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)

Skeletal uptake of diphosphonate was measured by emission tomography in 30 patients on chronic dialysis treatment. In 19 patients mean plasma aluminium concentrations, measured over the preceding 12 months, were 'high' (greater than 1.0 mumol/l, and in the other 11 were 'low' (less than 1.0 mumol/l). There was a strong correlation between serum alkaline phosphatase and skeletal uptake of diphosphonate in each group, but no difference in diphosphonate uptake between the groups. Additionally, when six patients with positive desferrioxamine tests were matched for serum alkaline phosphatase with six patients from the 'low' aluminium group there was no significant difference in uptake of diphosphonate (median and range 7.2; 5.2-16.5 and 5.9; 2.7-10.8 respectively). We conclude that skeletal uptake of diphosphonate is not suppressed in patients with moderate aluminium loading, but reflects bone turnover as indicated by serum alkaline phosphatase. Quantitative bone scintigraphy is not a useful discriminator for early aluminium osteomalacia.
Nephrol Dial Transplant 1989
PMID:Quantitative bone scanning in the diagnosis of aluminium osteomalacia. 251 81

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
Nephrol Dial Transplant 1989
PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Since 1980, moderately large doses of oral calcium (80 +/- 35 mmol/day as CaCO3 +/- calcium polystyrene sulphonate), in association if necessary with Mg(OH)2 (2.5 +/- 1 g/day), with a reduction in the dialysate Mg concentrations from 0.75 to 0.375 mmol/24 h, have replaced A1(OH)3 as phosphate binders in our centre. A1(OH)3 was previously given to our haemodialysis patients in association with small doses of Ca CO3 (less than or equal to 3 g/day) and if necessary with 1 alpha OH vitamin D3. To compare the long-term efficacy of this new approach with the former one in the prevention of renal osteodystrophy and soft-tissue calcification, 32 current patients were selected on the basis of at least 24 months of treatment in our centre and availability of a yearly bone survey (profile of lumbar spine and anteroposterior view of the pelvis, shoulders and hands). A group of 30 patients treated before 1980 were then selected on the same criteria and matched for age, sex, and duration on dialysis. Linear calcifications of the anterior and posterior walls of the aorta in front of L2, L3, L4 and on the lateral walls of the iliac and femoral arteries were measured and the para-articular calcifications and subperiosteal resorptions of the hands evaluated. The initial extent and the subsequent increase of the ocular and para-articular calcification were comparable in the two groups. Plasma alkaline phosphatase was stable in the normal range in both groups, as was plasma concentration of calcium. Plasma phosphate was slightly elevated (1.7 mmol/l) but stable and comparable in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1989
PMID:Prevention of osteitis fibrosa, aluminium bone disease and soft-tissue calcification in dialysis patients: a long-term comparison of moderate doses of oral calcium +/- Mg(OH)2 vs Al(OH)3 +/- 1 alpha OH vitamin D3. 251 25

The elective conversion of renal allograft recipients from cyclosporin (CsA) to azathioprine and prednisolone has the advantage that the long-term risk of CsA nephrotoxicity is reduced, but it may precipitate a rejection episode. We have monitored this period by fine-needle aspiration cytology (FNAC) in 24 patients undergoing conversion of immunosuppression 6 months after transplantation. As expected the serum creatinine and alkaline phosphatase were significantly reduced and the mean creatinine clearance was significantly increased after conversion. FNAC exhibited increased mononuclear cellular infiltration in 13 of the 24 patients. In nine patients there was a transient infiltration of lymphocytes and monocytes without changes in the normal parameters of renal function. In four others 'blast' cell infiltration was evident in association with rejection episodes. All four responded to pulsed doses of methylprednisolone. However, two other patients had late rejection episodes (2 and 6 months after conversion) which were steroid resistant and required reintroduction of CsA. No grafts were lost (median follow-up 9 months). This study has shown that although overt rejection occurred in only 16.6% of patients, cellular infiltration was present in over 50% during conversion of immunosuppression. FNAC failed to identify clearly the patients at risk of rejection during conversion of therapy.
Nephrol Dial Transplant 1988
PMID:Fine-needle aspiration cytology monitoring of elective conversion from cyclosporin to azathioprine and prednisolone. 314 Jan 33

