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)

Phosphorus (P) retention plays an important role in the pathogenesis of secondary hyperparathyroidism (2nd HPT) in chronic renal failure. In recent years, periodic intravenous or intermittent oral administration of high doses of 1,25(OH)2D3 has been reported to improve severe 2nd HPT in hemodialysis patients. The present study was performed to determine the effects of dietary P restriction on 2nd HPT in hemodialysis patients treated with intermittent oral high-dose 1,25(OH)2D3. A high dose of 1,25(OH)2D3 was administered orally twice a week at the end of hemodialysis in 20 hemodialysis patients with 2nd HPT. Dietary P content was estimated from records of the patients' food intake, made twice during the treatment period. Based on this information, dietitians developed appropriate meal plans and instructed the patients. After 8 weeks of the treatment, serum c-parathyroid hormone (c-PTH) and alkaline phosphatase (ALP) levels decreased significantly, from 18.8 +/- 1.9 ng/ml and 347.1 +/- 30.7 U/liter to 9.4 +/- 1.2 ng/ml and 268.3 +/- 19.6 U/liter, respectively. Serum P levels increased gradually during the first 4 weeks of the treatment. Dietary P intake was reduced significantly, from 908 +/- 49 mg/day to 734 +/- 39 mg/day, after the nutritional instructions. As a result of the dietary P restrictions, serum P levels were significantly decreased in the 8th week as compared with those in the 4th week. Serum Ca levels remained unchanged throughout the observation period. There was a significant relationship between the mean values for serum P levels during the study and the percent suppression of serum c-PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dietary phosphorus restriction on secondary hyperparathyroidism in hemodialysis patients during intermittent oral high-dose 1,25(OH)2D3 treatment. 182 Apr 36

In 21 patients with chronic renal failure spirometric and electromyographic examinations (including m. pectoralis, m. rectus abdomini, and m. obligus abdomini) were performed before and after hemodialysis. In 10 patients treated by peritoneal dialysis and, in 35 patients treated by hemodialysis serum PTH, thyroid hormones (T4, T3, rT3), CPK, aldolaze, pyruric acid, lactic acid, alkaline phosphatase were determined. In both groups before and after dialysis serum sodium, potassium, calcium, magnesium were determined. We observed negative correlation between PTH and respiratory muscles weakness indices. This fact may confirm the contribution of PTH in uremic myopathy evaluation.
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PMID:[Analysis of the causes of respiratory muscle hypotonia in patients with chronic renal failure treated by peritoneal dialysis and hemodialysis]. 183 10

Bone mineral content, estimated by single-photon absorptiometry of the forearm, serum values of intact parathyroid hormone (PTH(1-84], osteocalcin, alkaline phosphatase, 1,25-dihydroxycholecalciferol (1,25(OH)2D3), and aluminium were determined during treatment with calcium carbonate (CaCO3) or aluminium hydroxide (Al(OH)3) in 11 dialysis patients participating in a randomised cross-over study. Each treatment period lasted 6 months. Serum phosphorus was maintained in the range 1.5-2.0 mmol/l. During Al(OH)3 treatment bone mineral content (BMC) decreased by 11% per half-year (mean), but only by 3% per half-year during CaCO3 treatment (P less than 0.05). Comparing the CaCO3 and Al(OH)3 periods the following differences were found: serum calcium increased during CaCO3 treatment, PTH(1-84) decreased (79% of initial values during CaCO3 versus 196% during Al(OH)3, mean area under curve, P less than 0.05), osteocalcin decreased (89% versus 117%, P less than 0.01), alkaline phosphatase decreased (92% versus 116%, P less than 0.05), and aluminium decreased (56% versus 189%, P less than 0.05). 1,25(OH)2D3 remained unchanged in both periods. No increase in soft-tissue calcification was demonstrated on X-ray of the shoulders in any of the periods. Thus, CaCO3 treatment seems to slow down loss of bone mineral content, and using CaCO3 as phosphate binder may have a more beneficial effect on the progression of uraemic bone disease than Al(OH)3 due to the reduction of hyperparathyroidism and bone turnover.
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PMID:Comparison of calcium carbonate and aluminium hydroxide as phosphate binders on biochemical bone markers, PTH(1-84), and bone mineral content in dialysis patients. 185 34

