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)

The effects of low-level lifetime exposure to cadmium (Cd) on the skeleton mineral status and the risk of bone loss in the elderly were studied in an experimental model of human environmental exposure in non-Cd-polluted areas. Young female Wistar rats were exposed to 1 mg Cd/l in drinking water for 24 months. Bone mineral content (BMC), density (BMD) and area of the lumbar spine (L1-L5) and femur, and total skeleton BMD (T-BMD) were measured densitometrically at the baseline and after 6, 12, 18, and 24 months. Prevalence of osteopenia and osteoporosis was evaluated based on the BMD T score and Z score. Osteocalcin (OC) in the serum and total alkaline phosphatase (total ALP) in the serum, cortical and trabecular bone samples as bone formation markers, and C-terminal cross-linking telopeptide of type I collagen (CTX) in the serum and urine as bone resorption markers were measured. Calcium (Ca) and Cd concentrations in the serum/blood and urine were determined as well. In the Cd-exposed females, the L1-L5 and femur BMC and BMD at all the studied time points were lower compared to control. The exposure to Cd resulted in lower accumulation of peak bone mass, accelerated osteopenia, and enhanced the prevalence of osteoporosis in aged rats. The effect of Cd was more pronounced at the L1-L5 than at the femur. CTX concentration in the urine was decreased after 6 months and next increased compared to control, whereas the urinary loss of Ca was enhanced during the exposure to Cd. After 24 months of the treatment, the serum total ALP activity and the activity of this enzyme in cortical and trabecular bone decreased and serum CTX concentration increased, whereas the concentrations of OC and Ca were unchanged. The study clearly revealed that low-level lifetime exposure to Cd diminishes the accumulation of bone mass during skeletal growth and influences bone metabolism at maturity causing osteopenia, and enhances the age-related bone loss due to high turnover rate leading in consequence to osteoporosis in aged rats. The results together with our previous findings confirm the hypothesis that environmental exposure to Cd may be a risk factor for skeletal diseases.
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PMID:Low-level lifetime exposure to cadmium decreases skeletal mineralization and enhances bone loss in aged rats. 1554 44

A case of osteogenesis imperfecta (OI), which was successfully treated with alendronate is reported. A 41-year-old premenopausal woman with OI type I, who had frequently been experiencing fragile fractures, consulted our clinic because of back pain associated with spinal osteoporosis. She had experienced heart surgery (aortic valve replacement) due to aortic regurgitation 5 years before her first consultation with our clinic. After the surgery, she had been taking warfarin 3 mg/day, and this treatment was continued during our follow-up period. She was treated with alendronate (5 mg/day, daily) for 18 months. The bone mineral density of the lumbar spine (L2-L4) measured by dual energy X-ray absorptiometry (Norland XR-36) increased for 18 months, and back pain markedly decreased. The urinary cross-linked N-terminal telopeptides of type I collagen and serum bone-specific alkaline phosphatase, osteocalcin, and undercarboxylated osteocalcin levels also markedly decreased. No new fragile vertebral or non-vertebral fractures were observed during the 18 months of treatment. This report provides evidence indicating that treatment with oral alendronate may have the potential to decrease bone turnover, improve the lumbar BMD, reduce back pain, and prevent new fragile fractures in premenopausal women with OI type I.
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PMID:Effect of treatment with alendronate in osteogenesis imperfecta type I: a case report. 1564 30

