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 have investigated the clinical utility of a new quantitative two-site radioimmunometric assay specific for bone alkaline phosphatase (B-ALP) in 219 healthy control subjects and in 264 patients with various metabolic bone diseases. B-ALP was compared with total alkaline phosphatase (T-ALP) and with osteocalcin (BGP). B-ALP increased linearly with age in both sexes. In postmenopausal normal women B-ALP increased by 82% compared with premenopausal normal women, whereas the differences between pre- and postmenopausal women for T-ALP and BGP were 18% and 30% respectively. As assessed by Z-score, the highest values of B-ALP were found in patients with Paget's disease of bone, bone metastases or hyperparathyroidism and in patients on maintenance haemodialysis. In osteoporotic patients, B-ALP< but not T-ALP, showed a slight but significant (P < 0.05) difference compared with normal women. On the basis of bone turnover, osteoporotic patients were divided into two groups: high turnover and low turnover; B-ALP, like BGP, was significantly (P < 0.01) higher in patients with high turnover. In conclusion, B-ALP, measured by this new method, can be considered a sensitive marker of bone turnover and could be especially useful in identifying women at risk of developing osteoporosis.
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PMID:Bone alkaline phosphatase measured with a new immunoradiometric assay in patients with metabolic bone diseases. 879 66

We have examined healthy women (51 premenopausal women and 30 postmenopausal women; age 28-59) for lumbar bone mineral density (BMD) by dual energy X-ray absorptiometry (DXA) and assessed metabolic bone markers, such as type I procollagen carboxy-terminal propeptide (P1CP), pyridinoline (PYR), deoxypyridinoline (DPYR), osteocalcin (BGP) and alkaline phosphatase (ALP). BMD was assessed once a year in three consecutive years. Correlations among the BMD, BMD changes and levels of bone markers in samples at the first DXA assessment were studied. In pre-menopausal women, none of the biochemical markers were correlated with the BMD or changes in BMD. In contrast, BMD in post-menopausal women correlated (negatively) well with levels of P1CP, DPYR, PYR and ALP declining in this order, and a significant positive correlation was observed between the rate of bone loss in postmenopausal women and the P1CP concentration. PYR and DPYR also had a tendency to correlate. Combinations of several bone markers improved the correlation. These results show that by measuring several bone specific biochemical markers in postmenopausal women, one can estimate their rates of bone loss as well as their present BMDs. The measurement of biochemical bone markers will therefore be very useful in evaluating bone status and would be applicable in screening postmenopausal osteopenia.
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PMID:Estimation of bone mineral density and bone loss by means of bone metabolic markers in postmenopausal women. 882 22

Because of the previous controversial findings in non-insulin-dependent diabetes mellitus (NIDDM), we measured bone-mineral density (BMD) by two different methods, studied biochemical markers of bone remodeling and calciotropic hormones (parathyroid hormone and calcitonin) in women with NIDDM, and compared the results with age-matched controls. Forty-seven women with NIDDM and 252 healthy nondiabetic women as controls were recruited for this study. BMD was measured by dual X-ray absorptiometry (DEXA) and by quantitative computed tomography (QCT). Biochemical markers of bone remodeling included plasma alkaline phosphatase (AP), osteocalcin (BGP), tartrate-resistant acid phosphatase (TRAP), parathyroid hormone (PTH), calcitonin (CT), and 24-h urine calcium, hydroxyproline. Diabetic patients were more obese with a higher body-mass index (BMI) than controls. Bone mass was normal in NIDDM, both by DEXA and by QCT. Biochemical markers of bone remodeling, PTH and CT were also normal. There was no statistical correlation between bone mass and any of the other measurements studied. There is no evidence that NIDDM produces any change in bone metabolism or mass.
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PMID:Bone mineral metabolism is normal in non-insulin-dependent diabetes mellitus. 883 19