Cyclical treatments of osteoporosis utilizing a skeletal Activator of bone remodelling, and sequential therapy with a Depressor to selectively block the resulting phase of osteoclastic resorption have been dubbed 'ADFR' therapy; there is usually a treatment Free interval while the activated bone multicellular units complete the remodelling cycle before the protocol is Repeated. In this report an ADFR protocol was developed in which all patients received synthetic hPTH (1-38) for the first 14 days of a 100 day cycle. Half the patients received no other therapy (Group 1), but were followed closely with repeated vertebral bone mineral measurements over two full cycles. The remaining patients (Group 2) were randomly allocated to receive salmon calcitonin, at an average dose of 79 units per day for a 56 day depressor period immediately following each phase of activation. Detailed bone histomorphometry was performed on iliac biopsies obtained before treatment and at the end of the second cycle (Day 200). In Group 1, the serum alkaline phosphatase (Alk. P'ase) increased by 23 +/- 12% (P less than 0.01) and by 18 +/- 16% (P less than 0.03) of the baseline values following PTH treatment during the first and second cycles, respectively. The overall changes in serum Alk. P'ase across time were significantly less (P less than 0.04) in Group 2; however this parameter also increased by 15 +/- 15% during the first cycle and 8 +/- 6% during the second cycle. Vertebral BMC increased by 13% in Group I (P less than 0.01), but forearm BMC decreased by 11% (P less than 0.05) over the two cycles of therapy. There were no significant changes in bone mineral measurements in Group 2, but the differences between the two groups were not significant. Eighteen paired biopsies were available for histomorphometric analysis. There were no significant changes in static parameters measuring total bone tissue, osteoclastic function or osteoid formation after two cycles of treatment. Individual bone formation rates (surface referent) were not significantly different between the two groups; the pooled data for all biopsies showed a small but insignificant increase from 0.030 +/- 0.018 to 0.035 +/- 0.028 mm3/mm2/day. However there was a significant increase in the activation frequency (the probability of a remodelling event occurring on queiscent cancellous surface) from 13 +/- 7 to 27 +/- 26/day x 10(-4) (P less than 0.05) when calculated for the pooled data from both groups.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bone densitometric and histomorphometric responses to sequential human parathyroid hormone (1-38) and salmon calcitonin in osteoporotic patients. 186 70

Osteoblastic cells were cloned by culturing rat calvariae cells in agarose in the presence of TGF-beta and EGF. Two bone cell lines were established by immortalizing such an osteoblastic clonal cell population by the introduction of the avian v-mycOK10 gene in the form of a mouse ecotropic retrovirus. Although originating from the same clonal cell population, the two lines exhibited somewhat differing properties. IRC10/30-myc1 expressed alkaline phosphatase (AP), showed PTH- and PGE2-induced cAMP production, synthesized mainly collagen type I and a minor fraction of type III, and produced mRNA for the bone-specific protein osteocalcin. IRC10/30-myc3 did not express AP, showed no PTH responsiveness, and synthesized only about one-third as much collagen as IRC10/30-myc1 (4 versus 12% of total protein synthesis). However, the cell line IRC10/30-myc3 was induced to synthesize cAMP by PGE2 and produced osteocalcin mRNA. When cultured in vivo in diffusion chambers, both lines proved to be osteogenic. Besides bone, both lines also formed cartilage and fibrous tissue. Thus, by immortalizing a clonal cell population of the osteoblastic phenotype, cell lines expressing varying properties can emerge. Furthermore, the expression of alkaline phosphatase and PTH-inducible adenylate cyclase are not prerequisites for a cell to form bone in vivo. Finally, cells expressing the phenotype of differentiated osteoblasts, including osteocalcin synthesis, still have a multipotential differentiation capacity and form bone and cartilage in vivo.
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PMID:Establishment and characterization of two immortalized cell lines of the osteoblastic lineage. 188 24

A seventeen-year-old youth was presented with muscle cramps and convulsions. A brain CT scan showed calcification in the region of the ganglia, and a diagnosis of brain tumor was thus made and an anticonvulsant given for two years. At age nineteen, the patient developed pseudohypoparathyroidism owing to low serum calcium and high serum PTH levels. However, serum alkaline phosphatase and serum osteocalcin levels were high, lesion was detected in the femur neck. These data indicated that the bone remodeling response to PTH had remained intact in this patient. Serum osteocalcin is known to increase in primary hyperparathyroidism. However, unlike patients with hyperparathyroidism, those with pseudohypoparathyroidism show no increase in serum 1,25(OH)2D. The present case was thus useful for examining the direct effect of PTH on serum osteocalcin. The patient was administered 1 alpha (OH)D, and his condition monitored for two years. During this period, osteocalcin and PTH levels decreased while that of 1,25(OH)2D increased. Osteocalcin and PTH levels were found to be closely correlated (r = 0.68, p less than 0.01). The present results indicate the possibility that PTH may increase serum osteocalcin independent of Vitamin D.
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PMID:[Serum osteocalcin concentration in a patient with pseudohypoparathyroidism type Ib]. 188 14

