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PubMed1987

Impaired carboxylation of osteocalcin in warfarin-treated patients.

The total circulating osteocalcin and ratio of inactive (noncarboxylated; GLU) to active (carboxylated; GLA) form of circulating osteocalcin were measured in patients receiving long term warfarin treatment (n = 20), age-matched control patients not receiving warfarin treatment (n = 10), and normal subjects before and after the administration of 30 mg warfarin (n = 7). There was no significant difference in the total osteocalcin concentrations between the control patients and the patients receiving long term warfarin treatment, and it did not significantly change after warfarin ingestion in the normal subjects. The GLU/GLA ratio was significantly increased (P less than 0.002) in the patients receiving long term warfarin treatment compared with that in the control patients. There was a significant increase (P less than 0.01) in the GLU/GLA ratio after warfarin ingestion in the normal subjects. This study demonstrates that osteocalcin carboxylation in humans is a vitamin K-dependent process and that circulating osteocalcin is structurally altered by warfarin administration. This finding has pathophysiological implications for the fetal warfarin embryopathy syndrome, bone disease associated with chronic liver diseases, and possibly for osteoporosis, in which vitamin K deficiency has been implicated.

1-Carboxyglutamic Acid↗
PubMed1991

Differential effects of inhaled budesonide and oral prednisolone on serum osteocalcin.

Inhaled glucocorticosteroids have been developed for the treatment of asthma in an attempt to minimize the suppression of endogenous adrenal function that complicates oral or injected steroid usage, but it is unclear whether this strategy leads to reduced systemic complications in other areas, such as the skeleton. In this study we evaluated serum osteocalcin levels as a marker of skeletal metabolism in healthy volunteers treated with oral and inhaled steroids alone and in response to an oral calcitriol stimulation test. Forty subjects, aged 33 +/- 9 (mean +/- SD) yr were randomized to receive either high or low dose oral prednisolone (40 vs. 10 mg/day) or inhaled budesonide (3.2 vs. 0.8 mg/day). Each dose of budesonide is known to have a greater antiasthmatic potency than the dose of prednisolone with which it was compared. In addition 10 control subjects received placebos containing no active steroid drugs. During the second week of treatment, half of the subjects in each of the 4 steroid-treated groups and all subjects in the control group received oral calcitriol (2.0 micrograms/day). There was a marked dose-dependent reduction in serum cortisol levels, but this reduction was significantly less pronounced during budesonide treatment, such that low dose budesonide was without effect. During the first week of steroid therapy there were significant dose-dependent reductions in serum osteocalcin (P = 0.003), but this reduction was not significantly different between budesonide and prednisolone treatments. In response to calcitriol, serum osteocalcin increased by 35% in the control group (P = 0.06). Osteocalcin levels increased by 56% and 50% in the low dose budesonide and prednisolone groups and by 106% in the high dose budesonide group, but did not change in the high dose prednisolone group. The osteocalcin response to calcitriol was significantly higher in the budesonide groups (P = 0.03, by analysis of variance). High dose prednisolone caused increases in serum 1,25-dihydroxyvitamin D3 (P less than 0.02), urinary calcium excretion (P = 0.07), and urinary hydroxyproline (P less than 0.01). None of these changes was seen during budesonide therapy. There are as yet no data for these variables after long term use of inhaled budesonide in asthmatic patients, but our acute studies suggest that this potent topical glucocorticoid may have considerably less impact on the skeleton than oral prednisolone, even if used at doses high enough to suppress endogenous adrenal function.

Administration, Inhalation↗
PubMed1997

DNA sequences downstream from the vitamin D response element of the rat osteocalcin gene are required for ligand-dependent transactivation.

