Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-nine postmenopausal women (aged 55-75 years) with at least one osteoporotic fracture were allocated to one year of treatment with the anabolic steroid nandrolone decanoate (50 mg i.m. every 3 weeks) or placebo injection. Both groups also received a daily intake of 500 mg calcium. Thirty-six women (92%) completed the study. In the nandrolone decanoate-treated group the fat corrected bone mineral content in the proximal part of the distal forearm (measured by single photon absorptiometry) showed a significant increase of 3% compared with placebo (P less than 0.01), and the same tendency was seen in the bone mineral content of the distal part of the distal forearm and density of the lumbar spine (measured by dual photon absorptiometry). However, this did not reach significance. In the placebo group all bone mineral measurements remained unchanged. The biochemical estimates of bone formation (plasma bone Gla protein (BGP), serum alkaline phosphatase) and whole body retention (WBR) of 99mTc-diphosphonates were not statistically significantly changed by the nandrolone decanoate therapy. We conclude that treatment with nandrolone decanoate does increase the bone mineral content; however, this may not be due to a direct increase in bone formation. The mechanism may theoretically be a combination of decreased bone resorption and increased muscle mass, which both play a beneficial role in conserving bone.
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PMID:Treatment of postmenopausal osteoporosis: is the anabolic steroid nandrolone decanoate a candidate? 266 84

In order to determine the prevalence of secondary hyperparathyroidism in patients with Paget's disease of bone, we measured serum parathyroid hormone levels (N-terminal assay) in 39 patients with a wide range of pagetic activity. All patients had normal serum calcium levels. A total of 30 patients were either untreated or had received no treatment for 6 months or longer when studied; the other 9 were receiving either salmon calcitonin (3) or EHDP (6). The results showed that in 7 of the 39 patients (18%) parathyroid hormone levels were increased above normal. These were among the most severely affected cases, as manifested by the degree of elevation of three pagetic biochemical indices: serum alkaline phosphatase, plasma bone Gla protein, and 24 h urinary hydroxyproline-creatinine ratios. Levels of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 were normal. We examined the relationships between parathyroid hormone and each of the three pagetic indices as well as serum calcium for the entire group of 39 patients. Parathyroid hormone values did not correlate with serum calcium measurements (r = -0.241, p = NS) but did correlate significantly with serum alkaline phosphatase (r = 0.496, p less than 0.001), plasma bone Gla protein (r = 0.537, p less than 0.001), and urinary hydroxyproline (r = 0.450, p less than 0.011). We conclude that relative or absolute increases in parathyroid hormone may occur in moderately active Paget's disease, possibly in the setting of greater calcium demands during periods of increased pagetic new bone formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid function in Paget's disease of bone. 271 81

Dual photon absorptiometry (DPA) has been used to measure the effect of short and medium-term administration of tamoxifen on bone density in the axial skeleton of women with mastalgia. This provided a unique opportunity to monitor the effect of this 'anti-oestrogenic' agent in predominantly premenopausal women, not suffering from malignancy. In addition, plasma levels of calcium, phosphate, alkaline phosphatase and serum levels of oesteocalcin (GLA) have been assayed, both before and after 3 months of starting either tamoxifen or placebo treatment. No significant alterations in bone density were seen. Osteocalcin, alkaline phosphatase and electrolytes were unchanged and there was no dose response observed in women receiving either 10 mg or 20 mg of tamoxifen. Although possessing anti-oestrogenic properties, tamoxifen is also a partial agonist. Administration for the short periods does not measurably influence spinal or femoral bone density and thus the agent can probably be given safely for the short-term treatment of mastalgia.
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PMID:Bone mineral content of women receiving tamoxifen for mastalgia. 276 77

Sera from five patients with skeletal fluorosis were investigated for total calcium, ionized calcium, phosphate, alkaline phosphatase, 25 hydroxyvitamin D (25 OHD), 1,25 dihydroxyvitamin D (1,25[OH]2D), parathyroid hormone, and osteocalcin concentrations. Total and ionized calcium concentrations were normal in four and subnormal in one, but PTH concentration was elevated in all five. The patient with a subnormal calcium concentration also had subnormal 25 OHD and 1,25(OH)2D concentrations and a supranormal PTH concentration. The remaining four had supranormal PTH concentrations despite normal total and ionized calcium concentration, and normal 25 OHD and 1,25(OH)2D levels. Osteocalcin concentration was markedly elevated in all patients, as was alkaline phosphatase activity. These observations show for the first time that patients with fluorosis have markedly elevated osteocalcin, a marker of osteoblastic activity, and that they may have significantly elevated PTH concentrations in the presence of normal total and ionized calcium concentrations.
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PMID:Normal ionized calcium, parathyroid hypersecretion, and elevated osteocalcin in a family with fluorosis. 278 18

