients underwent conversion from aluminium hydroxide to calcium carbonate and were followed for 5 months, with subsequent addition of alfacalcidol for a further 5 months. Standard CAPD dialysate (1.75 mM calcium) was used, reducing to 1.45 mM and, if necessary, to 1.00 mM in patients who became hypercalcaemic. While receiving calcium carbonate alone, 12 of the 17 patients became hypercalcaemic, this responding in four to dialysate calcium reduction to 1.45 mM. In the remaining eight patients, further reduction to 1.00 mM was required and in two patients even this failed to control hypercalcaemia adequately, necessitating reversion to aluminium hydroxide. Phosphate control remained unchanged, as did calcium x phosphorus product. There were transient increases of blood ionised calcium, and decreases of parathyroid hormone, with progressive reduction of serum aluminium and alkaline phosphatase. The addition of alfacalcidol (0.25 microgram/day) led to hypercalcaemia in six subjects, successfully countered by dialysate calcium reduction in four. The results show that standard CAPD dialysate calcium at 1.75 mM is too high for the majority of calcium carbonate treated patients and that substantial reductions of the dialysate calcium concentration are required if calcium carbonate is to be used effectively.
Nephrol Dial Transplant 1992
PMID:Dialysate calcium reduction in CAPD patients treated with calcium carbonate and alfacalcidol. 131 83

To reduce parathyroid hormone concentrations in uraemic patients refractory or hyporesponsive to calcium supplements and active metabolites of vitamin D, we developed in 1982 a new parathyroid ablative technique consisting of percutaneous fine-needle ethanol injection (PFNEI) into enlarged parathyroid glands under ultrasonic guidance. Fifty uraemic patients have been treated. Decreases in carboxy terminal parathyroid hormone (PTH) were 50% or more in 13 of 50 patients followed up (26%) at 1 month, in 13 of 48 (27%) at 6 months, and in 9 of 25 (36%) at 12 months. Decreases of 30% or more in PTH were obtained in 21 of 50 (42%), in 25 of 48 (52%), and in 15 of 25 (60%). In 'responsive' patients, serum total alkaline phosphatase was significantly reduced [from 579 +/- 645 U/l to 360 +/- 354 U/l (P less than 0.01) at 6 months, and to 273 +/- 311 U/l (P less than 0.01) at 12 months] and bone isoenzyme decreased similarly [from 482 +/- 608 U/l to 256 +/- 344 U/l (P less than 0.005), and to 225 +/- 354 U/l (P less than 0.01)]. The best results were in seven patients who had relapsed after subtotal parathyroidectomy. Declines in PTH of 30% or more were observed in four of seven patients at 1 month, in six of the seven (85%) at 6 months, and in all four patients seen after 12 months. The treatment corrected hypercalcaemia, making it possible to start or to increase daily vitamin D treatment. Side-effects were mild, rare, and transient.
Nephrol Dial Transplant 1992
PMID:Ultrasound-guided percutaneous fine-needle ethanol injection into parathyroid glands in secondary hyperparathyroidism. 132 77


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