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)

An increase in parathyroid hormone (PTH) levels in chronic renal failure (CRF) induces bone abnormalities known as renal osteodystrophy (ROD). The aim of the present study was to evaluate alternative biochemical methods to bone biopsy, to evaluate changes in bone remodeling in renal patients. Intact PTH (iPTH) and bone markers were measured in 43 predialysis (PD), 49 hemodialysis patients (HD) and 185 controls. betaCTXs, bone alkaline phosphatase (bAL), iPTH were higher and creatinine clearance (Ccr) was lower in PD and HD compared with controls (p < 0.0001). In both renal groups, a positive correlation was found between iPTH and both betaCTXs and bAL (p < 0.0001) and between betaCTXs and bAL (p < 0.002). PD patients with Ccr < 40 ml/min had higher iPTH, bAL and betaCTXs (p<0.004, p<0.05 and p<0.001, respectively) than patients with Ccr > 40 ml/min. betaCTXs (p < 0.05) in PD and betaCTXs and bAL in HD patients were higher than controls, even when iPTH was within normal range (< 65 pg/ml). Patients with severe secondary hyperparathyroidism showed higher bone markers than patients with normal or moderately increased iPTH (p < 0.001). These results suggest that even when there is no increase in iPTH, bone remodeling increases (possibly due to other factors) exhibiting higher bone resorption, and betaCTXs would seem to be an adequate non-invasive tool to assess early bone changes in CRF and prevent future fractures. Bone marker measurements in ROD would be useful to identify patients who may require bone biopsy. However, further studies comparing both methods must be performed before replacing bone biopsy with serum beta-CTX.
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PMID:[Serum beta-type I collagen carboxyterminal telopeptide (beta-CTXs) and bone involvement in chronic renal failure]. 1619 10

The goal of the present study was to compare mobilization rate of calcium (Ca) from bone in pregnant and lactating goats and sheep. Blood samples were collected from goats and sheep monthly during pregnancy and at 1, 2, and 4 weeks postpartum (pp) and monthly during lactation until 6 months after parturition. Total bone mineral content (BMC) and total bone mineral density (BMD) were quantified using peripheral quantitative computed tomography at the same intervals as the blood was taken. Bone resorption was assessed by immunoassays quantitating two epitopes of the carboxyterminal telopeptide of type I collagen (ICTP, CTX). Bone formation was estimated by quantifying serum osteocalcin (OC) and bone-specific alkaline phosphatase (bAP). In addition, Ca and 1,25-dihydroxy vitamin D (1,25-VITD) concentrations were determined in serum. Mean ICTP and CTX concentrations of both animal species increased the first week after parturition. By the second week pp, the concentrations of both markers had decreased toward early gestation levels. In contrast, mean OC concentrations continually decreased until the 1st week pp. By the 2nd week pp, the mean concentrations of OC started to increase again. Mean bAP activities decreased during gestation and reached a nadir in the first week pp in goats and 4 weeks pp in sheep. Afterwards, mean bAP activities increased again in goats and sheep. 1,25-VITD concentrations peaked the first week pp and returned to early gestation values thereafter. Total BMC and BMD decreased from the 4th month of pregnancy until the 1st week pp in both species. Afterwards, BMC increased throughout the first month pp in goats and the first 3 months pp in sheep. BMD levels of sheep and goats returned to prepartum levels during lactation. The resorptive phase of bone remodeling is accelerated at parturition and in early lactation and is uncoupled from the process of bone formation. This allows the animal to achieve Ca homeostasis at the expense of bone. Increased bone remodeling during lactation may represent physiological mechanisms to help replace the maternal skeleton lost as the animal adapted to enormously increased Ca losses to the fetus and milk in late gestation and early lactation.
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PMID:The effects of first gestation and lactation on bone metabolism in dairy goats and milk sheep. 1636 7

