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)

We performed bone histomorphometry in thirty hemodialysed patients. Ten patients had a double iliac bone biopsy to estimate bone histomorphometry reproductibility. There was no difference between the mean results for each of the 10 patients at each site. However, there was an intra-individual variation which was small for the parameters of formation and particularly osteoid thickness and mineralizing rate and greater for resorption parameters. Mineralization rate appeared the most reliable and discriminant parameter. These 30 patients were separated in two groups according to their mineralizing rate (MR); patients with an MR greater than 0.3 mu/day were in group I and had severe hyperparathyroidism without major impairment of bone mineralization and high formation rate. They also had high serum alkaline phosphatases and high serum parathyroid levels measured with a COOH terminal antibody (iPTH). Patients with a low MR less than 0.3 mu/day (group II) had a severe mineralization defect with low formation rate, normal alkaline phosphatase and significantly lower levels of iPTH than in group I. This last type of histological bone lesion could not be due to aluminum intoxication since the level of serum aluminum was the same in the two groups. The mineralizing defect appeared to be inversely correlated with the percent of osteoid surfaces covered by osteoblast and with the iPTH level. These data suggest that during the course of renal osteodystrophy PTH stimulates not only bone resorption but also bone mineralization by increasing osteoblastic number.
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PMID:Bone histomorphometry in hemodialysed patients. 734 93

Clinically asymptomatic patients undergoing hemodialysis and with histologically proven renal osteodystrophy were treated with 1,25-dihydroxycholecalciferol (1,25[OH]2D3) or with placebo for 9-37 weeks. Serum concentrations of total calcium were frequently increased when the ionized calcium was raised into the normal range. Serum magnesium was in the upper normal range due to the presence of magnesium in the aluminum hydroxide used to lower the hyperphosphatemia, which was difficult to control. Basal serum parathyroid hormone (PTH) levels were increased and seven times higher when measured with a radioimmunoassay recognizing mainly COOH-terminal fragments of human PTH-(1-84) (C-terminal assay) as compared to another assay measuring predominantly intact PTH-(1-84) (N-terminal assay). During treatment with 1,25 (OH)2D3, serum PTH returned towards the normal range with increasing calcium levels. Mean PTH concentrations decreased significantly by 34% (p less than 0.05) when measured with the N-terminal assay and by only 14% (p greater than 0.1) in the C-terminal assay. Serum alkaline phosphatase activity and the mineral content of the forearm estimated by photon absorptiometry remained unchanged.
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PMID:1,25-Dihydroxycholecalciferol in dialysed patients with clinically asymptomatic renal osteodystrophy. A controlled study. 735 81

Nine non-dialyzed patients with creatinine clearance below 20 ml/min and histological and biochemical signs of renal osteodystrophy received 1 alpha-hydroxy vitamin D3 for 6 months in a mean daily dosage of 0.9 microgram. The serum concentrations of calcium and phosphate increased, and the serum concentrations of alkaline phosphatase and parathyroid hormone decreased during treatment. Quantitative histological examination of iliac crest bone biopsies showed a marked improvement of uremic bone changes, including normalization of the initial low mineralization rates evaluated by tetracycline uptake in bone. No significant change was seen in bone mineral content in the forearm measured by photon absorptiometry. An accelerated loss of kidney function was observed during the treatment period with 1 alpha-OH-vitamin D3 as compared with control periods before and after the treatment.
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PMID:1 alpha-hydroxy vitamin D3 treatment of non-dialyzed patients with chronic renal failure. Effects on bone, mineral metabolism and kidney function. 737 58

Growth arrest and renal osteodystrophy are major problems in renal insufficiency of children. The present report describes our experiences in managing renal osteodystrophy in 14 dialyzed children using 1,25-DHCC for 12 months. Values in plasma of Ca, P, Mg, alkaline phosphatase, iPTH, 25-OH-D, and 1,25-DHCC were determined regulary. Skeletal X-rays and analysis of iliac crest biopsies were obtained in each child. In treatment with 1,25-DHCC episodes of severe but reversible hypercalcemia occurred. Alkaline phosphatase and iPTH normalized completely. Radiographic examinations revealed marked improvement. Histological signs of fibro-osteoclasia and resorptive defects disappeared but there was no recovery of osteomalacia. A reduction of osteoblast population and of bone transformation was obvious. 1,25-DHCC failed to normalize growth in uremic children. In short, neither vitamin D nor 1,25-DHCC can guarantee complete recovery of renal osteodystrophy and growth arrest in uremic children.
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PMID:[Renal osteodystrophy in children. Therapy with 1,25-dihydroxy-cholechalciferol (author's transl)]. 739 29