The sequences in the rat osteocalcin gene that lie 3' to the vitamin D response element (VDRE) have been shown to augment transcriptional activation by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. These DNA sequences, however, are unable to bind the VDR or mediate 1,25-(OH)2D3 responsiveness independently of the VDRE. To further characterize this region, the functional properties of a series of mutant oligonucleotides were examined in transiently transfected ROS 17/2.8 cells. When these mutant oligonucleotides were expressed upstream of the heterologous herpes simplex virus thymidine kinase promoter, the bases between -420 and -414 of the rat osteocalcin gene were identified as critical for maximal transactivation by 1,25-(OH)2D3. Furthermore, mutation of these sequences in the context of the native osteocalcin promoter and enhancer totally abolished the ability of the VDRE to mediate 1,25-(OH)2D3 responsiveness. These bases, which are essential for the 1,25-(OH)2D3 responsiveness of the rat osteocalcin gene, are also present in a similar position, relative to the VDRE, in the human osteocalcin gene. To explore whether these sequences could enhance transactivation by other inducible transcription factors, they were examined for their ability to synergize with the chick vitellogenin estrogen response element and the rat somatostatin cAMP response element. When placed upstream to the herpes simplex virus thymidine kinase promoter and transfected into ROS 17/2.8 cells, these sequences were able to enhance transcriptional responsiveness to 17beta-estradiol and forskolin, respectively, demonstrating that they also contribute to transactivation by other inducible transcription factors.

Animals↗
PubMed1998

Changes in the expression of Fas, osteonectin and osteocalcin with age in the rabbit growth plate.

Chondrocytes of the growth plate are generally assumed to undergo apoptosis, but the mechanisms which induce this cell death are not known. The Fas receptor is a mediator of the apoptotic signal in some systems. We studied its expression in situ in growth plates of rabbits aged from five to 20 weeks. In addition, we investigated the immunolocalisation in the growth plates of the bone proteins, osteonectin and osteocalcin, and the changes in their expression with age. The Fas-positive chondrocytes were found mostly in the hypertrophic zone, as were the osteonectin-positive and osteocalcin-positive cells. The percentage of Fas-positive cells increased with age whereas little change was found in the number of osteonectin-positive and osteocalcin-positive chondrocytes. Many of the Fas-positive chondrocytes were also TUNEL-positive. This strongly suggests that apoptosis in the growth plate is mediated through the Fas system. Double immunostaining for osteocalcin and Fas showed that not all hypertrophic chondrocytes were of the same cell type. Some chondrocytes stained for osteocalcin only, others for Fas only, while some were positive for both.

Aging↗
PubMed2005

Identification of a new pebp2alphaA2 isoform from zebrafish runx2 capable of inducing osteocalcin gene expression in vitro.

UNLABELLED: The zebrafish runx2b transcription factor is an ortholog of RUNX2 and is highly conserved at the structural level. The runx2b pebp2alphaA2 isoform induces osteocalcin gene expression by binding to a specific region of the promoter and seems to have been selectively conserved in the teleost lineage. INTRODUCTION: RUNX2 (also known as CBFA1/Osf2/AML3/PEBP2alphaA) is a transcription factor essential for bone formation in mammals, as well as for osteoblast and chondrocyte differentiation, through regulation of expression of several bone- and cartilage-related genes. Since its discovery, Runx2 has been the subject of intense studies, mainly focused in unveiling regulatory targets of this transcription factor in high vertebrates. However, no single study has been published addressing the role of Runx2 in bone metabolism of low vertebrates. While analyzing the zebrafish (Danio rerio) runx2 gene, we identified the presence of two orthologs of RUNX2, which we named runx2a and runx2b and cloned a pebp2alphaA-like transcript of the runx2b gene, which we named pebp2alphaA2. MATERIALS AND METHODS: Zebrafish runx2b gene and cDNA were isolated by RT-PCR and sequence data mining. The 3D structure of runx2b runt domain was modeled using mouse Runx1 runt as template. The regulatory effect of pebp2alphaA2 on osteocalcin expression was analyzed by transient co-transfection experiments using a luciferase reporter gene. Phylogenetic analysis of available Runx sequences was performed with TREE_PUZZLE 5.2. and MrBayes. RESULTS AND CONCLUSIONS: We showed that the runx2b gene structure is highly conserved between mammals and fish. Zebrafish runx2b has two promoter regions separated by a large intron. Sequence analysis suggested that the runx2b gene encodes three distinct isoforms, by a combination of alternative splicing and differential promoter activation, as described for the human gene. We have cloned a pebp2alphaA-like transcript of the runx2b gene, which we named pebp2alphaA2, and showed its high degree of sequence similarity with the mammalian pebp2alphaA. The cloned zebrafish osteocalcin promoter was found to contain three putative runx2-binding elements, and one of them, located at -221 from the ATG, was capable of mediating pebp2alphaA2 transactivation. In addition, cross-species transactivation was also confirmed because the mouse Cbfa1 was able to induce the zebrafish osteocalcin promoter, whereas the zebrafish pebp2alphaA2 activated the murine osteocalcin promoter. These results are consistent with the high degree of evolutionary conservation of these proteins. The 3D structure of the runx2b runt domain was modeled based on the runt domain of mouse Runx1. Results show a high degree of similarity in the 3D configuration of the DNA binding regions from both domains, with significant differences only observed in non-DNA binding regions or in DNA-binding regions known to accommodate considerable structure flexibility. Phylogenetic analysis was used to clarify the relationship between the isoforms of each of the two zebrafish Runx2 orthologs and other Runx proteins. Both zebrafish runx2 genes clustered with other Runx2 sequences. The duplication event seemed, however, to be so old that, whereas Runx2b clearly clusters with the other fish sequences, it is unclear whether Runx2a clusters with Runx2 from higher vertebrates or from other fish.