In order to evaluate whether changes of adrenal steroid serum levels occurring during the prepubertal period influence the degree of osteopenia, dehydroepiandrosterone sulfate (DHEAS) was longitudinally monitored as marker of the onset of adrenarche. Fifteen thalassemic patients, 9 girls (Group 1) and 6 boys (Group 2), with chronological age (CA) from 6.1 to 10.3 years and bone age (BA) from 6 to 9.6 years, were studied. Two observations, 14 months apart, were made. All patients had no pubertal signs according to Tanner during the period of observation, and auxological data (height, BMI and height velocity) were evaluated in respect to bone age. There was a statistically significant difference between the two groups for serum DHEAS, BGP serum levels, height velocity and bone mineral density expressed as standard deviation score (BMDsds) in respect to both bone age and height age (the latter was calculated in order to eliminate the influence of height on BMD). Alterations of bone metabolism were excluded by determination of calcium, phosphorus, alkaline phosphatase activity, parathormone, 25-OH-D3, IGF-I serum levels, all these values being normal. In conclusion, our data show that a delayed adrenarche occurs in thalassemic boys which is correlated with a severe degree of osteopenia, even though the relationship between them is not yet established.
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PMID:Can adrenarche influence the degree of osteopenia in thalassemic children? 888 50

Hyperthyroidism is characterized by increased bone turnover and resorptive activity. Similar changes in remodeling are seen after menopause. To study the role of thyroid hormone in the menopause-related changes in bone metabolism, we investigated thyroid status and the sensitivity of bone to thyroid hormone in 14 premenopausal and 15 early postmenopausal women. Triiodothyronine (T3) was administered to the two groups as 20 micrograms doses three times daily for 7 days. The skeletal response was assessed by monitoring bone alkaline phosphatase (BAP), osteocalcin (BGP), pyridinium crosslinked telopeptide domain of type I collagen (ICTP) in serum and urinary excretion of hydroxyproline (OHP), pyridinoline (PYR), and deoxypyridinoline (DPR) at days 0, 8, 15, and 57. The early postmenopausal women had increased bone turnover as reflected in sBAP (p < 0.05), sBGP (p < 0.05), and uOHP (p < 0.01) when compared with premenopausal controls. T3 stimulation of early postmenopausal and premenopausal women significantly increased the markers of bone resorption: sICTP (56% vs. 44%), uOHP (45% in both groups), and UPYR (83% vs. 17%) without any significant differences between groups. Of the formative markers, only sBGP increased significantly after stimulation (34% vs. 41%), but both sBGP and sBAP displayed significant increases from days 15 to 57. Thus, stimulation with thyroid hormone results in an immediate stimulation of ongoing bone formation and bone resorption, but also initiation of new remodeling which, after 8 weeks, reached the formative phase. PTH decreased (p < 0.01) in both groups but serum calcium and serum phosphate were unaltered. In conclusion, menopause is not characterized by altered levels of thyroid hormones or altered skeletal responsiveness to thyroid hormones.
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PMID:Skeletal responsiveness to thyroid hormone is not altered at menopause. 892 57

We measured bone mineral density (BMD) at lumbar (L2-L4) vertebrae and proximal femurs of 385 healthy Chinese women aged 40-70 years and 156 healthy Chinese men aged 20-85, and four markers-bone alkaline phosphatase isozyme (BAP), procollagen-I C terminal propeptide (PICP), osteocalcin (BGP) in serum, and a bone resorption marker, urinary cross-linked N-telopeptide of type I collagen (NTX), of these subjects. The results indicate that in postmenopausal women, levels of all the markers increased with age. In men, serum BAP, PICP, and urinary NTX decreased significantly, and serum BGP decreased with borderline significance (P = 0.08). With increasing age, bone density decreased at both sites in postmenopausal women and at the proximal femur in men. The lumbar bone density showed no significant age-related changes in men. In premenopausal women, BMD at either site showed no significant change with increasing age. Despite the different trends between men and women of age-related changes in BMD and bone markers, bone density of both proximal femur and spine in both sexes correlated inversely with levels of the bone markers in a manner independent of age or body weight. The meaning of opposite age effects on bone markers in men and women needs further investigation. In addition, higher bone marker levels, implying faster bone turnover rate, are associated with lower BMD in both sexes.
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PMID:Sexual differences in bone markers and bone mineral density of normal Chinese. 893 71

