D3 Levels (d3 + level)

Distribution by Scientific Domains

Kinds of D3 Levels

  • hydroxyvitamin d3 level


  • Selected Abstracts


    Bone mineral metabolism and histomorphometry in rats with cholestatic liver disease

    LIVER INTERNATIONAL, Issue 2 2002
    Zvi Ackerman
    Abstract: Background: The etiology of osteopenia in cholestatic liver disease is uncertain. An animal model is needed in order to study the efficacy of therapeutic agents. Aims: In order to characterise the bone disease in rats with cholestatic liver disease. Methods: Four-month old male Sprague,Dawley bile duct-ligated (BDL) and sham-operated (SO) rats were studied. Twenty-eight days after surgery serum osteocalcin, a bone-formation marker, urinary deoxypyridinoline (DPD) cross-links, a resorption marker, and 25-hydroxyvitamin D3 were determined. Static and dynamic (tetracycline-based) histomorphometric analysis was performed on femurs and tibiae. Results: All BDL rats developed biliary cirrhosis. Bile duct-ligated rats had lower bone mass, reflected in statistically significantly 13.5% lower femoral dry-weight, 16% lower femoral ash-weight, 42.7% lower tibial cancellous bone area and 19% lower trabecular thickness, compared with SO rats. Bile duct-ligated rats exhibited decreased bone formation manifested by statistically significantly 70% lower tetracycline double-labelling, 40% lower mineralising surface, 51% lower bone-formation rate and 47% lower osteocalcin compared with SO rats. Deoxypyridinoline levels were 20% lower in BDL rats. Bile duct-ligated rats had 52% lower serum 25-hydroxyvitamin D3 level, but no significant increase in cortical osteoid area. Conclusions: Bile duct-ligated rats develop osteopenia characterised by low bone-formation rate, and can be used for studying therapeutic agents for patients with cholestatic liver disease displaying similar bone changes. [source]


    Vitamin D status is associated with relapse rate in pediatric-onset multiple sclerosis

    ANNALS OF NEUROLOGY, Issue 5 2010
    Ellen M. Mowry MD
    Objective We sought to determine if vitamin D status, a risk factor for multiple sclerosis, is associated with the rate of subsequent clinical relapses in pediatric-onset multiple sclerosis. Methods This is a retrospective study of patients with pediatric-onset multiple sclerosis or clinically isolated syndrome who were consecutively recruited into a prospective cohort at their clinical visit at the pediatric multiple sclerosis center of University of California, San Francisco or State University of New York at Stony Brook. Of 171 eligible patients, 134 (78%) with multiple sclerosis/clinically isolated syndrome were included in the cohort; a further 24 were excluded from this analysis due to lack of available serum (n = 7) or lack of follow-up (n = 17). Serum 25-hydroxyvitamin D3 levels were measured and were adjusted to reflect a deseasonalized value. The adjusted serum 25-hydroxyvitamin D3 level was the primary predictor in a multivariate negative binomial regression model in which the main outcome measure was the number of subsequent relapses. Results Among the 110 subjects, the mean unadjusted 25-hydroxyvitamin D3 level was 22 ± 9ng/ml. After adjustment for age, gender, race, ethnicity, disease duration, disease-modifying therapy, and length of follow-up, every 10ng/ml increase in the adjusted 25-hydroxyvitamin D3 level was associated with a 34% decrease in the rate of subsequent relapses (incidence rate ratio, 0.66; 95% confidence interval, 0.46,0.95; p = 0.024). Interpretation Lower serum 25-hydroxyvitamin D3 levels are associated with a substantially increased subsequent relapse rate in pediatric-onset multiple sclerosis or clinically isolated syndrome, providing rationale for a randomized controlled trial of vitamin D supplementation. ANN NEUROL 2010;67:618,624 [source]


