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)

It has been suggested that post-thyroidectomy hypocalcaemia is related to the presence of a thyrotoxic osteodystrophy for which a high serum concentration of bone alkaline phosphatase is a marker. Changes in serum-calcium (corrected to a standard albumin concentration of 40 g/l), alkaline phosphatase (A.P.), inorganic phosphate, and albumin were studied prospectively in 54 euthyroid patients with drug-treated Graves' disease, and in 17 controls with simple non-toxic goitre, before and serially after partial thyroidectomy. All data were paired and results indicate that the pattern of biochemical change was the same in both types of patient and that the degree of change was not related to the serum-A.P. concentration in the Graves'-disease patients. Of the patients studied within the first 24 h of operation, 5 out of 12 with Graves' disease and raised serum-A.P. (group I), 9 of 20 with Graves' disease and normal serum-A.P. (group II), and 7 of 15 controls (group III) showed a fall in serum-calcium below the lower limit of the reference range. In all three groups there was a highly significant fall in serum-calcium 24 h after operation but there was no significant difference in serum-calcium between the groups either immediately before or 24 h after operation. Serum-calcium returned to pre-surgical concentrations within 7 days of thyroidectomy and serum-A.P. concentrations by 4 to 6 weeks in all groups. There was no evidence that post-thyroidectomy hypocalcaemia is related to thyrotoxic osteodystrophy and the pattern of the biochemical changes was thought to be consistent with release of thyrocalcitonin at operation.
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PMID:Post-thyroidectomy hypocalcaemia: A feature of the operation or the thyroid disorder? 6 27

A significant correlation between the activity of the bone isoenzyme or serum alkaline phosphatase and the urinary hydroxyproline excretion in osteomalacia, osteoporosis, primary hyperparathyroidism with osteodystrophy, Paget's disease, secondary bone tumours, and in a control group was found (P less than 0.001). This close correlation was not observed between these variables in patients with active acromegaly. Diagnosis determined from these indices of formation and turnover of bone matrix agreed with that established by histological and histochemical examination of bone, by X-ray investigation of the skeleton, and by the radionuclear 85Sr test. The relationship between the activity of bone isoenzyme and urinary hydroxyproline excretion differed in metabolic bone diseases with a high bone turnover, in patients with osteoporosis and in patients with early osteoclastic bone metastases.
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PMID:Relationship of the activity of the bone isoenzyme of serum alkaline phosphatase to urinary hydroxyproline excretion in metabolic and neoplastic bone diseases. 10 9

We conducted a 7-month randomized, single, double, single-blind comparison of calcitriol (1,25(OH)2D3) with vitamin D3 in 22 hemodialysis patients to study the effects on the biochemical abnormalities associated with osteodystrophy. Calcitriol was given for 3 mo. All patients had initial prestudy calcium values less than or equal to 9.5 mg/100 ml, and phosphate values less than or equal to 4.5 mg/100 ml. Data were analyzed using the Normalized Trend Index (NTI). Calcitriol induced a rise in calcium (8.7 to 10.25 mg/100 ml) (p less than 0.001) and a fall in alkaline phosphatase (p less than 0.005), while D3 had no appreciable effect. The mean dose of calcitriol during treatment was 0.579 microgram/day while that for D3 was 706 IU/day. The effect on serum phosphate concentration was variable. Hypercalcemia as high as 13.2 mg/100 ml occurred in 2 of 13 patients on 1,25(OH)2D3, but in every instance promptly returned to normal with dose reduction. No other adverse effects were noted with therapy. We conclude that calcitriol reverses the biochemical abnormalities of osteodystrophy. Since its effects are rapidly reversed with discontinuation, the drug is probably safe as well as effective.
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PMID:Calcitriol in dialysis patients. 20 82

In six infants aged between 4 and 8 months with chronic renal failure, we have studied blood levels of calcium (Ca), phosphorus (P), alkaline phosphatase, immunoreactive parathyroid hormone (PTH), and calcitonin (CT), as well as urinary excretion of Ca, P, hydroxyproline and cyclic AMP under basal conditions and during an infusion of 20 mg/kg of 10% Ca gluconate in normal saline over 4 h. Under basal conditions four infants had normal serum Ca and P values, alkaline phosphatase levels at the upper limit of normal, and very high PTH (range: 1450--2550 pg Eq/ml) and CT (range: 700--1900 pg/ml) levels. The urinary Ca excretion was low, whereas the urinary excretion of P, hydroxyproline and cyclic AMP was high. During Ca infusion, the total serum Ca and CT levels increased, PTH fell without however reaching the normal upper limit, and urinary P and cyclic AMP excretion decreased. In two infants with osteodystrophy and the highest levels of PTH (2900 and 3500 pg Eq/ml respectively) there was no suppression of PTH during Ca infusion.
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PMID:Parathyroid hormone and calcitonin secretion in uraemic infants. 21 73

