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)

Parathyroid hormone (PTH), osteocalcin and alkaline phosphatase (AP) were investigated before and after parathyroidectomy in 12 patients receiving hemodialysis. Early post-parathyroidectomy, PTH decreased (p less than 0.001), AP increased (p less than 0.05), but osteocalcin remained unchanged. At 3 months, osteocalcin and AP declined. A negative correlation was observed between aluminum staining and post-parathyroidectomy osteocalcin. In conclusion, early post-parathyroidectomy, osteocalcin and AP reflect persistent osteoblastic activity, which declined after 3 months. In patients receiving hemodialysis both variables may represent different aspects of osteoblastic activity and osteocalcin allows mixed uremic osteodystrophy after parathyroidectomy.
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PMID:Evolution of osteocalcin, alkaline phosphatase and parathyroid hormone after parathyroidectomy in patients receiving chronic maintenance hemodialysis. 157 55

Intestinal disease might contribute to osteopenia. Measurements of IgA antibodies to gliadin have been established as an accepted screening procedure for detection of coeliac disease. When we applied these measurements to 92 patients with verified osteoporosis, 11 subjects (12%) were found to have elevated levels. This is markedly higher than the incidence in healthy subjects (3%). However, the patients with raised levels of IgA antibodies displayed no clinical symptoms and no laboratory evidence of calcium malabsorption. Thus their values for serum calcium, phosphate, parathyroid hormone (PTH), alkaline phosphatase and osteocalcin, as well as the fasting urinary excretion of hydroxyproline and calcium, were similar to those found in other patients with osteoporosis. Intestinal biopsy verified coeliac disease in three patients and was normal in another three. This gives an incidence of verified coeliac disease in this patient group that is approximately tenfold higher than that in the healthy population. Subclinical coeliac disease appears to be unusually over-represented among patients with idiopathic osteoporosis, and screening for gliadin antibodies might therefore be a valuable addition to the routine assessment of the osteopenic patient. The mechanisms underlying the relationship are not clear, but calcium malabsorption is not evident.
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PMID:Screening for antibodies against gliadin in patients with osteoporosis. 158 66

Thirty seven postmenopausal women aged under 65 with densitometric osteoporosis defined by a bone density value below the 80th percentile of the osteoporotic population but without identifiable crush fractures, were treated and monitored for two years using clinical, laboratory and densitometric parameters. Sixteen of them were given hormonal replacement therapy combining percutaneous or transdermal 17 beta estradiol with a progestogen and the other 21 sodium fluoride at the dose of 50 mg/d combined with calcium and vitamin D. There was a significant increase in vertebral bone density in both groups: 6.3 +/- 0.9 per cent for hormone treatment and 7.1 +/- 1.5% for fluoride after 2 years, while it fell in a control group. The increase was linear with fluoride, while 2/3 of the gain was acquired by the end of the first year of hormonal therapy. Nine of the 16 patients on hormonal therapy and 9 of the 21 taking fluoride showed a significant vertebral gain at 2 years (greater than or equal to 0.043 g/cm2). There was no parameter which enabled the identification of "responders" before treatment. There was no difference in changes in femoral bone density between patients treated with fluoride and controls. From a laboratory standpoint, hormonal therapy caused a significant fall at 12 months in the urinary calcium/urinary creatinine ratio, and a non-significant fall in osteocalcin at 2 years. With fluoride, there was a marked rise in osteocalcin and a more moderate rise in alkaline phosphatase, reflecting stimulation of bone formation without any variation in resorption. In conclusion, this study shows the ability of both these types of treatment of increasing, by different mechanisms, the vertebral bone density of osteoporotic women. However, it does not indicate the extent to which this gain in bone density might have a positive influence on fracture risk.
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PMID:[Comparative effects of sodium fluoride and hormonal replacement therapy on bone metabolism in osteoporotic women with high fracture risk. Results of monitoring for 2 years]. 160 21

To assess bone metabolism during treatment with gonadotropin-releasing hormone analogue (GnRHa), serum osteocalcin (BGP), alkaline phosphatase (ALP), parathyroid hormone (PTH), calcitonin (CT), calcium (Ca) and phosphorus (P) were determined before and after 6 months of GnRHa treatment in 15 premenopausal women with clinically diagnosed endometriosis. The bone mineral content (BMC) of the lumbar spine (L3) was measured by single energy quantitative computed tomography in 9 women, and in 6 of these 9 women microdensitometry was performed simultaneously during the treatment. BMC decreased significantly to 92.5 +/- 6.8% (mean +/- SD) of the pretreatment value after 6 months of treatment. On the other hand, microdensitometry revealed no significant change during treatment. Serum BGP and ALP were significantly higher after 6 months of treatment than before treatment, indicating an increase in bone formation. These data indicate that the GnRHa treatment induces an increase in bone turnover and a significant bone loss.
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PMID:[Bone mineral content in premenopausal women treated with gonadotropin-releasing hormone analogue]. 161 17

