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)

In order to assess the correlation between menopause and osteoporosis, both in pathogenetic and therapeutical terms, a study was carried out in four comparable group of patients at Department B of the Institute of Gynaecology and Obstetrics at the University of Turin. Patients were divided as follows: 24 patents affected by evident osteoporosis, 39 patients with the first symptoms of osteoporosis, 27 with hypercalcemia and 33 healthy controls. The following tests were performed in all subjects: serum assay of androstenedione, estrone, 17-beta-estradiol, PTH, calcium, phosphorus, alkaline phosphatase and creatinine. Laboratory tests were repeated monthly in all patients and control subjects. Dual chromatic ray bone densitometry was performed in all patients at the start and end of treatment. With regard to therapy, each group was subdivided into two equal subgroups which were treated with carbocalcitonin or conjugated estrogens. From the findings, it is clear that there is a non-significant difference between serum levels of androstenedione, estrone and estradiol in the three groups examined and control subjects. Although the possibility that the fall in steroid hormones might contribute to bone load cannot be excluded, it is not possible to demonstrate that this is the most important factor in the pathogenesis of osteoporosis given that many women do not develop osteoporotic symptoms after menopause. In addition, in therapeutic terms, all bone density parameters considered in patient osteoporosis improved after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative analysis of therapeutic effects of carbocalcitonin and and conjugated estrogens in post-menopausal osteoporosis]. 208 96

Bone gamma-carboxyglutamic acid containing protein (BGP) has been utilized effectively as a serum marker of bone turnover in healthy normals and in individuals with a variety of metabolic bone disorders including postmenopausal osteoporosis and Paget's disease. The utility of this serum marker in other bone disorders, including that associated with the maintenance of patients on long-term parenteral nutrition, still requires definition. Because of our interest in this clinical syndrome and the availability of serum and of bone formation rates (BFR) measured directly from double tetracycline labeling in 11 long-term parenteral nutrition patients, we measured BGP levels in these patients and attempted to correlate this measure with BFR. Serum vitamin D metabolites, immunoreactive parathyroid hormone (PTH), and alkaline phosphatase (alk phos) were also measured. Serum BGP was only weakly and not significantly correlated (r = 0.24, p = NS) with bone formation rate for the group as a whole. However, in a subgroup of 10 patients without hyperparathyroidism, there was strong and significant correlation (r = 0.81, P less than 0.01) between BGP and BFR. There was also a strong correlation between bone formation rate and serum 1,25 dihydroxyvitamin D [1,25(OH)2D] levels (r = 0.89, P less than 0.01, n = 11). The mechanism of this association could not be established. A correlation of borderline significance was observed between bone formation rate and serum alk phos (r = 0.60, P = 0.05, n = 11). The current data suggest that additional studies may help to more fully define the utility of serum measurements in quantifying bone dynamics in parenteral nutrition patients, and that measures of vitamin D metabolites, BGP, and alk phos may prove useful.
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PMID:Serum markers of bone formation in parenteral nutrition patients. 191 94

The effect of long-acting medroxyprogesterone acetate (MPA) on the trabecular bone density in patients with glucocorticoid-induced osteoporosis (GCO) was evaluated. Thirteen steroid-dependent asthmatic male patients with GCO were administered 200 mg MPA intramuscularly at 6-week intervals and 1 g of elemental calcium daily for a period of 1 year. Ten additional matched steroid-dependent asthmatic male patients received 1 g of elemental calcium daily (controls). All 23 patients involved in the study had vertebral trabecular bone densitometry (TBD) by quantitative computed tomography (QCT) at baseline and at 6 and 12 months into the study. A 17% increase in TBD was found in the MPA-treated patients at 1 year (from 68.5 +/- 5 to 80.2 +/- 4 mg K2HPO4/cc) in contrast to the control group who experienced a 21% decrease in TBD during the same period of time (from 80.5 +/- 7 to 63.7 +/- 8 mg K2HPO4/cc) (T = 6.90, P = 0.0001 df = 21). There were no significant changes in other parameters followed during the study in the MPA-treated group (serum calcium, phosphorus, magnesium, PTH, alkaline phosphatase, triglycerides, total and HDL cholesterol, urinary excretion of calcium, phosphate, creatinine) except for a decrease in the serum luteinizing hormone (LH) and testosterone (P less than 0.01) as well as of the hydroxyproline-creatinine ratio (P less than 0.01). The results lend support to the hypothesis of a progesterone-glucocorticoid competitive antagonism at the bone level, though other possibilities can be entertained, and suggest MPA as an effective therapy for glucocorticoid-induced osteoporosis in men.
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PMID:Effective therapy of glucocorticoid-induced osteoporosis with medroxyprogesterone acetate. 214 69