Osteocalcin (OC), also called Bone Gla Protein (BGP), is a bone matrix protein of 5800 MW synthesized by osteoblasts. Since OC is mainly metabolized in the kidney, its blood concentration is altered in renal failure. The relationship between OC and the calcium-phosphorus regulating hormones (parathyroid hormone, calcitonin) and the biochemical parameters of bone metabolism (serum calcium, serum phosphorus and serum alkaline phosphatase) was studied in 30 patients on chronic hemodialysis (mean age: 51 years; mean duration of dialysis treatment: 39 months). OC levels were significantly elevated in all patients on chronic hemodialysis (34.7 +/- 31.5 ng/ml) when compared to healthy subjects (6.25 +/- 1.39 ng/ml, p less than 0.001). In 2 patients the OC levels were excessively high (127.54 ng/ml; 148.02 ng/ml), which was associated with severe renal osteodystrophy due to secondary hyperparathyroidism. When divided into 2 groups in the patients with secondary hyperparathyroidism the mean OC value was markedly elevated (50.5 +/- 12.7 ng/ml) compared to the patients without secondary hyperparathyroidism (24.1 +/- 2.8 ng/ml) (p less than 0.05). 70 per cent of the patients on chronic hemodialysis with OC levels greater than 30 ng/ml showed moderate to severe scintigraphic findings of bone disease. In neither of the 2 groups could a correlation between OC and serum alkaline phosphatase be demonstrated. The results indicate, that OC levels could be useful additional parameter in hemodialyzed patients with secondary hyperparathyroidism and OC levels could reflect bone formation in these patients.
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PMID:[Osteocalcin in chronic hemodialysis patients as an additional parameter in the diagnosis of advanced secondary hyperparathyroidism]. 278 25

The authors evaluated bone mineralization by single photon absorptiometry and mineral homeostasis in 7 patients with anorexia nervosa. The patients with anorexia nervosa showed a reduction of bone mineralization in respect to age-sex matched normal values. Serum levels of calcium, ionized calcium, phosphate, magnesium, alkaline phosphatase, calcitonin and 25-hydroxyvitamin D were normal as well as phosphate and hydroxyproline urinary excretion. Osteocalcin levels were significantly low as compared to normal values (5.0 +/- 3.0 ng/ml vs 14.3 +/- 5.2 ng/ml, p less than 0.01) as well as urinary calcium excretion (0.02 +/- 1.01 vs 0.08 +/- 0.06, p less than 0.05); 1,25-dihydroxyvitamin D values were low only in 4 patients. Parathyroid hormone means levels were increased in respect to normal values (74.1 +/- 12.7 pg/ml vs 38.0 +/- 12.0, p less than 0.02). We confirm that adolescents with anorexia nervosa showed a reduced bone mineral content and alterations of mineral homeostasis that may contribute to the development of bone mineral loss.
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PMID:[Calciotropic hormones in osteoporosis caused by anorexia nervosa]. 278 86

10 healthy early postmenopausal women were treated with oestrogen and progestagen for two cycles of 28 days. Serum alkaline phosphatase and bone Gla protein increased during progestagen administration, whereas urinary excretion of calcium and hydroxyproline fell significantly during treatment, independently of progestagen intake. Thus, bone formation increases when progestagen is added to oestrogen treatment, whereas bone resorption may be kept constantly low during oestrogen plus progestagen treatment, leading to a positive calcium balance. This makes possible effective treatment of postmenopausal osteoporosis--treatment of elderly postmenopausal women with substantial bone loss before their bones have fractured or when they have just started to fracture. This study design can be used for easy and rapid screening of potential drugs for the prevention and treatment of postmenopausal bone loss.
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PMID:Uncoupling of bone formation and resorption by combined oestrogen and progestagen therapy in postmenopausal osteoporosis. 286 32

