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PubMed2002

[Use and indication of vitamin D and vitamin D analogues in patients with renal bone disease].

Vitamin D plays a pivotal role in the pathogenesis and treatment of renal bone disease. Vitamin D levels decline in the early phase of renal failure; however, through a compensatory mechanism parathyroid hormone (PTH) stimulates the production of calcitriol to return it to normal circulating concentrations. Nevertheless, resistance to calcitriol is observed and may be related to the decreased presence of the heterodimeric, DNA-binding partner for the vitamin D receptor protein. In end-stage kidney disease (ESKD) the circulating levels of calcitriol are invariably low. The indications of vitamin D therapy are the replacement of the missing hormone versus suppression of hyperparathyroidism requiring daily low-dose oral versus intermittent pulse or oral administration. However, this therapy must be accompanied by careful patient monitoring to avoid hypercalcemia and low bone turnover. Low bone turnover is not merely a histologic entity, but a clinical condition associated with high risk of extraosseous calcifications, in particular in the cardiovascular system, leading to increased morbidity. Thus, determination of bone turnover in patients with ESKD is essential. Bone biopsy is the gold standard to assess bone turnover, however, it is not always available and nephrologists rely on PTH levels. The intact PTH assay measures PTH (1-84) and large C-PTH fragments, which may antagonize the PTH (1-84) effects on bone. An assay that measures exclusively PTH (1-84) has recently become available and a calculated PTH (1-84) /C-PTH fragment ratio has been shown to be the best predictor of bone turnover in patients with ESKD not treated with vitamin D or with other medications known to affect bone metabolism. 22-Oxacalcitriol is a vitamin D analogue that could control serum PTH concentrations without deleterious effects on bone.

English Abstract↗
PubMed2003

Vitamin D and vitamin D analogs as cancer chemopreventive agents.

Epidemiologic studies have associated vitamin D, attained through nutrition and sun exposure, with reduced cancer risk. Although dose-limiting hypercalcemia has limited the use of natural vitamin D in cancer prevention, several promising new synthetic vitamin D analogs (deltanoids) are under development. Examples are KH-1060, EB-1089, 1alpha-hydroxyvitamin D5, vitamin D2, and QW-1624F2-2. Clinical targets for deltanoids include colon, prostate, and breast. Studies to elucidate the molecular mechanisms underlying the observed efficacy of deltanoids are ongoing. The vitamin D receptor, a steroid/thyroid receptor superfamily member, appears to control most deltanoid effects on proliferation, apoptosis, differentiation, and angiogenesis.

Animals↗
PubMed1979

Analysis of fat-soluble vitamins. XXI. High pressure liquid chromatographic assay methods for vitamin D in vitamin D concentrates.

Two high pressure liquid chromatographic methods, a straight and a reverse phase system, were developed and compared with the official (chemical) AOAC method for vitamin D concentrates. The effects of the systematic error and the reproducibility of using an internal or external standard were studied, as well as the effect of using peak height or peak height X retention time for calculating the potential vitamin D content. A method is given for determining the conversion factor to calculate previtamin D as vitamin D. Based on the results of the comparison, the following conditions were selected for collaborative study: straight phase, amyl alcohol-hexane mobile phase, external standard, and calculation of potency by peak height.

Cholecalciferol↗
PubMed1990

Bone disease in chronic childhood cholestasis. II. Better absorption of 25-OH vitamin D than vitamin D in extrahepatic biliary atresia.

Infants with extrahepatic biliary atresia (EHBA) commonly develop rickets in infancy, whereas long-term survivors with EHBA commonly develop osteopenia with increasing age. We evaluated baseline vitamin D (D2 and D3), 25-OH vitamin D2 and D3, 1,25(OH)2 vitamin D, bone mineral content, and vitamin D2 and 25-OH vitamin D3 absorption in six infants and children (age 4-22 mo) with EHBA whose portoenterostomy failed to produce bile flow (group 1) and five infants and children (age 10/12 to 8-4/12 y) with EHBA whose portoenterostomy repair led to good postoperative bile flow (group 2). Baseline serum vitamin D2 and D3 were undetectable in all subjects in group 1 despite supplements of 2500-5000 IU/day, whereas all group 2 subjects given supplements (doses 400-5000 IU/d) had measurable levels. Baseline serum 25-OH vitamin D was less than 15 ng/mL in five of six (three with rickets) in group 1, whereas only one in group 2 had concentrations less than 15 ng/mL. A significantly blunted rise of vitamin D2 above baseline and reduced area under the absorption curve after 1000 IU/kg vitamin D2 were found in group 1 patients compared to group 2 (both p less than 0.01), and five pediatric controls (both p less than 0.01). The peak change and area under the absorption curve for serum 25-OH vitamin D3 from baseline after 10 micrograms/kg 25-OH vitamin D3 were significantly reduced for group 1 (both at least p less than 0.05) and group 2 compared to controls (both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Biliary Atresia↗
PubMed1980

Vitamin D and vitamin D dependency.