Parathyroid hormone (PTH) has been proposed as a skeletal activator for cyclical protocols of treatment for osteoporosis; among several potential drugs that might serve to depress the subsequent phase of osteoclastic bone resorption, calcitonin is the most selective. Twenty patients aged 50-78 years were enrolled in a study of their biochemical responses during a 14-day activation cycle with synthetic hPTH 1-38, given as a subcutaneous injection of 400 IU/day; half the patients were randomly allocated to receive a subsequent 56-day depressor cycle with calcitonin in a dose of 100 U/day, while the remainder received no further treatment. All patients received an initial 24-h intravenous infusion of hPTH 1-38 (0.5 U/kg/h) to evaluate the PTH-dependent renal synthesis of 1,25(OH)2D. Serum calcium increased from 2.20 +/- 0.07 mmol/l to 2.56 +/- 0.16 (P less than 0.005) during PTH infusion, but was not significantly different from baseline during intermittent treatment. Baseline concentrations of serum 1,25(OH)2D were 22.8 +/- 8.2 pg/ml, increased to 52.2 +/- 25.1 (P less than 0.005) during infusion and remained significantly higher than baseline after 14 days intermittent therapy (33.1 +/- 19.4, P less than 0.05). Gastrointestinal absorption of 45Ca, as represented by alpha (peak fractional absorption/h), increased from 0.397 +/- 0.173 to 0.552 +/- 0.210 (P less than 0.01) during hPTH 1-38 therapy and was moderately correlated with the increment in serum 1,25(OH)2D levels (r = 0.5, P less than 0.03). Daily calcium excretion was significantly increased above baseline during hPTH 1-38 therapy, but there were no correlations between changes in urinary calcium, alpha or serum 1,25(OH)2D levels. Baseline fasting urinary excretion of OH-proline increased during hPTH 1-38 treatment from 30.5 +/- 13.9 mol/mmol creatinine to 43.4 +/- 17.5 immediately after hPTH 1-38 infusion (P less than 0.025), and mean excretion was persistently higher than baseline during intermittent treatment; the increased urine calcium and OH-proline excretion are consistent with PTH-induced activation of bone resorption. Serum alkaline phosphatase and osteocalcin levels increased significantly during a 90-day period of observation after the hPTH 1-38 cycle, which is consistent with increased osteoblast activity in association with coupled bone formation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical responses to sequential human parathyroid hormone (1-38) and calcitonin in osteoporotic patients. 216 92