Twenty-two patients with chronic renal failure were randomly assigned to a conventional low-protein diet containing 0.6 g protein/kg/day or a very-low-protein diet containing 0.4 g protein/kg/day supplemented with essential amino acids; they were followed up for 9 months. There were no significant changes in body mass index, arm muscle area, percentage body fat, serum albumin and transferrin levels in any of the groups; neither was there any difference between the groups in respect of these parameters. Renal function, as measured by the reciprocal of serum creatinine over time, stabilised in both groups during intervention, with no significant difference between the groups. There was however no correlation between changes in renal function and changes in blood pressure, or dietary intake of protein, phosphorus, cholesterol, polyunsaturated and saturated fatty acids. There were also no significant changes and no significant differences between the groups in serum levels of parathyroid hormone and alkaline phosphatase, urine cyclic adenosine monophosphate, tubular reabsorption of phosphate, and the theoretical renal threshold for phosphate. The results of this study suggest that the supplemented very-low-protein diet was not superior to the conventional low-protein diet in terms of its effect on protein-energy status, renal function and biochemical parameters of renal osteodystrophy.
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PMID:Supplemented low-protein diets--are they superior in chronic renal failure? 763 85

The authors classified sixty chronic renal failure (CRF) patients receiving hemodialysis (HD) treatment into four groups for clinical study. Forty patients received HD for more than five years and the remaining twenty patients received HD for less than two years. These two groups were further divided into two subgroups according to whether they took Rocaltrol or not. The levels of parathyroid hormone (PTH), calcitonin (CT), alkaline phosphatase (AKP) and bone X-ray were studied in each patient. The results showed: the levels of PTH and CT were obviously increased in all the patients. The levels of PTH and CT were higher in the patients having received HD for more than five years than those for less than two years. They were also higher in patients who had not taken Rocatrol than those who had. Ninety-five percent of the patients having received HD for more than five years had renal osteodystrophy (ROD) without receiving Rocaltrol treatment, while only sixty-five percent of the patients developed ROD with Rocatrol treatment. The longer the HD time, the higher the ROD incidence. The cause, prevention and treatment of ROD were discussed.
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PMID:[A study on the relative factors for secondary parathyroidosis and renal osteodystrophy in long-term hemodialysis patients]. 764 35

The assay of serum peptides of bone collagen formation and degradation could potentially provide an indirect estimate of the rate of bone turnover. In our study we have measured serum levels of the carboxy-terminal propeptide of type I procollagen (PICP) as a marker of bone formation and serum levels of the pyridinoline cross-linked telopeptide domain of type I collagen (ICTP) as a marker of bone resorption in 53 patients (47.7 +/- 10 years, M +/- SD) on haemodialysis (for 9.5 +/- 3.8 years) and affected by renal osteodystrophy. Besides PICP and ICTP, patients were also sampled for serum intact and C-terminal PTH, osteocalcin (BGP) and alkaline phosphatase (AP). A transiliac bone biopsy for histomorphometry was also performed in all. As expected both PTH assays, BGP and AP, were correlated reciprocally and to histomorphometric parameters. As for serum levels of PICP, they were on average increased (268.5 +/- 104.9 ng/ml, M +/- SD) compared to normals (range 66-176), but not correlated to classical humoral markers of hyperparathyroidism (PTH and AP), with the exception of BGP (with a rather low r value: 0.365, P < 0.01), nor to histomorphometric indices of bone resorption and formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic value of serum peptides of collagen synthesis and degradation in dialysis renal osteodystrophy. 772 29