Administration of large doses of vitamin D2 brought about a marked increase of 25-hydroxyvitamin D in both the patients with vitamin D dependency and hypophosphatemic vitamin D-resistant rickets. During the administration of vitamin D2, increment of 1,25-dihydroxyvitamin D was marked in hypophosphatemic vitamin D-resistant rickets, but far smaller in vitamin D dependency. In the latter, however, the 1,25-dihydroxyvitamin D reached the level close to the normal adult values. 1 alpha-hydroxyvitamin D3 was found 50 approximately 100 times as effective as vitamin D2 in 2 patients with vitamin D dependency (optimum maintenance dose: 0.05 micrograms/kg/day). It was concluded that 1 alpha-hydroxylation in the renal tubules is markedly defective in the patients with vitamin D dependency, but that a large dose of vitamin D2 is able to cause a definite increase in serum concentration of 1,25-dihydroxyvitamin D resulting in improvement of the rickets.

Alkaline Phosphatase↗
PubMed2005

Plasma 25-hydroxy vitamin D concentrations, vitamin D receptor genotype and breast cancer risk in a UK Caucasian population.

Low levels of 25-hydroxy vitamin D (25(OH)D) and polymorphisms in the vitamin D receptor gene (VDR) have been found separately to increase risk of breast cancer. The aim of this study was to determine whether low 25(OH)D levels, alone and in combination with BsmI VDR genotype, increased breast cancer risk in a United Kingdom (UK) Caucasian population. Breast cancer patients (n=179) and control women (n=179) were recruited and 25(OH)D levels measured by enzyme-linked immunosorbent assay (ELISA). VDR genotype was determined by polymerase chain reaction (PCR) and restriction enzyme digest. Analysis showed that subjects with 25(OH)D levels <50 nM and the bb BsmI VDR genotype are 6.82 times more likely to have breast cancer than subjects with levels of 25(OH)D>50 nM and either the BB or Bb genotype (95% confidence interval (CI) 2.31-14.7, P<0.001). This study indicates that low levels of circulating 25(OH)D, both alone and in combination with BsmI VDR genotype, may increase risk of breast cancer in a UK Caucasian population.

Adult↗
PubMed2006

[Vitamin D-vitamin D receptor system regulates antithrombogenicity in vivo].

Although it has been well documented that vitamin D receptor (VDR) activation influences the expression of various genes involved in calcium homeostasis and cell differentiation, the physiological role of VDR action in hemostasis remains unclear. We studied thrombogenicity in normocalcemic VDR knock-out (KO) mice on a high calcium diet in comparison with that in wild-type mice and that in hypocalcemic VDRKO mice fed a regular diet. Platelet aggregation was significantly enhanced in normocalcemic VDRKO mice. Aortic endothelial nitric-oxide (NO) synthase expression and urinary NOx excretion were reduced in hypocalcemic VDRKO mice but not in normocalcemic VDRKO mice. The gene expression of antithrombin in the liver and that of thrombomodulin in the aorta, liver and kidney were down-regulated in hypo- and normocalcemic VDRKO mice, whereas tissue factor gene expression in the liver and kidney was up-regulated in VDRKO mice regardless of plasma calcium level. Furthermore, VDRKO mice manifested an exacerbated multi-organ thrombus formation after exogenous lipopolysaccharide injection regardless of the calcemic conditions. These results demonstrate that the vitamin D-VDR system plays a pivotal role in antithrombogenicity in vivo.

Animals↗
PubMed1981

Analysis of fat-soluble vitamins. XXIV. High performance liquid chromatographic determination of vitamin D in vitamin D resin containing powders: collaborative study.

Further study of vitamin D methodology solved the discrepancy between the AOAC chemical method, 43.068-43.078, and the HPLC assay for vitamin D3 in resin containing dry powders. The discrepancy is caused by the difference in solubility of the vitamin D3 resin in benzene and in pentane. The method has been modified accordingly, and has been adopted official first action for vitamin D3 resins and vitamin D3 resin containing powders and aqueous dispersions.