Osteoporosis associated with estrogen deficiency results from an imbalance between bone resorption and formation, causing deterioration of bone architecture and decreased bone mass. Anti-osteoporotic therapies that have been developed so far include either anticatabolic or anabolic drugs. Strontium ranelate is a newly developed drug that induces opposite effects on bone resorption and formation. This dual original mode of action was demonstrated in experimental studies on bone cells and pharmacological studies in animals. In vitro, strontium ranelate was shown to decrease bone resorption. This effect resulted from a decreased differentiation and resorbing activity of osteoclasts and increased osteoclast apoptosis. In contrast, strontium ranelate was shown to enhance preosteoblastic cell replication and collagen synthesis in culture without affecting bone mineralization. In vivo, strontium ranelate promoted bone formation and reduced bone resorption in intact mice, an effect which resulted in increased vertebral bone mass. Additionally, strontium ranelate was found to reduce resorption and long bone loss induced by hind limb immobilization in rats. Finally, strontium ranelate administration decreased bone resorption and maintained bone formation in adult ovariectomized rats, which resulted in prevention of bone loss. In clinical trials (Spinal Osteoporosis Therapeutic Intervention [SOTI]), bone alkaline phosphatase levels increased, whereas C cross-linking telopeptide of type I collagen (CTX) levels decreased in patients treated with strontium ranelate compared with placebo at all time points. These pharmacological and clinical studies suggest that strontium ranelate acts by increasing bone formation and decreasing bone resorption and that these effects result in improved bone mass in vivo.
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PMID:Strontium ranelate: a physiological approach for optimizing bone formation and resorption. 1643 91

The purpose of this study was the investigation of serum concentration of serum C-telopeptide of type I collagen (s-CTX) and bone alkaline phosphatase (BALP) in Polish healthy children aged 2-18 years. We studied 141 healthy children (64 girls, 77 boys) divided into 3 age groups of both genders: prebubertal, pubertal and postpubertal. The level of s-CTX was determined by Serum CrossLaps One Step ELISA kit (Osteometer Bio Tech, Denmark) and the activity of BALP was measured using an enzyme immunoassay Alkphase-B kit (Metra Biosystems, USA). We observed that both markers of bone turnover showed sigmoid regression curves with increasing age. The peak values of s-CTX and BALP occurred during puberty in the girls aged 8-13 years (2266 +/- 368 ng/ml; 113.4 +/- 21.9 U/L) and in the boys aged 10-15 years (2139 +/- 489 ng/ml; 117.8 +/- 24.7 U/L). In all children after puberty, we observed a gradual lowering of both markers. However, girls showed decreased postpubertal values of s-CTX and BALP 2-3 years earlier than boys, reflecting the earlier completion of puberty in girls. The correlation between s-CTX and BALP was statistically significant (r = 0.578; p < 0.0001) in tested children. The results of this study will be useful in the diagnosis and monitoring of therapy in bone diseases.
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PMID:[Some bone turnover markers in serum of healthy children and adolescents in relation to age and gender]. 1652 55

Bone remodelling is a process by which bone grows and turns over. This process involves a series of highly regulated steps that depend on the interaction of two cell lineages, the osteoclasts and the osteoblasts. Information on metabolic activity of bone tissue are achieved with the determination, in blood and in urine, of biochemical products derived from the activity of this cells. The ability to determine bone turnover with biochemical markers has been enhanced considerably in recent years with the development of new assays for more sensitive and specific markers. These new markers can now replace the outdated and non-specific markers of bone remodeling such as serum total alkaline phosphatase (ALP) and urinary hydroxyproline (Hyp) determination. Biochemical markers of bone turnover can be classified according to the process that underlie in markers of bone formation, products of the osteoblast activity [bone ALP, osteocalcin (OC), procollagene I C- and N-terminal propeptides] and markers of bone resorption, products of the osteocalst activity [pyridinuim crosslinks, collagen I C- and N-terminal telopeptides (CTX-I and NTX-I), tartrate resistent acid phosphatase (TRACP) isoform 5b]. The interpretation of laboratory results should always include the consideration of potential sources of variability. Variation in the results of biochemical markers of bone metabolism can compromise their ability to characterize disorders of bone metabolism. Variation can be categorized into pre-analytical, analytical and biological sources. However, the determination of biochemical markers of bone turnover offers many advantages in clinical practice, since they are non-invasive, can be repeated often, and major changes occur in a short time.
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PMID:Markers of bone turnover: biochemical and clinical perspectives. 1655 Jul 16