The bone histology of renal osteodystrophy is classified into osteitis fibrosa, osteomalacia, those of mixed, osteoporosis and low turnover bone. Osteitis fibrosa is the most frequent skeletal abnormality and is caused by various degrees of hyperparathyroidism. The main factors inducing hyperparathyroidism which is a well known complication in patients with renal failure include (a) phosphorus retention: 1) hypocalcemia and 2) decreased levels of 1 alpha, 25(OH)2 Vitamin D3, (b) reduced number of 1 alpha, 25(OH)2 Vitamin D3 receptors in parathyroid tissue, (c) skeletal resistance to set-point for calcium-regulated parathyroid hormone secretion. Serum or plasma levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcitonin and tartrate resistant acid phosphatase are measured to evaluate hyperparathyroidism and metabolic bone disease. Dietary phosphorus restriction in chronic renal insufficiency prevents secondary hyperparathyroidism and renal osteodystrophy. Other treatment of phosphorus binders, Vitamin D metabolites or analogues, carcitonin and bisphosphonate are useful for the management of renal bone disease.
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PMID:[Secondary hyperparathyroidism and tertiary hyperparathyroidism chronic renal failure, uremia]. 775 92

Predicting the course of parathormone (PTH)-elicited bone turnover in both humans and experimental rat models with moderate chronic uremia, using only standard clinical chemistry analyses, is often difficult. Consequently, rat bone from 1 + 2/3 nephrectomized animals, after 230 days of progressive renal failure, was examined for PTH-stimulated adenylate cyclase (AC) and phospholipase C (PL-C) activities. Correlations to biological parameters related to the function of bone and kidney were made. Reduced renal function was demonstrated by increased serum creatinine; circulating 1,25 dihydroxyvitamin D3 below detection level; diminished renal PTH-elicited AC activity; and decreased urinary cAMP excretion. PTH-activated renal PL-C was also reduced. However, no significant differences were seen in urine creatinine, calcium, phosphate, and hydroxyproline, nor in serum PTH, alkaline phosphatase, calcium, and phosphate. Notwithstanding, renal osteodystrophy developed as estimated by increased plasticity of the long bones, as well as reduction of the diaphyseal (Dd) and inner femoral mid-shaft (Di) diameters. Femoral cancellous bone exhibited a substantial elevation of both eroded surface (ES) and osteoid surface (OS) as well as a marked reduction in trabecular bone volume (TBV). Calvarial PTH-activated AC was enhanced, whereas corresponding PL-C was markedly reduced. PTH-enhanced AC correlated positively with ES and negatively with Di, respectively. PTH-enhanced PL-C, however, correlated positively with bone calcium content and negatively with ES. Our results indicate that bone modeling and remodeling are to a large extent related to PTH-elicited signaling systems, and cannot easily be predicted by standard clinical chemistry analyses.
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PMID:Surgically induced uremia in rats. II: Osseous PTH-susceptible signaling systems as predictors of bone resorption. 782 Jul 79

Intermittent calcitriol therapy is commonly used to treat secondary hyperparathyroidism in patients undergoing regular dialysis, but there is little available information about the histologic response of bone to this form of therapy. Accordingly, 14 children and adolescents with biopsy-proven secondary hyperparathyroidism were treated with intermittent oral or intraperitoneal doses of calcitriol for 12 months. Biochemical indices of mineral metabolism including serum intact PTH levels were measured monthly throughout the study, and bone biopsies were repeated at the end of treatment. Before treatment, 11 patients had osteitis fibrosa and three had mild lesions of secondary hyperparathyroidism. Histologic improvement was seen in 12 of 14 patients, and osteitis fibrosa resolved in 10 of 11 cases. Bone formation decreased in all patients during intermittent calcitriol therapy, falling from 861 +/- 380 to 150 +/- 170 microns2/mm2/day, P < 0.001. Bone formation decreased to normal in six patients, but six patients developed adynamic lesions of bone with subnormal bone formation rates. Serum PTH and alkaline phosphatase levels declined in those who developed adynamic bone, but values remained elevated in patients with normal rates of bone formation at follow-up evaluation. Neither the mean dose of calcitriol nor the average dose per kilogram body weight differed in patients with adynamic lesions. Thus, adynamic renal osteodystrophy develops in a substantial number of patients during intermittent calcitriol therapy. Although declining serum PTH and alkaline phosphatase levels suggest the development of the adynamic lesion, bone formation decreases in some patients despite persistently high serum PTH levels. Calcitriol may directly suppress osteoblastic activity in patients with secondary hyperparathyroidism when given in large doses to patients undergoing peritoneal dialysis.
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PMID:Development of adynamic bone in patients with secondary hyperparathyroidism after intermittent calcitriol therapy. 786 12


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