We investigated bone mineral content and factors related to decreased bone mineral content in maintenance hemodialysis patients. Bone mineral contents, epsilon GS/D, radius-bone mineral content (R-BMC) and L3-bone mineral density (L3-BMD), were measured with a micro densitometer, a bone mineral analyzer and a dual energy quantative CT scanner, and relative bone mineral contents (% epsilon GS/D, %R-BMC and %L3-BMD) were calculated respectively. The desferrioaxmine infusion test was carried out for diagnosis of aluminium associated bone disease, and an elevated level of aluminium (delta aluminium) was observed. There was reverse correlation between epsilon GS/D and age in female hemodialysis patients. Serum bone gla protein, alkaline phosphatase and PTH-C levels were high in cases with increased epsilon GS/D and who were receiving little medication with activated Vitamin D in maintenance hemodialysis patients. A correlation was observed between delta aluminium and total medication of aluminium hydroxide-gel. Hemodialysis patients with bone pain had long term hemodialysis, high total medication of aluminium and high aluminium. Relative bone mineral contents (% epsilon GS/D, %R-BMD) were useful for estimating bone mineral content in hemodialysis patients. Hemodialysis patients were divided in four groups by PTH-C and delta aluminium levels as follow, 1) normal, 2) aluminium associated bone disease, 3) secondary hyperparathyroidism with aluminium associated bone disease, 4) secondary hyperparathyroidism. These results indicate that secondary hyperparathyroidism, and medication with aluminium may play a role in decreased bone mineral content in hemodialysis patients, and menopause may also be an important factor in female hemodialysis patients.
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PMID:[Clinical study of concerning factors of decreased bone mineral content in hemodialysis patients]. 192 Sep 39

Micromolar concentrations of aluminum sulfate consistently stimulated [3H]thymidine incorporation into DNA and increased cellular alkaline phosphatase activity (an osteoblastic differentiation marker) in osteoblast-line cells of chicken and human. The stimulations were highly reproducible, and were biphasic and dose-dependent with the maximal stimulatory dose varied from experiment to experiment. The mitogenic doses of aluminum ion also stimulated collagen synthesis in cultured human osteosarcoma TE-85 cells, suggesting that aluminum ion might stimulate bone formation in vitro. The effects of mitogenic doses of aluminum ion on basal osteocalcin secretion by normal human osteoblasts could not be determined since there was little, if any, basal secretion of osteocalcin by these cells. 1,25 Dihydroxyvitamin D3 significantly stimulated the secretion of osteocalcin and the specific activity of cellular alkaline phosphatase in the human osteoblasts. Although mitogenic concentrations of aluminum ion potentiated the 1,25 dihydroxyvitamin D3-dependent stimulation of osteocalcin secretion, they significantly inhibited the hormone-mediated activation of cellular alkaline phosphatase activity. Mitogenic concentrations of aluminum ion did not stimulate cAMP production in human osteosarcoma TE 85 cells, indicating that the mechanism of aluminum ion does not involve cAMP. The mitogenic activity of aluminum ion is different from that of fluoride because (a) unlike fluoride, its mitogenic activity was unaffected by culture medium changes; (b) unlike fluoride, its mitogenic activity was nonspecific for bone cells; and (c) aluminum ion interacted with fluoride on the stimulation of the proliferation of osteoblastic-line cells, and did not share the same rate-limiting step(s) as that of fluoride. PTH interacted with and potentiated the bone cell mitogenic activity of aluminum ion, and thereby is consistent with the possibility that the in vivo osteogenic actions of aluminum ion might depend on PTH. In summary, low concentrations of aluminum ion could act directly on osteoblasts to stimulate their proliferation and differentiation by a mechanism that is different from fluoride.
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PMID:Aluminum stimulates the proliferation and differentiation of osteoblasts in vitro by a mechanism that is different from fluoride. 192 12

Fourteen patients with chronic renal failure and secondary hyperparathyroidism were treated by subtotal parathyroidectomy. Bone pain and hypercalcemia were the main indications to surgery respectively in 13 and 1 patients. Bone pain disappeared or was significantly reduced in 12/14 patients. Two patients had a persistent hyperparathyroidism. Serum alkaline phosphatase returned to normal in 12 patients and PTH in 11 of 12 patients with pretreatment high levels.
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PMID:[Secondary hyperparathyroidism in chronic renal failure. Role of subtotal parathyroidectomy]. 192 66

The mechanisms by which glucocorticoids cause osteopenia are incompletely understood. It is generally accepted that bone formation is depressed during corticosteroid treatment, but the cause of the ongoing bone resorption is less clear. Secondary hyperparathyroidism and changes in vitamin D metabolism are thought to play a role. This is based mostly on data from cross-sectional studies in heterogeneous patient groups. We, therefore, studied longitudinally the course of biochemical parameters and the hormones influencing bone turnover in a homogeneous group of 10 euthyroid patients with Graves' ophthalmopathy, all euthyroid for at least 1 yr before, during, and after a 12-week course of prednisone. Bone formation was depressed as reflected by a fall in serum osteocalcin (3.0 +/- 2.1, 1.7 +/- 1.1, and 2.4 +/- 1.9 micrograms/L at weeks 0, 4, and 12, respectively; P = 0.02) and in total alkaline phosphatase (1.15 +/- 0.33, 0.83 +/- 0.22, and 0.88 +/- 0.40 mukat/L; P = 0.001). Parameters of bone resorption (urinary hydroxyproline/creatinine ratio, serum acid phosphatase) and the levels of vitamin D metabolites remained unchanged. Serum intact PTH seemed to decrease slightly. Our findings suggest that glucocorticoid induced osteopenia is caused by a depressed bone formation in the presence of an unaltered but ongoing bone resorption. Secondary hyperparathyroidism and changes in vitamin D metabolism are apparently not involved.
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PMID:The course of biochemical parameters of bone turnover during treatment with corticosteroids. 199 8


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