Signaling through the vitamin D receptor has been shown to be biologically active and important in a number of preclinical studies in prostate and other cancers. Epidemiologic data also indicate that vitamin D signaling may be important in the cause and prognosis of prostate and other cancers. These data indicate that perturbation of vitamin D signaling may be a target for the prevention and treatment of prostate cancer. Large studies of vitamin D supplementation will be required to determine whether these observations can be translated into prevention strategies. This paper reviews the available data in the use of vitamin D compounds in the treatment of prostate cancer. Clinical data are limited which support the use of vitamin D compounds in the management of men with prostate cancer. However, clinical trials guided by existing preclinical data are limited.
Antineoplastic Combined Chemotherapy Protocols/therapeutic use* ; Calcifediol/blood* ; Calcitriol/therapeutic use* ; Clinical Trials as Topic ; Ergocalciferols/therapeutic use* ; Humans ; Male ; Prostatic Neoplasms/prevention & control* ; Signal Transduction ; Vitamin D/metabolism* ; Vitamin D Deficiency/epidemiology*

BACKGROUND: Determining the concentration profiles of serum 25-hydroxyvitamin D (25OHD) may aid in the clinical diagnosis and treatment of vitamin D deficiency. To date, the standardized liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay has been used for accurate and precise determination of 25-hydroxyvitamin D levels. Here, we evaluated the performance of the recently developed and introduced PerkinElmer Vitamin D kit and compared the measurements obtained by RIA and LC-MS/MS methods. METHODS: We evaluated the accuracy, precision, linearity, lower limit of quantification (LLOQ), recovery, and carry-over of the MSMS Vitamin D kit. Clinical specimens from 80 patients were used for the comparison between the MSMS Vitamin D kit (PerkinElmer, USA) and the RIA kit (DiaSorin, USA). RESULTS: The MSMS Vitamin D kit was found to produce intra-assay and inter-assay coefficients of variation (CVs) of less than 6% for precision and showed a bias of less than 5%. The MSMS Vitamin D kit displayed linearity within the range for total vitamin D levels of 4.5-150 ng/mL, and the lower limit of quantification for 25OHD was 0.38 ng/mL. The RIA measurements of 25OHD showed a correlation of y=0.9931x+0.2216 (r2=0.74) with the LC-MS/MS values. CONCLUSIONS: The LC-MS/MS assay of 25OHD3 and 25OHD2 showed excellent performance when using the MSMS Vitamin D kit and in terms of 4-phenyl-1,2,4-triazoline-3,5-dione (PTAD) derivatization. Further, the results obtained were well correlated with those obtained using the RIA method. Thus, assays using the MSMS Vitamin D kit are considered as more standardized, and they enable quicker and more accurate analysis and help reduce inter-laboratory variation than that by other existing methods.
25-Hydroxyvitamin D 2 ; Bias (Epidemiology) ; Calcifediol ; Humans ; Mass Spectrometry ; Tandem Mass Spectrometry ; Triazoles ; Vitamin D ; Vitamin D Deficiency ; Vitamins

PURPOSE: To evaluate the clinical characteristics of vitamin D deficiency and its association with iron deficiency anemia (IDA). METHODS: A total of 171 children aged less than two years underwent 25-hydroxyvitamin D3 tests between January 2007 and July 2009. The study was classified into two groups: normal and vitamin D insufficiency, by their vitamin 25-hydroxyvitamin D3 levels. RESULTS: In total, 120 children were in the normal group (mean age, body weight and heights 12.5+/-7.0, 9.3+/-0.9 kg and 76.8+/-1.1 cm), and 51 children in the vitamin D insufficiency group (9.9+/-5.4 months, 9.0+/-0.9 kg and 75.1+/-0.9 cm). Vitamin D insufficiency was most commonly diagnosed in the spring (44%). The proportion of complete breast-feeding was higher in the insufficiency (92%), and 25.5% of the children in the deficient group also experienced IDA compared that 12% of normal group. Ten children in the insufficiency group experienced bony changes. Six children received calcitriol medication in the normal group, in whom the mean vitamin 25-hydroxyvitamin D3 level increased from 39.6+/-14.6 ng/mL (pre-medication) to 41.8+/-17.2 ng/mL (post-medication), and 13 in the insufficiency group, in whom the mean vitamin 25-hydroxyvitamin D3 increased from 20.7+/-7.0 ng/mL to a mean post-treatment level of 43.7+/-23.8 ng/mL. CONCLUSION: This study demonstrated that approximately 30% of children aged < or =2 years experienced vitamin D insufficiency associated with subclinical rickets. Many children also experienced concurrent IDA. Guidelines for vitamin D supplement in such children must therefore be established.
Aged ; Anemia ; Anemia, Iron-Deficiency ; Body Weight ; Calcifediol ; Calcitriol ; Child ; Humans ; Iron ; Prevalence ; Rickets ; Vitamin D ; Vitamin D Deficiency ; Vitamins