Chromatography, High Pressure Liquid↗
PubMed2004

Prenatal and infant predictors of bone health: the influence of vitamin D.

Vitamin D is essential for the health of pregnant women and their infants. Vitamin D insufficiency and deficiency during pregnancy are reflected in lower maternal weight gain and biochemical evidence of disturbed skeletal homeostasis in the infant, with, in extreme situations, reduced bone mineralization, radiologically evident rickets, and fractures. Populations at risk for vitamin D deficiency are those for which, for environmental, cultural, or medical reasons, exposure to sunlight is poor and the dietary intake of vitamin D is low. The infants born in such populations have low vitamin D stores and may receive little additional vitamin D if they are breast-fed without supplements for long periods. In the short term, lack of vitamin D supplementation in infancy leads to biochemical disturbances, reduced bone mineralization, slower growth, and eventual alterations in bone shape and increased risk of fracture, the hallmarks of rickets. In the longer term, lack of vitamin D supplementation may result in reduced bone size and mass during childhood and an increased risk of type 1 diabetes mellitus. Clear recommendations are needed regarding the intake of vitamin D during pregnancy and infancy. Such recommendations should be based on functional outcomes, rather than biochemical measurements, so that the medical problems resulting from the lack of this essential nutrient can be overcome.

Bone and Bones↗
PubMedDate not supplied

Seasonal differences in serum vitamin D binding protein in exclusively breast-fed infants: negative relationship to sunshine exposure and 25-hydroxyvitamin D.

Vitamin D binding protein (DBP) is the major carrier for vitamin D and its metabolites in serum. DBP increases in pregnancy and decreases in cirrhosis; no seasonal variation has been reported in adults. We observed significant seasonal differences in 41 exclusively breast-fed infants who were less than 6 months of age. Winter DBP concentrations exceeded summer DBP concentrations: 398 +/- 22 versus 297 +/- 20 micrograms/ml (mean +/- SEM). The mean concentration for spring and fall was 329 +/- 25 micrograms/ml. Maternal DBP concentrations did not differ by season. A sunshine exposure score, previously verified, was used to document time and body surface exposed to the sun. DBP was inversely related to sun exposure (r = -0.46, p = 0.005). Infant DBP was significantly and negatively correlated with 25-hydroxyvitamin D concentrations (r = - 0.38, p = 0.02). We speculate that serum DBP fluctuations are a response to varying vitamin D needs: increased serum DBP occurs in low vitamin D status to maximize uptake of vitamin D from skin.

Breast Feeding↗
PubMed2003

[Renal osteodystrophy and vitamin D].

Vitamin D deficiency is one of major pathogeneses of renal osteodystrophy (ROD). Vitamin D deficiency produces osteitis fibrosa via secondary hyperparathyroidism and osteomalacia via hypocalcemia. To prevent and treat ROD, vitamin D supplementation is an inevitable tool. Recent progresses of vitamin D therapy including development of new vitamin D analogues and direct injection to parathyroid gland will contribute to the successful treatment of ROD.

English Abstract↗
PubMed1990

Osteoporosis and the metabolites of vitamin D.

Vitamin D is metabolized by sequential steps in the liver and kidney to its active form, a process that is strongly feedback-regulated. In old age, the activity of the enzyme, 25-hydroxyvitamin D 1 hydroxylase, which produces the vitamin D hormone, is diminished. The activities of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) extend beyond increasing intestinal absorption of calcium. The vitamin D hormone (or its analogs) is useful in the treatment of osteoporosis because it not only stimulates intestinal calcium absorption, but also is required for the stimulation of osteoblasts and many other cells in the body. Recent work demonstrates that it is possible to chemically synthesize analogs selective for specific actions of the vitamin D hormone, especially in inducing differentiation of promyelocytes and keratinocytes.

Animals↗
PubMed2002

Increased 25-hydroxyvitamin D3 1alpha-hydroxylase and reduced 25-hydroxyvitamin D3 24-hydroxylase expression in parathyroid tumors--new prospects for treatment of hyperparathyroidism with vitamin d.