    Vitamin D deficiency in a multinational refugee population

    INTERNAL MEDICINE JOURNAL, Issue 12 2007
    H. D. Wishart
    Abstract Background: Populations with increased skin pigmentation who have migrated to countries of high latitude are at increased risk of low vitamin D. This study aimed to determine the prevalence of low vitamin D among the refugee population arriving in New Zealand. Methods: An audit of all refugees arriving at the national refugee resettlement centre from May 2004 to May 2005 was carried out. Serum 25-hydroxyvitamin D3 levels were measured and defined as normal (50,150 nmol/L) or low, with low subdivided into insufficient (25 to <50 nmol/L) and deficient (<25 nmol/L). Whether vitamin D status varied with age and sex was determined. Results: Vitamin D was measured in 869 (99%) of the refugees and was low in 470 (54%, 95% confidence interval (CI) 51,57%). It was insufficient in 323 (37%, 95%CI 34,41%) and deficient in 147 (17%, 95%CI 15,20%). Female sex was associated with at least a 10 times increased risk of vitamin D deficiency (relative ratio 13.93, 95%CI 10.15,17.96). Women aged between 17 and 45 years and men aged 46 years and more were at greatest risk. Conclusion: Poor vitamin D status is prevalent among refugees arriving in New Zealand. Women, particularly those of child-bearing age are at greatest risk. Screening and ongoing surveillance for vitamin D deficiency should be considered for all recent refugee immigrants to New Zealand. [source]


    Vitamin D status is associated with relapse rate in pediatric-onset multiple sclerosis

    ANNALS OF NEUROLOGY, Issue 5 2010
    Ellen M. Mowry MD
    Objective We sought to determine if vitamin D status, a risk factor for multiple sclerosis, is associated with the rate of subsequent clinical relapses in pediatric-onset multiple sclerosis. Methods This is a retrospective study of patients with pediatric-onset multiple sclerosis or clinically isolated syndrome who were consecutively recruited into a prospective cohort at their clinical visit at the pediatric multiple sclerosis center of University of California, San Francisco or State University of New York at Stony Brook. Of 171 eligible patients, 134 (78%) with multiple sclerosis/clinically isolated syndrome were included in the cohort; a further 24 were excluded from this analysis due to lack of available serum (n = 7) or lack of follow-up (n = 17). Serum 25-hydroxyvitamin D3 levels were measured and were adjusted to reflect a deseasonalized value. The adjusted serum 25-hydroxyvitamin D3 level was the primary predictor in a multivariate negative binomial regression model in which the main outcome measure was the number of subsequent relapses. Results Among the 110 subjects, the mean unadjusted 25-hydroxyvitamin D3 level was 22 ± 9ng/ml. After adjustment for age, gender, race, ethnicity, disease duration, disease-modifying therapy, and length of follow-up, every 10ng/ml increase in the adjusted 25-hydroxyvitamin D3 level was associated with a 34% decrease in the rate of subsequent relapses (incidence rate ratio, 0.66; 95% confidence interval, 0.46,0.95; p = 0.024). Interpretation Lower serum 25-hydroxyvitamin D3 levels are associated with a substantially increased subsequent relapse rate in pediatric-onset multiple sclerosis or clinically isolated syndrome, providing rationale for a randomized controlled trial of vitamin D supplementation. ANN NEUROL 2010;67:618,624 [source]


    Vitamin D and systemic cancer: is this relevant to malignant melanoma?

