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)

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.
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PMID:Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol. 689 3

We describe a sporadic, vitamin-D-resistant osteomalacic syndrome in 19 patients undergoing hemodialysis. The syndrome was found in less than 1.5% of patients from referring dialysis centers. All 19 patients had multiple fractures, severe myopathy, and many developed spontaneous hypercalcemia. Severe osteomalacia without evidence of secondary hyperparathyroidism distinguished this syndrome from other forms of renal osteodystrophy. Bone aluminum, measured in six patients, was greatly elevated. Therapy with calcitriol (1 alpha, 25-dihydroxycholecalciferol) lad to clinical improvement in seven patients with reduced pain and myopathy, decreased serum alkaline phosphatase, or both, but no improvement in bone histology. Patients who did not respond clinically to calcitriol developed marked hypercalcemia. The cause of this severe osteomalacia, which occurs despite normal or slightly elevated levels of serum calcium and phosphorus and fails to mineralize with calcitriol, is unclear.
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PMID:Vitamin-D-resistant osteomalacia in hemodialysis patients lacking secondary hyperparathyroidism. 689 20

To confirm and extend previous observations of enhanced linear growth in children with chronic renal disease being treated with 1,25-dihydroxyvitamin-D3 and to characterize further the calcium, phosphorus, magnesium, and zinc disorders in renal failure, 11 children (mean age 8 +/- 5 years) with chronic renal insufficiency (glomerular filtration rate 18% +/- 13% of normal) were evaluated on the basis of their reciprocal serum creatinine concentrations, height-velocity curves, mineral balances, and radiologic findings. Reciprocal serum creatinine concentrations analyzed retrospectively and prospectively during 32 months of 1,25-dihydroxyvitamin-D3 therapy showed progression of renal failure at rates linearly identical with those before treatment, thus suggesting that the treatment did not accelerate the rate of deterioration of glomerular filtration rate in chronic anal insufficiency. Indeed, one patient manifested a lesser decline in renal function (P less than .05). The height velocity of six of the children (75%) less than 12 years of age improved markedly over that expected for chronologic and bone ages after one year of treatment with orally administered 1,25-dihydroxyvitamin-D3, 15 to 35 ng/kg/day. All other medications except vitamin D2 were continued at their pretreatment dosage levels throughout the study. Growth velocity was unimproved in two of three children older than 12 years at the initiation of 1,25-dihydroxyvitamin-D3 therapy. Mineral balance data showed significant retention of calcium, phosphorus, magnesium, and zinc (357 +/- 32 mg/sq m/day, 250 +/- 82 mg/sq m/day, 38 +/- 32 mg/sq m/day, and 1,157 +/- 283 microgram/sq m/day, respectively), after treatment for 12 months. In addition, serum calcium, alkaline phosphatase, and parathyroid hormone concentrations returned toward normal. Finally, healing of renal osteodystrophy was radiologically evident after six months of therapy.
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PMID:Effects of 1,25-dihydroxyvitamin-D3 on renal function, mineral balance, and growth in children with severe chronic renal failure. 689 62

gamma-Carboxyglutamic acid-containing protein of bone (BGP) is an abundant noncollagenous protein of mammalian bone. BGP has a molecular weight of 5,800 and contains three residues of the vitamin K-dependent amino acid, gamma-carboxyglutamic acid. We have applied a radioimmunoassay based on calf BGP for the measurement of the protein in the plasma of 109 normal humans and 112 patients with various bone diseases. BGP in human plasma was demonstrated to be indistinguishable from calf BGP by assay dilution studies and gel permeation chromatography. The mean (+/- SE) concentration of BGP in normal subjects was 6.78 (+/- 0.20) ng/ml, 7.89 (+/- 0.32) for males and 4.85 (+/- 0.35) for females. Plasma BGP was increased in patients with Paget's disease of bone, bone metastases, primary hyperparathyroidism, renal osteodystrophy, and osteopenia. Plasma BGP did correlate with plasma alkaline phosphatase (AP) in some instances, but there were dissociations between the two. It was additionally observed that patients with liver disease had normal plasma BGP despite increased plasma AP, a reflection of the lack of specificity of AP measurements for bone disease. Our studies indicate that the radioimmunoassay of plasma BGP can be a useful and specific procedure for evaluating the patient with bone disease.
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PMID:New biochemical marker for bone metabolism. Measurement by radioimmunoassay of bone GLA protein in the plasma of normal subjects and patients with bone disease. 696 55

Bone radiotracer uptake in renal osteodystrophy was investigated in 35 dialysis patients by correlating the results of quantitative bone scintigraphy with those of biochemical and bone morphometric studies. There were highly significant correlations (P less than 0.001) between the total skeletal activity and the biochemical (iPTH and alkaline phosphatase), and histologic parameters of hyperparathyroidism. These clinical results strongly suggest that increased bone turnover i.e. hyperparathyroidism, rather than osteomalacia is the major cause of increased skeletal uptake in renal osteodystrophy.
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PMID:Increased bone radiotracer uptake in renal osteodystrophy. Clinical evidence of hyperparathyroidism as the major cause. 707 18