1. To determine the relationships between parathyroid hormone activity and long-term sodium fluoride therapy in osteoporosis, cytochemical bioassays (for biologically active parathyroid hormone) were performed in 22 osteoporotic control patients and in 18 patients after 15 +/- 10 months of treatment (60 mg of sodium fluoride daily). Ten patients were studied longitudinally by repeated metabolic balances and were therefore common to both groups. All patients were receiving mineral supplements. 2. Cross-sectional data showed a fourfold mean increase in biologically active parathyroid hormone on fluoride treatment (P less than 0.005) together with a 51% increase in serum alkaline phosphatase (P less than 0.005). Longitudinal data showed, in addition, a significant increase in the calcium balance of 2.4 +/- 1.2 (SEM) mmol daily (P less than 0.05) and the development of a positive phosphorus balance (P less than 0.02). 3. Fluoride-treated patients were then analysed in two groups according to the level of biologically active parathyroid hormone. Thirty-two per cent of values were above the upper limit of normal (18 pg/ml). The mean serum alkaline phosphatase level in this group showed no elevation above that of the control patients, the overall rise being accounted for entirely by patients with normal levels of biologically active parathyroid hormone. High levels of biologically active parathyroid hormone were also associated with relative hypophosphataemia (P less than 0.01), relative hypercalciuria (P less than 0.05) and an increased urine/faecal calcium ratio (P less than 0.025). 4. Results show that long-term fluoride and calcium therapy increase biologically active parathyroid hormone in osteoporosis and that excessive parathyroid hormone activity may account for certain features of the refractory state.
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PMID:Fluoride therapy and parathyroid hormone activity in osteoporosis. 216 71

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76

A cohort of 101 patients were treated with enteric-coated sodium fluoride tablets and calcium supplements. Vitamin D was also given in supra-physiologic doses in 70% of the cases. Lumbar bone mineral density (BMD), as measured by dual-photon absorptiometry, increased in a linear fashion up to four years, irrespective of the value of initial BMD and of the underlying condition, be it involutional osteoporosis (the vast majority), glucocorticoid osteoporosis, or even osteogenesis imperfecta. Estrogen replacement therapy (ERT) seemed to promote the fluoride-induced increase in lumbar BMD, as did the vitamin D supplements. Of these patients, 17% proved "resistant" to the therapy. There was no way of predicting who would be in this category. Compared with an age- and sex-matched control group, women showed significantly different behavior of their bone mass. In the control group, the losses were highly significant at the lumbar spine and at all three scanning sites of the forearm, as measured by single-photon absorptiometry. In contrast, the fluoride group had a significant gain of BMD at the lumbar spine and changes of BMC at the forearm were not significant. Fluoride thus preserved bone mass at the appendicular skeleton, while increasing it at the axial skeleton. When comparing the patients who received vitamin D supplements and those who did not, there was a significant difference in the appendicular skeleton. The distal forearm in the vitamin D-supplemented group tended to gain, whereas the midforearm lost significant bone mass. The trend was reversed in the group without vitamin D-supplementation, a more favorable pattern. Therefore, vitamin D supplements should not, as a rule, be provided to such patients. The biochemical hallmark of the fluoride-induced changes is a slight rise of the alkaline phosphatase within the normal range. Alkaline phosphatase levels that exceed the upper limit of normal signal a warning that too much fluoride and/or too little calcium supplements are being administered, or that a fluoride-related complication is impending or has occurred (e.g., a stress fracture). Osteosclerosis was achieved in 69% of the cases who had a radiological followup of at least four years (average period of appearance: 1.8 years). Stress fractures in the lower limbs occurred in 17 patients, almost exclusively in females, and appeared on average 2.2 years after initiation of therapy. In this group of stress fractures there was significant cortical bone loss at midforearm.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment of the vertebral crush fracture syndrome with enteric-coated sodium fluoride tablets and calcium supplements. 218 27

There is increasing evidence that pamidronate and related compounds are effective in the prevention and treatment of osteoporosis. It is therefore of relevance to document the time course and mechanism of bisphosphonate action in this condition. To this end, the present study describes the biochemical responses to prophylactic treatment with oral pamidronate (APD, 150 mg/day) in 16 glucocorticoid-treated patients and contrasts them with those in 19 steroid-treated control subjects. Measurements were made over a period of 12 months. The treated patients showed a fall in urine hydroxyproline excretion at 6 weeks associated with a reduction in serum ionized calcium concentration, a rise in serum 1,25-(OH)2D3, and a nonsignificant rise in serum bone gla protein (BGP). In contrast to BGP, serum alkaline phosphatase activity declined at 6 weeks, falling further at 3 months. Between 3 and 12 months, BGP levels paralleled those of alkaline phosphatase and hydroxyproline, all these being significantly below their initial values, and the other parameters returned to baseline. There was a gradual increase in plasma phosphate concentrations in the treated group over the 12 month period. It is concluded that pamidronate produces an acute and sustained inhibition of bone resorption followed by a more gradual reduction in bone formation. This transient dissociation results in a reduction in serum calcium, leading to a rise in serum 1,25-(OH)2D3, which in turn stimulates BGP production. Thereafter, indices of bone turnover remain subnormal but serum calcium and 1,25-(OH)2D3 return to baseline.
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PMID:Prevention of glucocorticoid-induced osteoporosis. 220 Feb 39