Bone density, bone turnover and fracture susceptibility were evaluated in 1,132 randomly recruited women, all 75 years old. Seventy-four of the women had diabetes, while 1,058 women did not. Areal bone mineral density (aBMD) of the hip and lumbar spine was investigated by dual energy X-ray absorptiometry (DXA), and bone mass of the calcaneus was measured by ultrasound. Urinary deoxypyridinoline/creatinine (U-DPD/Crea) and serum C-terminal cross-linked telopeptide of type 1 collagen (S-CTX) were assessed as markers of bone resorption. Serum bone-specific alkaline phosphatase (S-bone ALP) and serum osteocalcin (S-OC) were assessed as markers of bone formation. Also, serum 25(OH) vitamin D and serum parathyroid hormone (S-PTH) were assessed. Fracture susceptibility was evaluated retrospectively and prospectively for up to 6.5 years. In diabetic women, the aBMD of the femoral neck was 11% higher (p<0.001), and BMD of the lumbar spine was 8% higher (p=0.002) than in non-diabetic women. There was no difference in bone mass by ultrasound of the calcaneus. Women with diabetes had higher BMD of the femoral neck (p<0.001) and lumbar spine (p=0.03) also after correction for differences in body weight. In diabetic women, U-DPD/Crea, S-CTX, and S-OC were decreased when compared with non-diabetic women (p=0.001 or less). After correction for covariance of body weight and plasma creatinine, S-CTX (p<0.001) and S-OC (p<0.001) were still lower in the diabetic women. Diabetic patients had hypovitaminosis D (p=0.008), a difference explained by differences in time spent outdoors and body weight. S-PTH did not differ between the groups. Women with diabetes had no more lifetime fractures (52%) than women without diabetic disease (57%), (p=0.31). This study shows that elderly women with diabetes and without severe renal insufficiency have high bone mass and low bone turnover. The high bone mass and low bone turnover is not likely to have a strong influence on fracture susceptibility.
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PMID:Increased bone density and decreased bone turnover, but no evident alteration of fracture susceptibility in elderly women with diabetes mellitus. 1582 89

Our aim was to evaluate changes in serum levels of selected bone metabolism indicators and bone density over 24 months following renal transplant. A partial objective was assessment of the effectiveness of prophylactic administration of vitamin D and calcium preparations to prevent progression of osteopathy after kidney transplantation. Forty patients after kidney transplantation were prophylactically given vitamins A and D (800 IU) and calcium (1000 mg) a day. During monitoring, the serum creatinine in all recipients was <200 micromol/L (subgroup A with creatinine concentration < 120 micromol/L versus subgroup B with creatinine 120 to 200 micromol/L). The concentration of serum parathormone, serum level of bone fraction of alkaline phosphatase, serum concentrations of phosphorus and calcium urinary 24-hour excretion of phosphorus and calcium were examined at 2 weeks and 2 years after transplantation. In the same time period, radiographs of thoracic, lumbar spine, and hip joints were obtained. Bone density (BMD) of the lumbar (L) spine and the hip was determined by dual-energy X ray (Lunar Prodigy). Two years after transplantation in subgroup A, the BMD showed decrease in 80% of recipients in the L spine area but hip showed a 15% BMD increase. In subgroup B, the BMD decreased in 95% recipients in L and hip and only 25% showed a BMD increase. No clinical or radiographic sign of fracture was detected in this group. We conclude that prophylactic administration of vitamin D and calcium is not sufficient to prevent the progression of osteopathy after renal transplantation. Changes in bone density evaluated after the kidney transplantation are affected by graft function.
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PMID:Changes in bone mineral density and selected metabolic parameters over 24 months following renal transplantation. 1584 9

Osteoporosis is a common concomitant disease in patients with rheumatic diseases on glucocorticoid (GC) therapy. Bone status is usually evaluated by determination of bone density in combination with clinical examinations and laboratory tests. However, the strength of individual biochemical bone makers in GC-induced osteoporosis has yet to be fully clarified. For this reason, different bone markers were investigated in correlation with bone density in patients with rheumatic diseases. Approximately 238 patients (212 women, 26 men) with a rheumatic disease and under GC therapy were examined consecutively for the first time with regard to bone density (BMD) and bone markers [osteocalcin, bone-specific alkaline phosphatase (precipitation method/tandem-MP ostase), crosslinks [pyridinoline (PYD), deoxypyridinoline (DPX), N-terminal telopeptide (NTX)]]. The daily glucocorticoid dose was 10 mg prednisone equivalent (median), and the cumulative dose was 12 g prednisone equivalent (median). None of the patients had previously taken medication for osteoporosis. Osteoporosis was demonstrated in 35.3% of the patients, osteopenia in 47.5%, and a normal BMD in 17.2%. The results of tandem-MP ostase correlated with the BMD of the lumbar spine and of the femoral neck. The values for N-terminal telopeptide and pyridinoline correlated only with the bone density of the femoral neck. All results were statistically significant, although the correlation coefficients were low. After classification of the patients according to their BMD values (osteoporosis, osteopenia and normal BMD), there were significantly more patients with bone markers above the norm in the osteoporosis group and in the osteopenia group than in the group with normal bone density. All bone markers recorded behaved similarly in relation to the bone density values. The same analysis was also undertaken for the different disease groups. In these subgroups there was also a correlation between ostase/crosslinks with BMD, but the correlation coefficients were low. A general recommendation for the routine use of a specific bone marker in patients with rheumatic diseases on glucocorticoid therapy cannot be made from a cost-benefit point of view mainly because of limited predictive power (low correlation coefficients, incomplete correlation with different sites of BMD measurement).
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PMID:Correlation of different bone markers with bone density in patients with rheumatic diseases on glucocorticoid therapy. 1588 44