Vitamin D analogues are in clinical use for prevention and treatment of secondary hyperparathyroidism (HPT) in chronic renal failure. Despite recent advances there is a need for vitamin D derivatives with maintained parathyroid hormone suppressive activity and less hypercalcemic and hyperphosphatemic toxicity. Here we show coincident increased expression of the vitamin D activating enzyme 25-hydroxyvitamin D(3) 1alpha-hydroxylase (1alpha-hydroxylase) and reduced expressions of the 1,25(OH)(2)D(3) catabolizing enzyme 25-hydroxyvitamin D(3) 1alpha-hydroxylase (1alpha-hydroxylase) in the majority of investigated parathyroid adenomas and secondary hyperplastic glands. In addition, this relationship was found for the mitochondrial CYP27A enzyme (25-hydroxylase), a potential physiological vitamin D(3) 25-hydroxylase. These findings should be considered in future development of vitamin D analogues for treatment of HPT.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1993

[Vitamin D dependency and vitamin D resistance].

Vitamin D dependency is classified into two clinical disorders which are caused by genetic defect of vitamin D metabolism. Vitamin D dependent rickets type I and type II are the deficiency of 25-hydroxyvitamin D-1 alpha-hydroxylase and the defect of receptor for 1 alpha,25-dihydroxyvitamin D, respectively. In contrast, vitamin D resistance shows hypophosphatemia derived from disorder(s) of phosphate transport system in renal brush border membrane. There are three clinical entities such as hereditary hypophosphatemic rickets with hypercalciuria, familial hypophosphatemic rickets and oncogenic hypophosphatemic osteomalacia. However, the real pathogenesis of these disorders have not well been understood at present.

Humans↗
PubMed2002

Vitamin D and vitamin D analogs in cancer treatment.

The secosteroid hormone 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is a key player in the regulation of bone mineralization and calcium homeostasis. In addition, 1,25-(OH)2D3 has antiproliferative and prodifferentiation effects on various cells in vitro and in vivo. The growth-inhibitory properties of 1,25-(OH)2D3 could be harnessed in the treatment of cancer. However, its use as an anti-cancer drug is limited because of the calcemic effects of pharmacological doses. In an attempt to dissociate the antiproliferative and calcemic effects, numerous vitamin D3 analogs were developed. The mechanisms by which 1,25-(OH)2D3 and 1,25-(OH)2D3 analogs exert their growth-inhibitory effects are not clear but include effects on cell differentiation, apoptosis, cell cycle regulation, metastases, and angiogenesis. In the current review aspects involved in the tumor suppressive activity of 1,25-(OH)2D3 and 1,25-(OH)2D3 analogs will be addressed. The use of vitamin D3 compounds, alone or in combination with other drugs, in cancer treatment and the potential drawbacks will also be discussed.

Animals↗
PubMed2000

The function of vitamin D receptor in vitamin D action.

Vitamin D has roles in a variety of biological actions such as calcium homeostasis, cell proliferation and cell differentiation to many target tissues. Most of these biological actions of vitamin D are now considered to be exerted through the nuclear vitamin D receptor (VDR)-mediated control of target genes. VDR belongs to the nuclear hormone receptor superfamily and acts as a ligand-inducible transcription factor. For the ligand-induced transactivation of VDR, coactivator complexes have recently been shown to be essential. The function of VDR as a ligand-induced transcription factor is overviewed, and the phenotype of VDR gene knock-out mice and the VDR-mediated transcriptional and negative regulation of the key enzyme in vitamin D biosynthesis are also described, based mainly on our recent findings, to gain a better understanding of the function of VDR in the transcriptional control of vitamin D target genes.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1985

Effect of race and diet on human-milk vitamin D and 25-hydroxyvitamin D.

Vitamin D-deficiency rickets continues to be reported in infants fed human milk, and the importance of human milk as a source of vitamin D for infants is controversial. Furthermore, effects of race and of normally consumed maternal vitamin D intake on human-milk vitamin D have not been reported. Milk, serum, and three-day-diet diaries were obtained from 25 mother-infant pairs. Human-milk vitamins D3 and D2 and 25-hydroxyvitamin D3 were lower in blacks vs whites, whereas 25-hydroxyvitamin D2 did not differ. Total-milk vitamin D, but not 25-hydroxyvitamin D, correlated with vitamin D intake. Milk vitamin D2 specifically was correlated with vitamin D intake even after controlling for race. Infant serum 25-hydroxyvitamin D did not correlate with milk vitamin D or 25-hydroxyvitamin D; we speculate that the contribution of vitamin D from human milk in these infants is insignificant relative to the contribution from sunshine exposure.

25-Hydroxyvitamin D 2↗