Amino Acid Sequence↗
PubMed1994

Cord blood levels of calcium-regulating hormones and osteocalcin in premature infants.

We measured cord blood levels of calcium-regulating hormones and osteocalcin in 34 premature infants of various gestational ages. 1,25(OH)2D levels were low in mid-gestation and increased with advancing gestation. Parathyroid hormone levels were low, and calcitonin levels were high in mid-gestation. Both of them declined with advancing gestation. Osteocalcin levels were high in mid-gestation. They increased from 22 weeks through 27 weeks of gestational age, and decreased thereafter. Circulating osteocalcin is considered as a clinical marker of bone turnover. However, cord blood osteocalcin decreased between 27 and 36 weeks of gestation during which period calcium accumulation by the fetus increases. Therefore, cord blood osteocalcin does not appear to reflect fetal bone formation.

Calcitonin↗
PubMed1993

The effect of single doses of inhaled beclomethasone dipropionate on the circadian rhythm in serum osteocalcin in normals.

A single dose of 2.5 mg prednisone leads to a significant transient decrease in serum osteocalcin, which is only demonstrated by frequent serum sampling. The aim of the present study was to evaluate whether a single dose of inhaled beclomethasone dipropionate causes transient changes in serum osteocalcin, indicating a systemic effect on bone cells. In a double-blind, placebo controlled, cross-over design we evaluated the effects of single doses of 250 micrograms and 1000 micrograms beclomethasone on the circadian rhythm in serum osteocalcin. Fifteen normal subjects aged 23-38 years were studied twice with an interval of one week with hourly blood sampling from 16.30 until 17.00 the following day; 1000 micrograms beclomethasone, but not 250 micrograms, suppressed serum cortisol by 14.4 +/- 6.7% (p = 0.03). Neither of the beclomethasone doses significantly altered the time pattern of serum osteocalcin. We conclude that a single inhaled dose of beclomethasone in the therapeutical range does not acutely influence osteoblastic activity as judged from serial measurements of serum osteocalcin.

Administration, Inhalation↗
PubMed1994

Cortical bone osteocalcin content and matrix composition in autosomal dominant osteopetrosis type I.

Several bone matrix protein constituents, including the major component collagen type I and the hydroxyapatite binding protein, osteocalcin, have been implicated in the regulation of bone turnover. Cortical bone osteocalcin, collagen and mineral content were studied in autosomal dominant osteopetrosis type I (ADO), a disorder characterized by diffuse symmetrical osteosclerosis. Iliac crest bone biopsies were obtained from eight patients (mean age 43.0 years, range 17-63 years) and compared with 16 age- and sex-matched normal controls (mean age 44.1 years, range 20-61 years). The osteocalcin level in cortical bone was increased (p < 0.03) in ADO (51.4 +/- 3.9 mg/kg bone) compared with controls (38.0 +/- 3.6 mg/kg bone). Total collagen, protein and calcium expressed per kilogram bone dry weight were without significant difference between patients and controls. The pathogenesis of ADO is most likely not related to cortical bone osteocalcin content, a protein implicated in osteoclast ontogeny and activation. These observations are in contrast to recent observations of reduced bone osteocalcin levels in osteopetrotic mutations in the rat and underscore the interspecies heterogeneity of this disorder.

Adolescent↗
PubMed2004

Serum osteocalcin levels in hyperthyroidism before and after antithyroid therapy.