Structural and functional impairment of skeletal system is a relevant cause of morbidity and disability in patients with Cushing's syndrome (CS). Approximately 30-50% of patients with CS experience fractures (particularly at the spinal level) consistent with the 50% incidence of osteoporosis. Growth failure, pubertal arrest are the hallmarks of CS in children and growing adolescents leading to reduced final adult height and peak bone mass. The decrease in osteoblast number and function, through different mechanisms, seems to play a central role in the bone loss in CS. Patients with CS have decreased serum levels of osteocalcin and alkaline phosphatase. Considering the preferential bone loss in the cancellous skeleton it is reasonable to measure BMD, possibly with Dual X-rays absorptiometry (DEXA) at lumbar spine, in all patients with CS. Patients cured from CS have increased prevalence of spine damage: therefore, a radiological follow-up of the skeleton should be included in the management of patients with CS not only during the active phase but also after cure. Glucocorticoid-induced osteoporosis is reversible. The recovery of bone loss in CS is slow, taking approximately ten years to become complete. In the meanwhile, patients with severe osteopenia are exposed to a high risk of fracture. Alendronate may induce a more rapid improvement in BMD than cortisol normalization alone and it could be useful in patients with persistent postsurgical hypercortisolism to prevent further bone loss. The decision to discontinue antiresorptive therapy should be based on clinical monitoring and DEXA measurements.
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PMID:Cushing's syndrome and bone. 1601 Apr 58

Osteopenia and osteoporosis are currently receiving particular attention as late effects of therapy in survivors of childhood acute lymphoblastic leukemia (ALL). The aim of this study was to evaluate abnormalities in bone mass and mineral homeostasis in children with ALL after induction therapy (during consolidation treatment). Lumbar spine (L2-L4) bone mineral density (BMD, g/cm(2)) was measured by dual energy X-ray absorptiometry in 20 children with ALL, a median of 25.9 months postdiagnosis and results were expressed as z-scores relative to healthy Caucasian children (controls). Serum levels of intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), calcium, phosphate, and magnesium were also analyzed. In addition, the body mass indexes (kg/cm(2)) of patients and controls were calculated. Results were compared with those of 40 healthy controls. Among the 20 children with ALL (12 boys and 8 girls), 12 presented z-scores < 1 SD (normal) and 8 were osteopenic (z-score between 1 and 2.5 SD). In addition, children with ALL had reduced lumbar BMDs (z-score -0.817) in comparison to healthy controls (z-score -0.353) (p = .04). Moreover, alkaline phosphatase and intact parathyroid hormone values were significantly increased compared to controls values. The data demonstrate that bone metabolism in children with ALL during consolidation therapy is disturbed, resulting in a reduced BMD and z-score with respect to healthy controls. Since a reduced BMD predisposes to osteopenia and osteoporosis, specific attention and therapeutic interventions should be considered.
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PMID:Evaluation of bone metabolism in children with acute lymphoblastic leukemia after induction chemotherapy treatment. 1602 Jan 15

The MTHFR c.677C>T polymorphism has been shown to have significant effects on skeletal health in middle-aged to elderly women and men. Despite an accumulating amount of data on MTHFR genetics and the association between homocysteine levels and fracture, it remains unknown if MTHFR c.677C>T genotype affects bone mineral accretion in youth or bone loss in adulthood. The purpose of this cross-sectional study was to examine the effects of this common allelic polymorphism on peak bone mass and bone turnover. We performed MTHFR genotyping in 780 healthy Danish men, aged 20 to 29 years, participating in the Odense Androgen Study. BMD at the spine, hip and whole-body was measured using a Hologic QDR-4500 densitometer. Genotype frequencies were compatible with Hardy-Weinberg equilibrium. Spine BMD was significantly associated with genotype, with a decrease in BMD of 0.20 SD for each copy of the T-allele. Effects were independent of age, BMI, smoking and serum levels of vitamin D and IGF-I. Associations with BMD of the hip and whole body were short of statistical significance. MTHFR genotype showed no association with the bone turnover markers 1-CTP, bone specific alkaline phosphatase or osteocalcin. In conclusion, significant skeletal effects of this common polymorphism were present at the lumbar spine in men at the age of 25 years.
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PMID:MTHFR c.677C>T polymorphism as an independent predictor of peak bone mass in Danish men--results from the Odense Androgen Study. 1616 7