We studied the effects of a single oral phosphate (Pi) dose as well as those of three consecutive oral phosphate doses on calcium and bone metabolism. In the first part of the study (P1 study) 10 female volunteers were given orally 1500 mg of Pi in water, as a single dose, or plain water in randomized order at two different sessions. In the second part of the study (P3 study), 10 female volunteers were given orally 1500 mg of Pi, as three separate 500 mg doses in water, or plain water in randomized order. Calcium and bone metabolism was monitored for 24 h by measuring the concentrations of serum ionized calcium (S-iCa), urinary calcium, serum phosphate (S-P), urinary P, serum intact parathyroid hormone (PTH), serum carboxy-terminal propeptide of type I collagen (PICP), serum osteocalcin (BGP), serum carboxy-terminal telopeptide of type I collagen (ICTP), urine deoxypyridinoline (DPD) and bone-specific alkaline phosphatase activity (B-ALP). The S-P increased (p = 0.00005 and p = 0.0005, in the P1 and P3 studies, respectively), the S-iCa concentration declined significantly only in the P1 study (p = 0.0014), the urinary calcium excretion decreased (p = 0.02 and 0.013, in the P1 and P3 studies, respectively), and the PTH concentration rose (p = 0.0083 and p = 0.014, in the P1 and P3 studies, respectively) during the phosphate experiment as compared with the control session. Of the three markers of bone formation studied, PICP declined in the P1 study (p = 0.04), and B-ALP declined in both parts of the study (p = 0.027, p = 0.026, in the P1 and P3 studies, respectively) after phosphate administration, whereas there was no significant change in BGP in either of the studies. The markers of bone resorption, ICTP and DPD, were unaffected by the phosphate load in both studies. In conclusion, acute ingestion of phosphate leads to an increase in S-P, a decrease in S-iCa, and an increase in intact PTH secretion. Our results indicate that these events may lead to an acute inactivation of the early phases of bone formation. In this setting, there was no indication of enhanced bone resorption despite the increase in PTH secretion, which could be due to the combined effect of phosphate and PTH on bone resorption.
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PMID:An acute intake of phosphate increases parathyroid hormone secretion and inhibits bone formation in young women. 897 Aug 92

This study was designed to test the hypothesis that a short treatment course of 1,25(OH)2D3 elicits a stimulation of osteoblast activity without any action on the osteoclast. To test this, oral daily doses of 0.5 microgram or 1 microgram of 1,25(OH)2D3 were administered for 7 days to two groups (n = 5 and n = 7, respectively) of postmenopausal women with low bone mineral density. Markers of osteoblast activity, i.e. osteocalcin (BGP), total alkaline phosphatase activity (ALP) and bone alkaline phosphatase activity (BALP), and markers of osteoclast activity, i.e. hydroxylysyl-pyridinoline (Pyr), lysyl-pyridinoline (D-Pyr), and galactosyl-hydroxylysine (GHyl) were measured in plasma and in fasting urinary samples, respectively, at sequential times during and after 1,25(OH)2D3 administration. It resulted that short term 1 microgram 1,25(OH)2D3 oral administration induced a significant (P < 0.05) rise of BGP serum level without any associated increase of D-Pyr and GHyl, the latter also expressed as GHyl to GGHyl ratio. Urinary Pyr increased significantly after 1 microgram daily doses of 1,25(OH)2D3. Thus, a short course of 1 microgram daily doses of 1,25(OH)2D3 elicits a stimulation of osteoblast activity without any enhancement of D-Pyr, the most specific marker of osteoclast activity. The enhancement of Pyr after 1 microgram daily doses of 1,25(OH)2D3 might be due to the activation of extraosseous metabolic pathways rather than to the activation of osteoclast.
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PMID:Effect of short course of 1,25-dihydroxyvitamin D3 on biochemical markers of bone remodelling in postmenopausal women. 897 58

