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)

The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.
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PMID:Effect of correction of metabolic acidosis on bone mineralisation rates in patients with renal osteomalacia. 23 58

By means of a photon densitometer utilizing a 125I-source, bone mineral content was measured in 15 chronic renal failure patients on conservative management, 46 patients on maintenance hemodialysis and 20 patients after renal transplantation. The determinations were made at 4 sites in both radius and tibia. In patients with chronic renal failure on conservative treatment the bone mineral content did not differ significantly from that in normals. Patients on hemodialysis showed a low bone mineral content in 61 percent of females and 53 percent of males. Especially low values were obtained from 5 females who had undergone bilateral nephrectomy. After renal transplantation all female patients showed low values, whereas 50 percent of male patients showed decreased values. No correlations were found between bone mineral content and serum parameters (calcium, phosphate, alkaline phosphatase, creatinine), duration of renal failure, hemodialysis treatment or steroid medication.
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PMID:[Mineral content of the skeleton in chronic kidney insufficiency treated with dialysis and after kidney transplantation. Results of isotope densitometry]. 33 6

A case of fatal viscerotropic Rocky Mountain spotted fever with virtual absence of cutaneous lesions was diagnosed at autopsy by specific immunofluorescent demonstration of Rickettsia rickettsii in spleen, kidney, epididymis and skin. The clinical presentation was that of insidious onset of fever, renal failure, hypotension, hyponatremia and obtundation over a 10 day period. The patient had respiratory insufficiency, hypocalcemia, increases in creatinine phosphokinase (CPK), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase, billirubin and serum phosphate, grand mal seizure, myalgia and unremitting shock with death occurring on day 12 of illness. Postmortem examination revealed severe vasculitis with interstitial nephritis and multifocal tubular necrosis, pericholangitis with bile stasis, glial nodules in the brain, multifocal rhabdomyonecrosis, interstitial pneumonitis and mild interstitial myocarditis. Risk factors which this patient shared with other patients with fatal Rocky Mountain spotted fever were failure to recognize a rash, failure to obtain a tick bite history, male sex, black race and age greater than 30 years.
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PMID:Fatal viscerotropic Rocky Mountain spotted fever. Report of a case diagnosed by immunofluorescence. 34 5

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

A group of 25 patients with chronic terminal renal failure, treated regularly by haemodialysis, was examined. Activity of the bone serum alkaline phosphatase isoenzyme was significantly elevated in 12 patients with signs of bone disease, either isolated or combined with liver damage, even when total alkaline phosphatase activity was within normal limits. The intensity and incidence of raised bone isoenzyme activity increased with the duration of dialysis therapy. Elevated activity of liver alkaline phosphatase isoenzyme correlated with the other laboratory and clinical signs of liver involvement in 16 patients. Activity of the intestinal isoenzyme was elevated in over half the patients, unrelated to liver or bone damage, and was in an inverse correlation to the total serum calcium level. The evaluation of total serum alkaline phosphatase activity had no diagnostic value.
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PMID:The source and clinical significance of serum alkaline phosphatases in patients treated by chronic dialysis. 61 70

Immunoreactive parathyroid hormone (iPTH) and 25-hydroxycalciferol (25(OH)D) serum levels were determined in 32 patients with renal osteopathy, they were correlated with the results of bone biopsy and other clinical parameters. iPTH was closely related to bone histology, it did not correspond to serum calcium and alkaline phosphatase, but the correlation to serum phosphate was statistically significant. 25(OH)D levels were not related to the histological findings of osteomalacia or increased bone resorption, while a correlation between the vitamin D metabolite and serum calcium could be observed. Since iPTH and 25(OH)D levels exhibited a significant correlation, an inhibitory effect of 25(OH)D on parathyroid gland function in renal failure was discussed.
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PMID:[Immunoreactive parathyroid hormone, 25-hydroxycalciferol and bone histology in renal osteodystrophy (author's transl)]. 94 Feb 99

Synthetic 1alpha-hydroxycholecalciferol (1alpha-OH-D3) was given intravenously in a dose of 2.5-10 mug per day to three patients with chronic renal failure. As little as 10 mug of 1alpha-OH-D3 daily for a week improved intestinal calcium absorption to a normal level, raised serum calcium, and reduced serum alkaline phosphatase. Severe rickets which had not responded to large amounts (greater than 200 mg in total) of vitamin D2 was markedly cured with 2.5 mug of 1alpha-OH-D3 given daily for 3 weeks. These clinical data hold promise that is certainly useful in the improvement of intestinal malabsorption of calcium and bone diseases in renal failure.
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PMID:Curative effects of 1alpha-hydroxycholecalciferol on calcium metabolism and bone disease in patients with chronic renal failure. 121 80