Recently, several new bone metabolic markers have been developed and applied for diagnosis of bone metastasis. We have investigated the efficacy of several bone metabolic markers : serum carboxy-terminal telopeptide of type 1 collagen ( I CTP), C-terminal cross-linked telopeptide of type I collagen (CTX) and urinary free deoxypyridinoline (fDPD) as bone resorption markers, serum carboxy-terminal propeptide of type 1 collagen (P I CP), osteocalcin (OC), and bone alkaline phosphatase (BAP) as bone formation markers for diagnosis of bone metastasis. I CTP was most useful for diagnosis of bone metastasis in breast cancer patients because of no increase in postmenopausal osteoporosis. Combination of resorption and formation markers increased sensitivity. In follow-up, bone metabolic markers seemed more useful for predicting therapeutic response of bone metastasis than tumor markers. Bone metabolic markers were also useful for predicting survival or occurrence of skeletal-related events. These findings suggest that bone metabolic markers would be useful to detect, to monitor, and to predict prognosis of bone metastases.
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PMID:[Evaluation of cancer-induced bone diseases by bone metabolic marker]. 1658 8

The present study was undertaken to examine the effect of melatonin (25 microg/mL of drinking water, about 500 microg/day) on a 10-wk long treatment of male rats with methylprednisolone (5 mg/kg s.c., 5 days/wk). Bone densitometry and mechanical properties, calcemia, phosphatemia and serum bone alkaline phosphatase activity and C-telopeptide fragments of collagen type I (CTX) were measured. Both melatonin and methylprednisolone decreased significantly body weight (BW) and the combination of both treatments resulted in the lowest BW values found. Consequently, all results were analyzed with BW as a covariate. Densitometrically, methylprednisolone augmented bone mineral content (BMC), bone area (BA) and bone mineral density (BMD) in the entire skeleton, BMC in cortical bone, and BMC and BMD in trabecular bone. Melatonin increased BMC and BA in whole skeleton and BMC and BMD in trabecular bone. For BMC and BA of whole skeleton, BMC of cortical bone, and BMC and BMD of trabecular bone, the combination of glucocorticoids and melatonin resulted in the highest values observed. Femoral weight of rats receiving methylprednisolone or melatonin increased significantly and both treatments summated to achieve the greatest effect. In femoral biomechanical testing, methylprednisolone augmented ultimate load and work to failure significantly. Rats receiving the combined treatment of methylprednisolone and melatonin showed the highest values of work to failure. The circulating levels of CTX, an index of bone resorption, decreased after methylprednisolone or melatonin, both treatments summating to achieve the lowest CTX values found. Serum calcium increased after methylprednisolone and serum phosphorus decreased after treatment with methylprednisolone or melatonin while serum bone alkaline phosphatase levels remained unchanged. The results are compatible with the view that low doses of methylprednisolone or melatonin decrease bone resorption and have a bone-protecting effect.
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PMID:Melatonin effect on bone metabolism in rats treated with methylprednisolone. 1663 16