Hyperthyroidism is characterized by accelerated bone turnover, caused from direct stimulation of bone cells by increased thyroid hormones. In this study, we aimed to investigate serum osteocalcin levels as a bone formation marker, before antithyroid (propylthiouracil) therapy at hyperthyroid stage and after antithyroid therapy at euthyroid stage of the patients. Twenty four hyperthyroid patients (18 females, 6 males) and 20 (13 females, 7 males) healthy controls were included into this study. Blood and urine samples were taken before medical treatment at hyperthyroid state, and after the antithyroid therapy until the patients reached the euthyroid state. Serum alkaline phosphatase, osteocalcin, calcium, phosphorus, Free T3, Free T4, TSH and urine calcium/creatinine levels were assessed. We found a significant decrease in serum osteocalcin (p=0.006), urinary calcium/creatinine (p=0.004), and serum phosphorus (p=0.038) levels in euthyroid state in comparison to hyperthyroid state. The increases in serum bone formation marker osteocalcin and bone resorption marker urinary calcium/creatinine levels in hyperthyroid state compared to euthyroid state in our study confirmed that hyperthyroid patients have high bone turnover. We conclude that, hyperthyroid patients has high bone turnover of formation and resorption even after attainment of euthyroidism. Osteocalcin and urine calcium/creatinine are sensitive markers in documenting bone remodeling during treatment of hyperthyroidism.

Alkaline Phosphatase↗
PubMed1990

Plasma osteocalcin: biological variations and reference limits.

Osteocalcin, the most abundant non-collagenous protein in the bone matrix, is partly released in blood. We have measured its concentration by a radio-immunoassay procedure in 1096 apparently healthy subjects from both sexes who came for a health screening examination. Their ages varied from 4 years to over 65 years. Venous blood was drawn in the morning from fasting subjects. Plasma osteocalcin was higher in men than in women. Its level increased significantly with age, body weight, height and bone age until age 12-13 years in girls and 14-15 years in boys. In women, osteocalcin level increased after the age of 50 years and was higher than in men. It remained constant over age 60 years in both sexes, but was higher in women. There was no effect of menstrual cycle in girls at puberty. Plasma osteocalcin did not vary with follicular and luteal phases or with the use of oral contraceptive drugs in women. The usual nonsteroid anti-inflammatory drugs had no effect on blood osteocalcin level. Reference limits according to age and sex are provided.

Adolescent↗
PubMed1999

Characterization of an enhancer required for 1,25-dihydroxyvitamin D3-dependent transactivation of the rat osteocalcin gene.

The sequences in the rat osteocalcin gene that lie 3' to the vitamin D response element (VDRE) contain a GGTTTGG motif (-420 to -414) that is essential for transcriptional activation of osteocalcin-CAT (OC-CAT) fusion genes by 1,25(OH)2D3. A second copy of this motif, present on the antisense strand is unable to compete for nuclear protein binding to the VDRE-associated motif, suggesting that the core element extends beyond the GGTTTGG motif. In order to examine the base requirements for both function and nuclear protein interactions with the VDRE-associated GGTTTGG enhancer motif, deletion and substitution of flanking sequences was performed in the context of both the native osteocalcin promoter and a heterologous viral promoter. These data demonstrate that the base requirements for protein-DNA interactions and transactivation are located between -430 and -414. The position of the element with respect to the VDRE is flexible and insertion of additional copies either 5' or 3' to the VDRE further enhances transactivation, both in the context of the native osteocalcin promoter and a heterologous viral promoter. These data demonstrate that VDR-dependent transactivation of the rat osteocalcin gene requires not only the VDRE (-456 to -442) but also sequences between -430 and -414. The protein(s) that interacts with these sequences is capable of enhancing transcription in both a position and orientation-independent fashion.

Animals↗
PubMedDate not supplied

[Osteocalcin--a marker of bone metabolism in rheumatoid arthritis patients].

Blood serum concentration of osteocalcin was studied in 53 patients with rheumatoid arthritis. Osteocalcin (noncollagenous protein of bony tissue) is a marker of bony tissue formation known to be of high informative value. There were no significant differences in values for osteocalcin concentration between patients with rheumatoid arthritis and healthy people. Reduction of osteocalcin content and, correspondingly, of process of bony tissue formation was observed in rapidly progressing course of rheumatoid arthritis and in stage IV arthritis. Rises in osteocalcin concentration were recordable in those women in there postmenopause. Patients with rheumatoid arthritis were found out to experience adequate formation of bony tissue in spite of the osteopenia syndrome progression. Disordered structural and functional state of the bony tissue processes of remodelling may be explained by bony tissue remodeling processes dissociation.