31 adult patients (15 male and 16 female) with chronic renal failure were treated for 6 months with 1-alfa-hydroxycholecalciferol on a dose 0.25-2.0 micrograms/24 h. 15 patients with not very advanced renal failure (serum creatinine level 176.8-442 mumol/l) received conservative therapy (group I), 16 patients with serum creatinine value 884-1326 mumol/l were treated by intermittent hemodialysis (group II). The statistically significant decrease of serum alkaline phosphatase activity in group I and II (p < 0.01), the rise of serum calcium level in group I (p < 0.005) were determined. Half of the patients from both the groups stated the relief or disappearance of bone and joint pains and muscle weakness. Besides in group I significant decrease of creatinine clearance (p < 0.001) and increase of serum urea and creatinine value (p < 0.01) were noticed. On the basis of these results we can conclude that the treatment with 1-alfa-hydroxycholecalciferol, produced by "Polfa", ought to be introduced gradually with increasing doses and frequent monitoring of calcium-phosphate metabolism and renal function parameters.
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PMID:[Clinical estimation of 1-alpha-hydroxycholecalciferol in treatment of patients with chronic renal failure]. 130 33

Chronic renal failure (CRF) in the young is complicated by, among other conditions, growth retardation, hyperparathyroidism and uremic osteodystrophy. Many children with CRF are now being treated with growth hormone (GH). Since GH has a direct mitogenic effect on osteoblasts in culture, we studied the effects of GH therapy on osteoblastic activity, such as serum alkaline phosphatase (AP), bone GLA-protein (BGP) and bone mass density (BMD) in poorly growing children with and without CRF. Fifteen (4 girls, 11 boys) healthy children with short stature (SS) and 10 (3 girls, 7 boys) children with end-stage renal failure (CRF) 4.5-12.4 years of age were treated with daily subcutaneous injections of GH in a dose of 0.1-0.125 IU/kg/day for 1 year. IGF-I, BGP and BMD of the spine were determined before and after the year of treatment. During GH therapy, a similar increase in height velocity and IGF-I were noted in SS and CRF groups: 3.8 +/- 0.77 to 8.38 +/- 1.25 (p < 0.001) vs. 4.0 +/- 0.6 to 7.14 +/- 1.3 cm/year (p < 0.001) and 7.8 +/- 2.6 to 21.8 +/- 7.5 (p < 0.01) vs. 7.9 +/- 1.3 to 21.5 +/- 5.6 nmol/l (p < 0.01), respectively. AP increased from 205 +/- 27 to 274 +/- 50 IU/l (p < 0.01) in the SS group but not in CRF patients (223 +/- 58 pre- 218 +/- 51 IU/l post-GH therapy).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of growth hormone therapy on IGF-I, bone GLA-protein and bone mineral content in short children with and without chronic renal failure. 130 46

A nonisotopic assay of vitamin B-12 in human serum or plasma is described, performed with the Abbott IMx analyzer. The sample is first treated at pH > 12.5 to release bound vitamin B-12 and to convert all forms to cyanocobalamin. Next, the analyte is bound, at lower pH, by vitamin B-12-specific binding protein, immobilized to a solid phase of polymeric microspheres. Detection involves monitoring the activity of the tracer enzyme (alkaline phosphatase) coupled to a derivative of cyanocobalamin. Total assay precision is 7.9% for vitamin B-12 at 200 ng/L, 6.6% at 400 ng/L, and 6.7% at 800 ng/L. Assay sensitivity, calculated as 2 SD from the zero calibrator, is 37 (+/- 9) ng/L. The dynamic range extends to 2000 ng/L. Analytical recovery of 300 and 600 ng/L additions of vitamin B-12 to sera with basal concentrations of 30-400 ng/L was 102.5%. Results of the assay correlated well with those of commercially available radioisotope assays. No interference was observed in specimens from patients with pernicious anemia, chronic or acute myelogenous leukemia, or renal failure. Cross-reactivity with cobinamide (1 g/L) was < 0.00003%. Vitamin B-12 measurements for blood specimens drawn into serum, EDTA, or heparinized plasma-collection tubes agreed within 3%.
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PMID:Automated assay of vitamin B-12 by the Abbott IMx analyzer. 139 92


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