The effect on bone metabolism of an agonist analog of GnRH, nafarelin, was studied in 16 premenopausal women, who received 200 micrograms nafarelin/day for 6 months, and 9 premenopausal women, who received 400 micrograms nafarelin/day for 6 months, followed by a 6-month follow-up period. Bone mineral content in the forearm (measured by single photon absorptiometry) and in the spine (measured by dual photon absorptiometry) significantly decreased after 6 months of treatment with 400 micrograms nafarelin, but 6 months after termination of treatment all bone mineral measurements had returned to pretreatment levels. The bone mineral measurements in the 200 micrograms group did not change throughout the study. In both treatment groups the biochemical estimates of bone turnover increased significantly to postmenopausal levels. Withdrawal of treatment resulted in an abrupt decrease in the bone resorption parameters (fasting urinary hydroxyproline to creatinine and calcium to creatinine excretion ratios and serum phosphate), whereas there was a protracted fall in the bone formation parameters (plasma bone Gla protein and serum alkaline phosphatase) 6 months after termination of treatment. Our findings demonstrate that nafarelin in both doses increased biochemical indices of bone turnover, that 400 micrograms/day nafarelin resulted in a significant decrease in bone mineral content, and that these effects were reversible.
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PMID:The effect of a gonadotropin-releasing hormone agonist analog (nafarelin) on bone metabolism. 297 Oct 80

Bone turnover before and after withdrawal of estrogen/gestagen treatment was studied in a randomized trial with 110 healthy female volunteers, who had passed a natural menopause 6 months to 3 years before the start of the study. Urinary excretion of intravenously injected 99m-technetium diphosphonate was measured as an index of bone turnover; plasma bone Gla protein and serum alkaline phosphatase were measured as indices of bone formation; and fasting urinary excretion of hydroxyproline and calcium were measured as estimates of bone resorption. During 2 years of hormone treatment, all variables decreased highly significantly (p less than 0.001) to a constant low level. Three months after withdrawal all variables increased highly significantly (p less than 0.001) towards, but not above, pretreatment and placebo levels. We conclude that withdrawal of estrogen/gestagen replacement therapy in postmenopausal women increases bone turnover, but not in excess of pretreatment values. This indicates that bone loss (after withdrawal) is similar to that seen in the placebo group and that a rebound phenomenon is unlikely.
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PMID:Bone turnover in postmenopausal women after withdrawal of estrogen/gestagen replacement therapy. 297 70

Recent evidence suggests that the protein osteocalcin is like the bone alkaline phosphatase produced by osteoblasts and circulates in human blood. With the introduction of a radioimmunoassay for serum osteocalcin it was hoped that this test would provide a useful index of altered bone metabolism. Therefore serum osteocalcin was measured in 88 controls and 112 patients with disorders of calcium and phosphate metabolism, isolated elevation of alkaline serum phosphatase in the absence of disease (isolated hyperphosphatasaemia) and children prone to osteopenia. In the controls serum osteocalcin was higher in children less than 15 years (median and range: 11.9, 7.7-15.3 ng/ml) than in adults (3.7, 2.6-5.2 ng/ml) and was highly correlated to alkaline serum phosphatase activity (r = 0.87, n = 88, P less than 0.01). Osteocalcin was elevated in primary hypoparathyroidism, low in untreated hypoparathyroidism but normal in hypoparathyroidism (including pseudohypoparathyroidism) during vitamin D treatment. The bone protein was low-normal and increased to high-normal levels during vitamin D therapy in vitamin D deficiency rickets and familial hypophosphataemic rickets, but remained low in patients with end organ resistance to 1,25-dihydroxyvitamin D. Osteocalcin (and urinary hydroxyproline) were not elevated in isolated hyperphosphatasaemia, indicating that mechanisms other than increased bone turnover may account for the markedly elevated serum alkaline phosphatase activity in these subjects. Osteocalcin was decreased in children with diabetes mellitus type I and in patients on glucocorticoid treatment, indicating decreased bone formation. It is concluded that the measurement of serum osteocalcin seems to be a reliable index of bone formation provided that the vitamin D status and renal function are normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of serum osteocalcin as an index of altered bone metabolism. 301 28


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