Adult↗
PubMed2002

Divergent regulation by p44/p42 MAP kinase and p38 MAP kinase of bone morphogenetic protein-4-stimulated osteocalcin synthesis in osteoblasts.

In the present study, we investigated whether the mitogen-activated protein (MAP) kinase superfamily is involved in the bone morphogenetic protein (BMP)-4-stimulated synthesis of osteocalcin in osteoblast-like MC3T3-E1 cells. BMP-4 dose-dependently stimulated osteocalcin synthesis. BMP-4 markedly induced the phosphorylation of p44/p42 MAP kinase and p38 MAP kinase, while having little effect on SAPK (stress-activated protein kinase)/JNK (c-Jun N terminal kinase) phosphorylation. SB203580 and PD169316, specific inhibitors of p38 MAP kinase, significantly reduced the osteocalcin synthesis stimulated by BMP-4. In contrast, PD98059 and U0126, inhibitors of upstream kinase of p44/p42 MAP kinase, markedly enhanced the BMP-4-stimulated osteocalcin synthesis. The BMP-4-induced phosphorylation of p44/p42 MAP kinase was suppressed by PD98059, which did not, however, affect the BMP-4-induced phosphorylation of p38 MAP kinase. Taken together, our results strongly suggest that p38 MAP kinase takes part in BMP-4-stimulated osteocalcin synthesis as a positive regulator in osteoblasts, whereas p44/p42 MAP kinase acts as a negative regulator in the synthesis.

Bone Morphogenetic Protein 4↗
PubMed2003

Great increase in bone 66 kDa protein and osteocalcin at later stages with healing rat fractures: effect of zinc treatment.

Fracture healing has been demonstrated to increase production of bone growth factors, and this elevation has been shown to be enhanced by zinc treatment. Moreover, the effect of zinc treatment on production of bone osteocalcin, which is a kind of Ca2+-binding protein localized in bone matrix, at the later stages with bone fracture was investigated. Rats were sacrificed 7 (earlier stage) or 21 (later stage) days after fracture of femoral diaphysis. Femoral-diaphyseal tissues with fracture healing were cultured in a serum-free medium for 24 h. Many proteins in the bone tissues were released into the medium. Bone protein production was markedly elevated 21 days after bone fracture as compared with that of 7 days. A approximately 66 kDa protein molecule, a major protein component which was produced by the diaphyseal tissues during fracture healing, was predominantly increased at the later stages with fracture healing. Bone osteocalcin production was significantly increased during fracture healing. This increase was enhanced at the later stages with fracture healing. The presence of zinc acexamate (10(-4) M) in culture medium caused a significant increase in bone protein and osteocalcin production at 7 or 21 days after bone fracture. The effect of zinc acexamate in increasing bone total protein and osteocalcin production was remarkable at the later stages with fracture healing. Moreover, zinc treatment caused a significant increase in alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium content in the femoral-diaphyseal tissues of the later stages with fracture healing in vitro. The present study demonstrates that bone protein production is markedly increased at the later stages with fracture healing, and that zinc treatment can enhance production of bone protein components including osteocalcin in vitro. Zinc treatment may stimulate the healing of femoral fracture at earlier and later stages.

Animals↗
PubMed2001

[Changes of osteocalcin in serum of young SD rats after functional protrusion].

OBJECTIVE: The aim of this study is to investigate temporal and spatial change patterns of osteocalcin in serum of young growing SD rats, in conditions of different functional treatment time spans. METHODS: Totally, 72 SD rats are randomly divided into 3 groups, including the control group, the 24-hour wearing group (wearing functional appliance 24 hours a day), and the 12-hour wearing group (wearing appliance for 12 hours in daylight). One week after the experiment, rats were sacrificed and osteocalcin level in serum was measured by using radioimmunoassay. Date was processed using macroscopic and microscopic analysis. RESULTS: Serum osteocalcin had circadian rhythm and the peak was about 12:00 in a day. After wearing the functional appliance, serum osteocalcin level increased with treatment time, and serum osteocalcin level in the 24-hour wearing group rose more obviously than that in the 12-hour wearing group. CONCLUSION: For the functional appliance, better results can be achieved in the 24-hour wearing group.

Animals↗
PubMed2002

[Osteocalcin and type I collagen mRNA expression of rat marrow stromal cells under induction condition].