To test conditions under which thyroid hormone might be deleterious to bone, we studied a group of 58 patients who had undergone thyroidectomy because of thyroid cancer 1 to 21 years previously and were treated with steady doses of exogenous thyroid hormone. Vertebral bone density (BMD Z-score) was significantly reduced and biochemical indices of bone resorption (urinary hydroxyproline and plasma tartrate-resistant acid phosphatase activity) and of osteoblastic activity (plasma osteocalcin and bone isoenzyme of serum alkaline phosphatase) as well as the calculated prevalence of bone resorption relative to osteoblastic activity (HBP) were significantly increased in thyroid hormone-treated post-menopausal women but not in men and premenopausal women. The HBP as well as the biochemical indices of bone remodeling were significantly negatively correlated with serum TSH levels. In treated patients, BMD Z-score was significantly dependent on the HBP, menopausal state, duration of treatment and serum TSH levels. In conclusion, the further increase in bone resorption by thyroid hormone is predisposed by menopausal changes in bone turnover. The simultaneous evaluation of biochemical indices of bone resorption and formation improves the assessment of bone loss in patients treated with thyroid hormone in a suppressive dose.
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PMID:Biochemical assessment of bone loss in patients on long-term thyroid hormone treatment. 162 31

Circulating monomeric human calcitonin (hCT-M), parathyroid hormone, osteocalcin, alkaline phosphatase, urinary hydroxyproline, corrected serum calcium and inorganic phosphate were measured in 49 multiple myeloma patients and 49 matched controls. In patients with Durie-Salmon stage III disease hCT-M levels (16.9 +/- 5.8 ng/l, mean +/- SD) were significantly higher than controls and stage I patients (P less than 0.01), and correlated directly with corrected serum calcium (r = 0.74; P less than 0.001). In the same subgroup 14 of 15 patients had plasma hCT-M concentrations higher than the mean + 2SD of the controls. The calcium infusion test induced an increase of hCT-M in normocalcemic patients which was significantly greater in patients with advanced disease than in either controls or stage I patients. These findings suggest that hCT-M may be a biochemical index of bone resorption and disease activity in myeloma patients with osteolysis. In fact, its plasma concentrations were elevated in a large proportion (93%) of patients with severe bone involvement, and correlated directly with serum calcium. Moreover, our findings suggest the presence of a calcitonin-dependent calcium homeostatic mechanism, that protects against hypercalcemia due to tumor osteolysis.
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PMID:Plasma monomeric calcitonin as a marker of disease activity in multiple myeloma patients with osteolysis. 163 26

The study was carried out on a group of 20 women in reproductive age on chronic haemodialysis and on a control group of 11 healthy women. The women on a regular haemodialysis were divided into two subgroups: normoprolactinaemic and hyperprolactinaemic. The following parameters of bone metabolic changes were studied: serum calcium, phosphorus, alkaline phosphatase, pharathormon, osteocalcin, calcitonin, and also LH, FSH, prolactin and estradiol. The values of serum Ca, P, AP, PTH, CTC, OS and of LH and FSH were significantly higher in women on haemodialysis. The hyperprolactinaemic women on haemodialysis had lower values of bone metabolic parameters than normoprolactinaemic women. Hyperprolactinaemia did not significantly contribute to acceleration of bone metabolic changes which were already very accelerated due of secondary hyperparathyroidism.
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PMID:[The effect of hyperprolactinemia on biohumoral parameters of bone metabolism in women of reproductive age on chronic hemodialysis]. 164 94