Quantitative bone histology (on undecalcified sections following double tetracycline labeling), radiographs, and biochemistry were studied in 47 children, ages 1 to 17 years, with glomerular filtration rates (GFR) below 80 ml/min/1.73m2. The earliest histologic change was an increased osteoid surface accompanied by increased osteoblast and tetracycline surfaces. However, significant bone disease (increased osteoclastic surface, fibrosis, increased osteoid area, increased mineralization lag time, and reduced tetracycline uptake at osteoid surfaces) occurred only at GFR below 30 ml/min/1.73m2. Radiographs and alkaline phosphatase were normal in 25% of children with significant bone disease; parathyroid hormone was increased in 48% of children without bone disease. Thus, these noninvasive investigations were poor predictors of disease presence. GFR was the most sensitive indicator because bone disease occurred only at GFR below 30 ml/min/1.73m2 and was present in all children with GFR below 20 ml/min/1.73m2. It was concluded that bone histology is required for early detection of bone disease and is an essential tool in experimental studies of renal osteodystrophy. However, because the level of GFR will indicate the presence or absence of bone disease in most children, bone biopsy can be avoided generally in clinical practice.
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PMID:Quantitative bone histology in children with chronic renal failure. 713 53

Thirteen patients receiving regular haemodialysis, with biochemical or radiological evidence of renal osteodystrophy, were treated with alfacalcidol (1 alpha hydroxy vitamin D3) for four years. During the first eighteen months of treatment plasma alkaline phosphatase and serum parathyroid hormone concentrations fell and subperiosteal phalangeal erosions improved. Thereafter plasma alkaline phosphatase and serum parathyroid hormone concentrations rose and after four years' treatment only four patients had a normal plasma alkaline phosphatase, only five a normal serum parathyroid hormone level and in only six had the erosions healed completely. Hypercalcaemia occurred in twelve patients, plasma calcium exceeding 3.0 mmol/l in ten. Plasma calcium rose abruptly close to the time when plasma alkaline phosphatase became normal and often remained raised despite reduction in dosage of alfacalcidol. We have reservations about the ultimate value of long-term treatment with alfacalcidol in haemodialysed patients with renal osteodystrophy and urge caution in its use.
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PMID:Long-term experience of alfacalcidol in renal osteodystrophy. 714 11

Renal osteodystrophy in part due to secondary hyperparathyroidism, is one of the major unresolved problems affecting patients on chronic hemodialysis. In addition, evidence has shown that parathyroid hormone (PTH) is toxic to other organ systems besides bone. The results of a prospective study on the effect of propranolol in reducing PTH levels in chronic renal failure patients on hemodialysis are reported. Propranolol administration reduced PTH levels by over 50-75%. The levels of calcium, phosphorus, alkaline phosphatase and hematocrit were variable, but patients with severe derangements in these measurements also seemed to benefit from propranolol. It should now be determined by larger and longer studies whether these biochemical improvements can be translated into clinical benefits.
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PMID:Suppression of secondary hyperparathyroidism by propranolol in renal failure patients. 721 43

Renal osteodystrophy, a frequent complication of chronic renal failure, is usually assessed by periodic X-rays of bone which are both poorly reproducible and expensive. Seeking a better screening test for osteodystrophy, we evaluated the usefulness of serum alkaline phosphatase as a predictor of bone disease and of hyperparathyroidism. Alkaline phosphatase, despite nonspecificity, correlates with the severity of osteodystrophy and with the increase in serum parathyroid hormone concentration. Serial measurements of alkaline phosphatase can predict changes in these parameters.
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PMID:Prediction of radiographic severity of renal osteodystrophy by serum values. 723 40

Sixty radiological, clinical and biochemical features were simultaneously recorded in a population of 46 patients on maintenance hemodialysis. Radiological signs of bone reabsorption (hands, acromio-clavicular and sacro-iliac joints) were demonstrated in 65% and were quantified as a radiological index of hyperparathyroidism. The index was correlated with the levels of parathormone and of alkaline phosphatase (p less than 0.01) and with the duration of renal failure (p less than 0.01), and inversely related to bone densitometry (p less than 0.05). Discriminant analysis confirmed the redundant value of parathormone and alkaline phosphatases in predicting bone lesions. Factorial analysis showed the existence of 12 classes of patients statistically close to one another. These results demonstrate the heterogeneity of renal osteodystrophy.
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PMID:[Renal osteodystrophy in patients on maintenance hemodialysis: statistical study of clinical, radiological and biochemical features]. 728 Jun 47


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