OBJECTIVE: To investigate osteocalcin and type I collagen mRNA expression of rat marrow stromal cells under induction condition. METHODS: Cultured rat marrow stromal cells were induced by osteogenic compound(composed of dexamethasone 10(-3) mol/L, beta glyceralphosphate 10 mmol/L, ascorbic acid 50 micrograms/ml). Osteocalcin and type I collagen mRNA expression were measured using RT-PCR technique. RESULTS: It was found that rat marrow stromal cells in induced group have an increased time-dependent expression of osteocalcin and type I collagen mRNA, in comparison with control groups. And the necessity of 1,25-(OH)2D3 in induced osteocalcin mRNA expression was confirmed. CONCLUSION: The cultured rat marrow stromal cells kept the undifferentiated state and had osteogenic potential testified by increased osteocalcin and type I collagen mRNA expression when induced.

Animals↗
PubMed2003

Vitamin D supplementation to healthy children does not affect serum osteocalcin or markers of type I collagen turnover.

AIM: New serum markers have recently been introduced in the assessment of bone turnover. Such measures are osteocalcin, the C-terminal propeptide of type I procollagen (PICP), the N-terminal propeptide of type I procollagen (PINP) and the C-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP). This study aimed to determine whether supplementation with vitamin D3 to healthy children during the winter affects bone turnover in healthy children measured by serum osteocalcin, PICP, PINP or ICTP. METHODS: 12 girls and 8 boys aged 6.2-13.7 (mean 9.8) y, all proven healthy by medical examination and history, were enrolled in a double-blind, randomized, placebo-controlled, cross-over study with two 4 wk treatment periods and 2 wk washout. Vitamin D3 600 IU was given in one tablet of ABCDin daily. On the last day of the 4 wk periods blood was sampled for assessment of serum osteocalcin, PICP, PINP, ICTP, 25-OH-vitamin D, 1,25-diOH-vitamin D and parathyroid hormone (PTH). RESULTS: During supplementation and placebo periods serum osteocalcin (mean +/- SEM) was 53.9 +/- 5.7 and 54.4 +/- 3.8 microg l(-1) (p = 0.70), PICP was 437+/- 44 and 429 +/- 41 microg l(-1) (p = 0.73), PINP was 579 +/- 56 and 619 +/- 64 microg l(-1) (p = 0.33) and ICTP was 13.4 +/- 0.9 and 13.6 +/- 0.7 microg l(-1) (p = 0.52), respectively. Mean +/- SEM serum 25-OH-vitamin D was 47.0 +/- 2.3 and 33.0 +/- 3.0 nmol l(-1) during vitamin D3 supplementation and placebo (p < 0.001, t = 8.10, 95% CI = 10.3 to 17.6 nmol l(-1)), 1,25-diOH-vitamin D and PTH were 87.5 +/- 4.3 and 92.0 +/- 5.3 pmol l(-1) (p = 0.38), and 3.97 +/- 0.5 and 4.21 +/- 0.4 micromol l(-1) (p = 0.37), respectively. CONCLUSION: Supplementation with 600 IU vitamin D3 to healthy children in the winter does not affect bone turnover as measured by serum osteocalcin, PICP, PINP or ICTP. Vitamin D supplementation to healthy children may not be recommended on the ground of concern for bone turnover.

Child↗
PubMedDate not supplied

Abnormalities in serum osteocalcin values in children receiving chemotherapy including ifosfamide.

In patients undergoing high-dose ifosfamide treatment tubular nephrotoxicity with hypophosphatemia has been described. Long-lasting hypophosphatemia may be associated with bone disease including rickets. Serum osteocalcin is considered a sensitive marker for reduced osteoblast activity and bone formation. In our study we determined osteocalcin serum levels in 11 children with cancer and chemotherapy, comparing them with fractional reabsorption of phosphate, aminoaciduria and a1-microglobulin excretion. A decrease of serum levels of osteocalcin and serum phosphate during chemotherapy was found. Progressive hyperaminoaciduria, a1-microglobulin loss and a low fractional reabsorption of phosphate were also detected during chemotherapy. All parameters tended to become normal after treatment. We conclude that serum osteocalcin levels may decrease soon after the initiation of chemotherapy, indicating low osteoblast activity, probably as a result of phosphate loss. Patients with decreased osteocalcin levels may therefore be at risk for osteoporosis.

Adolescent↗