    BRITISH JOURNAL OF DERMATOLOGY, Issue 2 2002
    J.E. Osborne
    Summary 1,25-dihydroxyvitamin D3[1,25(OH)2D3] is a well-known potent regulator of cell growth and differentiation and there is recent evidence of an effect on cell death, tumour invasion and angiogenesis, which makes it a candidate agent for cancer regulation. The classical synthetic pathway of 1,25(OH)2D3 involves 25- and 1,-hydroxylation of vitamin D3, in the liver and kidney, respectively, of absorbed or skin-synthesized vitamin D3. There is recent focus on the importance in growth control of local metabolism of 1,25(OH)2D3, which is a function of local tissue synthetic hydroxylases and particularly the principal catabolizing enzyme, 24-hydroxylase. The classical signalling pathway of 1,25(OH)2D3 employs the vitamin D nuclear receptor (VDR), which is a transcription factor for 1,25(OH)2D3 target genes. Effects of this pathway include inhibition of cellular growth and invasion. Cytoplasmic signalling pathways are increasingly being recognized, which similarly may regulate growth and differentiation but also apoptosis. 1,25(OH)2D3 has a major inhibitory effect on the G1/S checkpoint of the cell cycle by upregulating the cyclin dependent kinase inhibitors p27 and p21, and by inhibiting cyclin D1. Indirect mechanisms include upregulation of transforming growth factor-, and downregulation of the epidermal growth factor receptor. 1,25(OH)2D3 may induce apoptosis either indirectly through effects on the insulin-like growth receptor and tumour necrosis factor-, or more directly via the Bcl-2 family system, the ceramide pathway, the death receptors (e.g. Fas) and the stress-activated protein kinase pathways (Jun N terminal kinase and p38). Inhibition of tumour invasion and metastasis potential has been demonstrated and mechanisms include inhibition of serine proteinases, metalloproteinases and angiogenesis. The lines of evidence for an effect of vitamin D3 in systemic cancer are the laboratory demonstration of relevant effects on cellular growth, differentiation, apoptosis, malignant cell invasion and metastasis; epidemiological findings of an association of the occurrence and outcome of cancers with derangements of vitamin D3/1,25(OH)2D3 and the association of functional polymorphisms of the VDR with the occurrence of certain cancers. In addition, vitamin D3 analogues are being developed as cancer chemotherapy agents. There is accumulating evidence that the vitamin D3/1,25(OH)2D3/VDR axis is similarly important in malignant melanoma (MM). MM cells express the VDR, and the antiproliferative and prodifferentiation effects of 1,25(OH)2D3 have been shown in cultured melanocytes, MM cells and MM xenografts. Recently, an inhibitory effect on the spread of MM cells has been demonstrated, low serum levels of 1,25(OH)2D3 have been reported in MM patients and the VDR polymorphisms have been shown to be associated with both the occurrence and outcome of MM. The relationship between solar irradiation and MM is more complex than for the systemic cancers. As in other cancers, there is evidence of a protective effect of vitamin D3 in MM, but ultraviolet radiation, which is a principal source of vitamin D3, is mutagenic. Further work is necessary on the influence of serum vitamin D3 levels on the occurrence and prognosis of MM, the effects of sun protection measures on serum vitamin D3 levels in temperate climates and epidemiological studies on geographical factors and skin type on the prognosis of MM. Meanwhile, it would seem mandatory to ensure an adequate vitamin D3 status if sun exposure were seriously curtailed, certainly in relation to carcinoma of breast, prostate and colon and probably also MM. [source]


    The Effect of Oxcarbazepine on Bone Metabolism

    ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009
    Y. Çetinkaya
    Objective,,, Long term use of several antiepileptic drugs is known to cause alteration in bone metabolism. Therefore, we investigated the effect of new antiepileptic drug, oxcarbazepine, on bone metabolism. Methods,,, Twenty eight patients who were on oxcarbazepin therapy (18 female, 10 males; mean age: 27.82 ± 10.98 years (range: 15,45)) with no additional antiepileptic drug use history in one year period prior to the study and 28 control subjects were involved in the study. Measurement of calcium, phosphate, alkaline phosphatase and Vitamin D3 levels and bone density measurements with DEXA method were performed in patient and age-matched control groups. The baseline parameters were compared with the control group and with those measured at the end of one year. Results,,, The biochemical (calcium, phosphate, alkaline phosphatase and Vitamin D3) parameters and densitometry values after one year of therapy were not different than the baseline values indicating that those were not affected by the therapy (P > 0.05). Conclusions,,, In previous studies, anticonvulsant drugs that induce enzymes increase bone degradation by causing vitamin D deficiency. According to the results of this study, oxcarbazepin with little effect on enzyme induction was shown not to affect bone mineral metabolism. [source]