Vertebral fractures due to osteoporosis are a common but frequently unrecognized complication in established ankylosing spondylitis (AS). It is known that inflammatory activity in rheumatic diseases (i.e., proinflammatory cytokines) itself plays a possible role in the pathophysiology of bone loss. The aim of this study was to analyze whether inflammatory activity and an alteration of the vitamin D metabolism play a substantial role in the loss of bone mass in AS. In this cross-sectional study, 58 patients with established AS and an age- and sex-matched control group were examined. The vitamin D status was investigated, as was, in parallel, the relationship to disease activity (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], Bath Ankylosing Spondylitis Disease Activity Index [BASDAI]), markers of bone metabolism (parathyroid hormone [PTH], 1.25 vitamin D3, 25 vitamin D3), calcium, bone alkaline phosphatase (bone-AP), urine cross-links, and plasma tumor necrosis factor alpha (TNFalpha). Bone mineral density was measured by quantitative computed tomography (QCT) of the lumbar spine. Osteoporosis was diagnosed in early as well as in progressive stages of AS (23/58=39.6%). Furthermore, serum levels of 1.25 vitamin D3 and PTH were negatively correlated with disease activity and TNFalpha. The excretion of cross-links showed a positive correlation with disease activity and TNFalpha, and 1.25 vitamin D3 and PTH were positively correlated with bone-AP. TNFalpha also positively correlated with disease activity. AS patients with osteoporosis showed significantly increased CRP, ESR, cross-links and PTH and a significantly decreased 1.25 D3. Osteoporosis is frequent in AS and high disease activity is associated with an alteration in vitamin D metabolites and increased levels of bone resorption in active AS. Our findings propose a close association of BMD, bone metabolism and inflammatory activity, possibly related to vitamin D inflammation interactions.
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PMID:Association of 1.25 vitamin D3 deficiency, disease activity and low bone mass in ankylosing spondylitis. 1617

Hypovitaminosis D is increasing worldwide and is associated with low bone mass. The effects of hypovitaminosis D on bone might be direct or mediated through decreased muscle mass and function and/or secondary hyperparathyroidism. This study systematically investigated the relative contribution of lean mass, PTH, and the direct effect of vitamin D as predictors of vitamin D mediated osteopathy in elderly individuals. 460 ambulatory subjects aged 65-85 years had their bone mass and lean body mass measured by a dual-energy X-ray absorptiometry. Serum calcium, phosphorus and alkaline phosphatase, intact parathyroid hormone (PTH) and 25-hydroxyvitamin D (25 OHD) were also measured. Serum 25 OHD correlated with lean body mass in men, r = 0.24, P = 0.002, but not in women; and with bone mass at all skeletal sites in men, r = 0.20-0.30, P < 0.02. Correlations were also noted at all skeletal sites in women except for the spine, r = 0.13-0.18, P < 0.04. In both genders, BMD at sites enriched in cortical bone was 0.4-0.7 SD lower in the group with the lowest vitamin D tertile than that in the group in the highest tertile. After controlling for PTH, the magnitude of the correlations between BMD and 25 OHD remained significant in both genders. After controlling for lean body mass, the magnitude of these correlations did not change in women and decreased but remained significant in men. After adjustment for age and height, both lean body mass and PTH had significant independent contributions to BMD variance at all skeletal sites. After adjustment for age, height, lean mass, and PTH, 25 OHD did not have any significant residual contribution to BMD variance except at the trochanter in men. This study demonstrates that vitamin D osteopathy in the elderly is in large part mediated through lean mass in men and through PTH levels in both genders, with a greater contribution of PTH in women than in men. There was little demonstrable independent relation between serum 25 OHD and bone mass.
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PMID:Hypovitaminosis D osteopathy: is it mediated through PTH, lean mass, or is it a direct effect? 1649 64


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