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

Six long-term hemodialysis patients with progressive skeletal deterioration during long-term pharmacologic vitamin D2 therapy were treated for six to 12 months with oral 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) to determine its therapeutic effectiveness in vitamin D2-unresponsive osteodystrophy. On bone biopsy, three of the patients had severe osteomalacia and three showed predominant osteitis fibrosa. Previous therapies, including phosphate binders and dialysis schedules, were maintained. The three patients with osteomalacia and the two with osteitis fibrosa showed clinical deterioration. There was no significant change in serum calcium, phosphate, alkaline phosphatase, bone densitometry, immunoreactive parathyroid hormone levels or bone histology. Roentgenograms showed multiple new fractures of ribs and femoral necks in the patients with osteomalacia and increased bone resorption in two of three patients with osteitis fibrosa. 1,25-(OH)2D3 dosage had to be decreased in all patients because of hypercalcemia with a mean tolerated dose of 0.22 microgram/day. In these patients, 1,25-(OH)2D3 was not effective therapy for progressive osteodystrophy unresponsive to pharmacologic vitamin D2.
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PMID:Experience with 1,25-dihydroxycholecalciferol therapy in undergoing hemodialysis patients with progressive vitamin D2-treated osteodystrophy. 38 92

Five radiologists graded 49 series of bone X-rays of 20 patients with chronic renal failure treated by hemodialysis. There was a high incidence of osteodystrophy which progressed identifiably over intervals exceeding 12 months. The severity grade of osteodystrophy was poorly reproducible among patients, among radiologists, and even between interpretations by the same radiologist after an interval of 10 months. Although the severity of osteodystrophy correlated with serum alkaline phosphatase values, the latter was not an accurate predictor of the severity of the bone lesions. Radiographic reassessment at intervals of one year or less in the asymptomatic patient has less reproducibility than the anticipated changes. More sensitive and reliable techniques are recommended.
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PMID:Inconsistency in radiographic evaluation of progressive renal osteodystrophy. 47 48

The effects of synthetic salmon CT, administered subcutaneously and intermittently (1 MRC U/kg/day for 15 days/month over 6 months) were investigated in 15 uremic patients on regular dialysis treatment (RDT), all presenting various degrees of osteodystrophy. Clinically, osteoarticular pain disappeared in 8 out of 10 cases; 1 patient with rib fractures had a rapid calcification of the bone fracture repair tissue. No significant changes were found in serum calcium and PTH levels. Phosphotemia showed a significant decrease within the first 20 days. The varying individual hypophosphatemic response proved to be related to the initial level of phosphatemia. The alkaline phosphatase, when increased, showed a decrease to the normal range. A significant decrease in osteoclastic hyperactivity (active resorption surface, osteoclast index) and a slight increase in osteoblastic pool (active osteoid surface) were documented. No change was noted when osteomalacia predominated. Side effects included: anorexia, nausea, vomiting, face flushing. Our data suggest that salmon CT may be usefully employed in chronic uremic patients on RDT, when secondary hyperparathyroidism predominates.
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PMID:Effect of calcitonin on bone lesions in chronic dialysis patients. 49 16

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

This paper explores in patients with dialysis osteodystrophy the relationship between clinical features and histological, radiological, and biochemical findings. Eighty-five patients treated by hemodialysis for more than 6 months were studied. The following conclusions were drawn: 1) Bone pain in patients on regular hemodialysis is usually a symptom of developing osteomalacia but not of hyperparathyroidism or osteoporosis. 2) Many patients with histological osteomalacia and radiological features of osteomalacia, such as fractures or Looser zones, have no symptoms. 3)In dialysis patients, biochemical and radiological abnormalities are not a reliable means of predicting the presence of osteomalacia, but a raised serum alkaline phosphatase is a good indicator of the presence of osteitis fibrosa. For early detection of osteomalacia, bone biopsy in necessary. 4)A number of our dialysis patients develop an unusual form of osteomalacia characterized by absent or minimal histological osteitis fibrosa, a normal serum alkaline phosphatase, and a high incidence of myopathy and fractures.
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PMID:Hemodialysis bone disease: correlation between clinical, histologic, and other findings. 68 26


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