Osteolytic bone disease is a major clinical feature of multiple myeloma (MM). Mechanisms of bone destruction are related to increased osteoclastic activity, which is not accompanied by a comparable increase in bone formation, as osteoblasts are functionally exhausted. Thus the lesions rarely heal and bone scans are often negative in myeloma patients with extensive lytic lesions, offering very little in the follow-up of bone disease. Biochemical markers of bone resorption, such as N- and C-terminal cross-linking telopeptide of type I collagen (NTX, CTX/ICTP, respectively), tartrate resistant acid phosphatase isoform-5b, bone formation (bone-specific alkaline phosphatase [BAP]), and osteocalcin provide useful information on bone dynamics. Several studies have shown that NTX, CTX, and ICTP are elevated in myeloma patients, reflect the extent of bone disease, and correlate with survival. Furthermore, they are useful in monitoring bone destruction during antimyeloma or bisphosphonate treatment. Markers of bone formation have produced conflicting results in trials. However, BAP correlates with bone pain, lytic lesions, and fractures in quite a few studies of MM. Novel markers, such as bone sialoprotein, receptor activator of nuclear factor-kappa B ligand (RANKL), osteoprotegerin, osteopontin, dickkopf-1, and soluble Frizzle-related protein-2 have been found of value in assessing bone lytic disease in MM, but their promising results must be confirmed in large trials. In conclusion, although no marker provides optimal analysis of MM or of MM treatments, combinations of markers have at times helped in assessing MM stages and lytic bone disease and in monitoring specific treatment modalities. The need for further research in this field is clear.
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PMID:Biochemical markers of bone metabolism in multiple myeloma. 1668 Aug 33

Following total hip arthroplasty (THA), femoral periprosthetic bone undergoes a remodeling process that results in bone loss in its proximal regions that may compromise the long-term outcome of THA. Periprosthetic bone loss mainly occurs during the first postoperative months. The question is whether a postoperative treatment with alendronate is effective in reducing periprosthetic bone loss and which doses and duration of treatment are required. In a 12-month prospective, randomized double-blind study, 51 patients undergoing cementless THA were treated postoperatively either with a daily dose of 20 mg alendronate for 2 months and 10 mg for 2 months thereafter (group I), with 20 mg of alendronate for 2 months and 10 mg for 4 months thereafter (group II), or treated with placebo (group III). Proximal femoral bone mineral density (BMD) was measured with dual-energy X-ray absorptiometry (DEXA) and serum biochemical markers of bone turnover bone specific alkaline phosphatase, osteocalcin, and C-terminal telopeptides (CTX-I) were assayed. Six months of alendronate treatment significantly reduced (p<0.001) bone loss in proximal medial region (-10%) compared with placebo (-26%). All biochemical markers of bone turnover were suppressed by alendronate. These data suggest that alendronate administered for the first 6 postoperative months following THA was effective in preventing early periprosthetic bone loss.
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PMID:Alendronate prevents femoral periprosthetic bone loss following total hip arthroplasty: prospective randomized double-blind study. 1670 19

The increased bone remodeling in women after menopause induces an imbalance between bone resorption and formation, leading to decreased bone mass, altered bone microarchitecture, and increased fracture risk. Current antiosteoporotic drugs decrease bone remodeling or increase bone formation. Strontium ranelate (Protelos) is a newly developed antiosteoporotic drug that acts by reducing bone resorption and promoting bone formation, thereby inducing a positive bone balance. In rat and mouse culture models, strontium ranelate enhances preosteoblastic cell replication and bone formation markers. In contrast, it decreases rodent osteoclastic cell resorbing activity and human osteoclast differentiation, and increases rabbit osteoclast apoptosis. In vivo, strontium ranelate increases bone formation and reduces bone resorption in mice, resulting in increased vertebral bone mass. In rats, strontium ranelate increases bone mass and improves microarchitecture and bone geometry, resulting in increased bone resistance. In ovariectomized rats, strontium ranelate decreases bone resorption but maintains high bone formation, resulting in improved bone microarchitecture and increased bone mass and strength. In clinical trials, serum alkaline phosphatase levels increased whereas serum CTX levels simultaneously decreased in patients treated with Protelos versus placebo at all time-points. In these trials, histomorphometric analysis of bone biopsies showed that the osteoblast surface and mineral apposition rate increased whereas bone resorption parameters tended to decrease in treated patients compared to the placebo group. These preclinical and clinical data indicate that strontium ranelate acts by increasing bone formation and decreasing bone resorption, thus rebalancing bone turnover in favour of bone formation, an effect that results in increased bone mass and strength.
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PMID:Strontium ranelate: a dual mode of action rebalancing bone turnover in favour of bone formation. 1673 40


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