Forty women aged 64.7 +/- 5.1 yr with established postmenopausal osteoporosis were blindly allocated to 1 yr's treatment with either continuous combined estrogen/progestogen therapy (2 mg estradiol + 1 mg norethisterone acetate + 500 mg calcium daily) or placebo + 500 mg calcium daily. In the group treated with hormones bone mineral density in the spine (dual photon absorptiometry) and bone mineral content in the ultradistal forearm (single photon absorptiometry) increased highly significantly by 8-10% during the 1 yr of treatment. Bone mineral content in the mid-shaft of the forearm (single photon absorptiometry) and the total body bone mineral (dual photon absorptiometry) increased by 3-5% when compared to that in the placebo group, which showed virtually unchanged values at all measurement sites. Seven of the women treated with hormones were examined after a further year of treatment. BMC increased by another 3-6%, reaching a 12% increase in bone mineral density in the spine after 2 yr of treatment. Biochemical estimates of bone resorption (fasting urinary calcium and hydroxyproline) and bone formation (serum alkaline phosphatase and plasma osteocalcin), decreased significantly (P less than 0.001) in the group treated with hormones, but remained unchanged in the placebo group. The reduction in indices of bone resorption was more pronounced than that in bone formation after one year, indicating a positive bone balance. No further changes were seen in these bone turnover parameters during the second year of treatment. In the group treated with hormones, serum levels of triglycerides, total cholesterol, and low density lipoprotein cholesterol decreased by about 12% (P less than 0.05-P less than 0.01), whereas high density lipoprotein cholesterol decreased by about 8% (P less than 0.001). The high density lipoprotein cholesterol/low density lipoprotein cholesterol ratio was unchanged. The hormone treatment did not produce any major side effects, and only minor bleedings were experienced by a few women. The present study demonstrates that treatment with female sex hormones in this particular combination is a realistic approach to the treatment of women with established postmenopausal osteoporosis.
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PMID:17 Beta-estradiol and continuous norethisterone: a unique treatment for established osteoporosis in elderly women. 220 24

A comprehensive analysis is reported in 376 healthy middle and old-age persons, including measurements of bone mineral content (BMC) of the mid-radias, pituitary sex hormones (RIA), serum calcium, phosphate, albumin, alkaline phosphatase, urinary calcium, phosphate, hydroxyproline (BCA), daily intake of protein and calcium, physical exercise and activity, body weight, amenorrhea etc. Results showed that the preponderance of bone resorption over bone formation is the essential pathophysiological change of involutional osteoporosis. For females, bone loss is regulated mainly by estrogen in presenile group, co-regulated by estrogen and androgen in senile group. For males, urinary hydroxyproline excretion is also regulated by estrogen A remarkable correlation was observed between BMC and the following factors: serum calcium, urinary calcium, hydroxyproline, body weight, physical exercise, amenorrhea, intake of protein and calcium. Our data indicated that the intake of calcium daily in old chinese should not be lower than 700 mg (male) and 900 mg (female), protein should not be lower than 60-70 g. The age of onset, prevalence rate and BMC average reduction rate of osteoporosis in chinese were also observed in the studies.
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PMID:[Etiological and influential factors of involutional osteoporosis in old Chinese]. 222 49


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