Administration of growth hormone (GH) to patients with growth hormone deficiency (GHD) has beneficial effects, but so far has been employed only empirically. We have, therefore, investigated the dose-dependent effect of GH on target tissue by studying biochemical markers of bone and collagen turnover in GHD. Then patients with GHD (nine males and one female aged 21-43 years, mean age 28 years) participated in the study. Growth hormone deficiency was defined as a peak serum GH response of less than 15 mU/l in two provocation tests. After a 4-week run-in period, the study population received increasing doses of GH at 4-week intervals (1, 2 and 4 U/m2). Blood samples were collected in the fasting state at 7.00 h on the last day of each period and assayed for serum levels of osteocalcin (S-BGP), bone alkaline phosphatase (B-ALP), C-terminal propeptide of type I collagen (S-PICP), carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (S-ICTP) and N-terminal propeptide of type III collagen (S-PIIINP). Following replacement therapy, serum insulin-like growth factor I and insulin-like growth factor binding protein 3 increased sequentially with time (p < 0.001 and p < 0.001, MANOVA) and the values were elevated significantly over baseline levels after treatment with 1 U/m2. Serum BGP values were below normal at the start of the study and increased gradually following GH treatment to levels in the low-normal range. Baseline values for serum bone alkaline phosphatase (B-ALP), PICP and PIIINP were within the normal range. The collagen parameters increased with GH replacement (p < 0.001, MANOVA) to levels above normal, whereas B-ALP stayed within normal limits. Serum ICTP values were elevated above the normal range at baseline, indicating increased bone resorption in GHD. A linear increase in values was observed with GH treatment (p < 0.001, MANOVA). Serum ICTP did not correlate significantly with the bone formative parameters but was correlated positively to PIIINP. The sensitivity of S-ICTP as a bone resorptive marker is thus questioned. In conclusion, a dose-dependent increase in markers of growth hormone metabolism and in biochemical markers of both bone and non-bone collagen synthesis was seen following incremental doses of GH in GHD.
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PMID:Dose-dependent effects of recombinant human growth hormone on biochemical markers of bone and collagen metabolism in adult growth hormone deficiency. 902 10

The processes of bone formation and resorption can be monitored in vivo by measuring enzymes and other protein products released by osteoblasts and osteoclasts respectively. The major validated biochemical markers of bone formation currently in use include the bone isoenzyme of alkaline phosphatase, osteocalcin (also known as BGP, bone Gla protein) and propeptides derived from the N or C terminal ends of the Type I procollagen molecule. The most useful markers of bone resorption are breakdown products of Type I collagen. The longest established of these is the measurement in urine of hydroxyproline in collagen peptides, but the assays are cumbersome. Furthermore, hydroxyproline is not specific to bone collagen and is also derived from the diet. There is therefore much current interest in collagen products that are more specific to bone, including galactosyl hydroxylysine, and the collagen crosslinks, pyridinoline and deoxypyridinoline. The pyridinolines and peptides derived from crosslinked regions in collagens appear to be the most promising markers of resorption and enable quantitative evaluation of rates of bone resorption in man. These biochemical methods are of use in the diagnosis and evaluation of bone diseases, in population studies, and for monitoring responses to hormones and drugs in clinical studies. It is important to remember that individual markers reflect different biochemical and physiological processes and may not, therefore, always show identical changes. There is an increasing amount of work being devoted to the study of bone biomarkers in osteoporosis. In population studies biochemical measurements may predict rates of bone loss and occurrence of fractures. However their value in the diagnosis and management of individual patients is less clear, partly because of the considerable biological and analytical variation in their measurement. There are exciting challenges ahead for improvements in technical methods and for the use of new markers derived from bone cells and bone matrix.
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PMID:The assessment of bone metabolism in vivo using biochemical approaches. 913 85


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