To control hyperphosphataemia without hyperaluminaemia, A1(OH)3, which was given in addition to high doses of oral calcium, was replaced by Mg(OH)2 for 6 months in 20 haemodialysed patients and for 20 months in 12. The treatment during the control period was 110 +/- 91 mmol/day of oral calcium element given as CaCO3 and/or Calcium Sorbisterit and 1.05 +/- 1.47 g/day of A1(OH)3. Haemodialysis treatment was 4 h, thrice weekly. To prevent hypermagnesaemia, dialysate magnesium was decreased from 0.75 mmol/l to 0.375 mmol/l. After a control period of 3 months, Mg(OH)2 was given at a mean dose of 2.6 +/- 2 g/day and oral calcium supplements were decreased to 76 mmol/day. Two subsequent bone histomorphometry studies were performed at 8 month intervals in four patients and at 20 month intervals in seven patients. The results show a good control of plasma calcium (mean +/- SD: 2.43 +/- 0.1 mumol/l); phosphate (1.76 +/- 0.4 to 1.66 +/- 0.3 mmol/l); aluminum (1.3 +/- 0.1 mumol/l to 0.6 +/- 0.1 mumol/l); alkaline phosphatase (135 +/- 65 to 125 +/- 40 IU); and PTH fragments (PTH C terminal decreased from 260 +/- 214 to 185 +/- 182 pg/ml, PTH medium from 4185 +/- 5113 to 2270 +/- 4880 pg/ml). Plasma magnesium increased from 0.96 +/- 0.2 to 1.54 +/- 0.2 mmol/l. Bone histomorphometry shows no change in mineralisation, and a borderline decrease of resorption parameters. The main side-effects are (1) diarrhoea, which was well controlled by transient treatment with karaya gum, and (2) an increased need for potassium binders.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1988
PMID:Magnesium hydroxide as a complementary aluminium-free phosphate binder to moderate doses of oral calcium in uraemic patients on chronic haemodialysis: lack of deleterious effect on bone mineralisation. 314 23

Twenty-seven patients on chronic haemodialysis were investigated for a mean of 4.8 years (3.0-6.5 years). Mean bone mineral content fell constantly and similarly at a rate of three to four per cent per year in both centre (n = 14) and home (n = 13) haemodialysis patients. Mean serum values of 25(OH)D3 (normal), 24,25(OH)2D3 (decreased to half the normal level and 1,25(OH)2D3 (severely decreased and almost non-detectable) were similar in patients with a rapid bone mineral content loss (greater than 10%/3 years) and a slow bone mineral loss (less than 10%/3 years). Mean serum parathyroid hormone was markedly elevated, but significantly higher (about twice the level) in the 'rapid losers' than in the 'slow losers'; whereas the two groups did not differ with regard to mean serum concentrations of calcium, phosphate and alkaline phosphatase.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Bone mineral loss during centre and home haemodialysis. Influence of vitamin D metabolites and serum parathyroid hormone. 399 37

In 42 uraemic patients radiological skeletal survey, biochemistry and bone histology were compared before and at 6-12 months (42 patients), 12-24 months (26 patients) or 24-48 months (12 patients) after parathyroidectomy. The presence of small vessel or non-visceral soft tissue calcification was not related to the age, sex, duration of end-stage renal failure treatment, total serum calcium, magnesium, phosphate, Ca x P product, alkaline phosphatase, ionised calcium, serum aluminium, iPTH, severity of radiological and histological osteitis fibrosa or parathyroid gland weight. Twenty-three patients (55%) had small vessel and 20 (48%) soft tissue calcification before parathyroidectomy. Despite a marked improvement in subperiosteal erosions (37 healed, 5 improved) and healing of osteitis fibrosa histologically, seven patients developed new and six developed increased peripheral arterial calcification while in 10 patients non-visceral soft tissue calcification disappeared and in two decreased. Successful parathyroidectomy improves non-visceral calcification but not arterial calcification despite reduction in Ca x P product and iPTH.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Ectopic calcification. The role of parathyroid hormone. 399 87

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

We have studied the effects of desferrioxamine (DFO) or successful renal transplantation on eight patients identified as having aluminium associated bone disease. All patients showed dramatic subjective improvement in their bone pain and/or fractures. All histological parameters studied improved, with the more normal bone being found in the transplanted patients. Bone aluminium fell by at least 50 per cent. Biochemically, increased bone activity was indicated by a rising alkaline phosphatase. This was particularly marked in the DFO treated group who tended to show the development of hyperparathyroidism.
Proc Eur Dial Transplant Assoc 1983
PMID:The efficacy of various treatment modalities on aluminium associated bone disease. 634 35

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.
Proc Eur Dial Transplant Assoc 1983
PMID:Controlled trial of calcitriol in the prevention of bone disease in haemodialysed patients. 634 40


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