22-Oxacalcitriol (OCT), a synthetic vitamin D analog, can mimic the ability of 1,25-dihydroxyvitamin D3[1,25-(OH)2D3] to differentiate leukemia and skin cells, to enhance the immune response and to suppress PTH secretion, but has much less calcemic activity. The mechanism for this selective action is not understood. OCT has been shown to have a diminished ability to mobilize calcium from bone in vivo, but in vitro findings are contradictory. Little is known about the effect of OCT on bone forming cells. Therefore, the present studies were designed to investigate the actions of OCT at the molecular level in the osteoblast-like cell line, ROS 17/2.8. 3H-OCT was bound to the vitamin D receptor (VDR) in intact cells at the same rate as 3H-1,25-(OH)2D3. As previously found for 1,25-(OH)2D3, the time course of specific binding of OCT was biphasic, with an initial plateau at 1 h and a further increase from 2-8 h. Scatchard analysis demonstrated that exposure to 3H-1,25-(OH)2D3 increased VDR from 24 fmol/mg protein at 2 h to 85 fmol/mg protein at 8 h. Exposure to 3H-OCT increased VDR from 22 to 76 fmol/mg protein, indicating that OCT is also capable of up-regulating the VDR in ROS 17/2.8 cells. In contrast to the lower affinity of OCT for VDR reported for chick intestine and HL-60 cells, the Kd for OCT in intact ROS 17/2.8 cells was identical to that for 1,25-(OH)2D3. The effect of OCT on osteocalcin secretion and alkaline phosphatase (ALP) activity in ROS 17/2.8 cells was also determined. Pretreatment for 24 h with either 1,25-(OH)2D3 or OCT resulted in a dose-dependent enhancement of osteocalcin secretion. A 2-fold stimulation by both compounds was observed with 10(-7)M. ALP activity was measured after a 72-h incubation with 10(-7)M 1,25-(OH)2D3 or OCT. Both compounds increased ALP activity to the same extent. Stimulation by OCT of VDR levels, ALP activity, and osteocalcin secretion were inhibited by the addition of 5 microM cycloheximide, indicating that these actions of OCT require new protein synthesis. Thus, OCT, like 1,25-(OH)2D3, up-regulates the vitamin D receptor, stimulates osteocalcin secretion, and increases ALP activity in ROS 17/2.8 cells, suggesting that the analog may be as active as 1,25-(OH)2D3 in stimulating bone formation in vivo. The low activity of OCT in mobilizing calcium from bone in vivo does not appear to be due to an inability of this compound to act on osteoblasts.
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PMID:The activity of 22-oxacalcitriol in osteoblast-like (ROS 17/2.8) cells. 164 45

Serum vitamin D metabolites and urinary calcium excretion; parameters of bone formation (serum alkaline phosphatase, serum osteocalcin); parameters of bone resorption (24 hour hydroxyprolinuria, 2 hour fasting urinary hydroxyproline/creatinine ratio); and parameters of cortical and trabecular bone density, parathyroid hormone (iPTH, COOH terminal assay), and serum minerals (calcium, phosphorus) were followed serially in 55 young adults (21 women and 34 men) from December 1985 until January 1987 at four different times during the year. The effect of a low-dose cyclooxygenase inhibitor (piroxicam 5 mg daily) on the same parameters of bone density and bone turnover when given from December until May, was also evaluated in this study. At the end of the treatment period parameters of bone turnover and bone density were comparable between placebo and piroxicam-treated groups. Therefore, the results of all subjects were pooled in order to investigate seasonal variation. In both sexes, seasonal variation was found not only for 250HD3 but also for 1,25(OH)2D3, serum calcium and phosphorus, urinary calcium excretion, and for bone density at the lumbar spine. Parameters of bone formation (serum osteocalcin and alkaline phosphatase), bone resorption (24 hour urinary hydroxyprolinuria and fasting urinary hydroxyproline/creatinine ratio) and PTH were influenced by this seasonal variation. We conclude that in young adults, a significant seasonal variation occurs, with low winter and high summer values, for serum 25 and 1,25(OH)2D3 for urinary calcium apparently without important influence on parameters of bone turnover or parathyroid activity and for lumbar spine density. Treatment with a low-dose cyclooxygenase inhibitor was without influence on the observed changes.
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PMID:Seasonal variation in bone metabolism in young healthy subjects. 165 77

An oral calcium (Ca) tolerance test was used to compare the acute calcaemic, calciuric, parathyroid and bone turnover responses in 21 women at 36 weeks of pregnancy, 27 breast-feeding women studied 22 weeks postpartum and 27 control women. In all groups the oral Ca load increased plasma Ca and urinary calcium excretion (CaE), reduced intact PTH concentration (and consequently reduced renal phosphate and cyclic AMP excretion) and reduced hydroxyproline excretion (HypE, a biochemical index of bone resorption). There were no changes in the biochemical indices of bone formation, serum osteocalcin (elevated in the lactating group) and alkaline phosphatase, in any group. The pregnant women had the same fall in HypE and a greater calcaemic response than the controls. These results suggest that there is increased intestinal Ca absorption efficiency and a normal rate of bone resorption in late pregnancy. In contrast, the lactating women had a greater fall in HypE (from a baseline twice that of controls) and a significantly lower (p less than 0.001) rise in CaE, despite a calcaemic response similar to that of controls. Therefore, in lactation there is increased bone turnover and an increased capacity to reabsorb Ca in the renal tubule, compared to controls. An oral calcium supplement may benefit breast-feeding women, by reducing lactation-related elevated rate of bone resorption and consequent loss of trabecular bone.
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PMID:Acute effects of an oral calcium load in pregnancy and lactation: findings on renal calcium conservation and biochemical indices of bone turnover. 166 6


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