Vitamin D is present in two forms, ergocalciferol (vitamin D2) produced by plants and cholecalciferol (vitamin D3) produced by animal tissues or by the action of ultraviolet light on 7-dehydrocholesterol in human skin. Both forms of vitamin D are biologically inactive pro-hormones that must undergo sequential hydroxylations in the liver and the kidney before they can bind to and activate the vitamin D receptor. The hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D], plays an essential role in calcium and phosphate metabolism, bone growth, and cellular differentiation. Renal synthesis of 1,25(OH)2D from its endogenous precursor, 25-hydroxyvitamin D (25OHD), is the rate-limiting and is catalyzed by the 1alpha-hydroxylase. Vitamin D dependent rickets type I (VDDR-I), also referred to as vitamin D 1alpha-hydroxylase deficiency or pseudovitamin D deficiency rickets, is an autosomal recessive disorder characterized clinically by hypotonia, muscle weakness, growth failure, hypocalcemic seizures in early infancy, and radiographic findings of rickets. Characteristic laboratory features are hypocalcemia, increased serum concentrations of parathyroid hormone (PTH), and low or undetectable serum concentrations of 1,25(OH)2D despite normal or increased concentrations of 25OHD. Recent advances have showed in the cloning of the human 1alpha-hydroxylase and revealed mutations in its gene that cause VDDR-I. This review presents the biology of vitamin D, and 1alpha-hydroxylase mutations with clinical findings.
Animals ; Biology ; Bone Development ; Calcitriol ; Calcium ; Cholecalciferol ; Clone Cells ; Cloning, Organism ; Dehydrocholesterols ; Ergocalciferols ; Humans ; Hydroxylation ; Hypocalcemia ; Kidney ; Liver ; Muscle Hypotonia ; Parathyroid Hormone ; Receptors, Calcitriol ; Rickets ; Seizures ; Skin ; Ultraviolet Rays ; Vitamin D ; Vitamins

PURPOSE: It is well known that obesity is related to vitamin D deficiency (VDD). We investigated the response to vitamin D replacement in normal-weight and overweight children. METHODS: This was a prospective study including 62 Korean children with VDD. VDD was defined as a serum 25-hydroxycholecalciferol (25(OH)D) concentration <20 ng/mL. Overweight was defined as a body mass index (BMI)≥the 85th percentile (n=21), and normal weight as a BMI between the 5th and 84th percentiles (n=41). All participants received vitamin D3 supplementation (2,000 IU/day) for 8 weeks. The serum levels of 25(OH)D, PTH and biochemical parameters were measured before and after treatment. RESULTS: The mean age was 10.0±1.4 years in normal-weight children and 10.0±2.1 years in overweight children (P=0.93). After 8 weeks of treatment, 61.9% of normal-weight children and 47.6% of overweight children achieved vitamin D sufficiency (P =0.30). The mean serum 25(OH)D levels after vitamin D replacement were 33.8±7.6 ng/mL and 30.3±6.6 ng/mL in normal-weight and overweight children, respectively (P =0.10). The mean calcium/creatinine ratios after treatment were 0.09±0.07 and 0.08±0.06 in the normal-weight and overweight groups, respectively, and no hypercalciuria was found. In multiple regression analysis, the response to vitamin D replacement was influenced by the BMI (β=-1.0, P=0.03) and sex (β=-4.0, P=0.04). CONCLUSIONS: Eight weeks of vitamin D replacement (2,000 IU/day) is sufficient to overcome vitamin D deficiency in normal-weight and overweight children without any complications.
Body Mass Index ; Calcifediol ; Child ; Cholecalciferol ; Humans ; Hypercalciuria ; Obesity ; Overweight ; Prospective Studies ; Vitamin D Deficiency ; Vitamin D ; Vitamins

BACKGROUND/AIMS: The exact relationship between vitamin D deficiency and inflammatory bowel disease (IBD) remains unclear. We evaluated the effect of vitamin D3 administration on inflammatory responses and disease severity in patients with IBD. METHODS: We investigated the serum 25-hydroxyvitamin D3 [25-(OH)D], C-reactive protein (CRP) levels and the partial Mayo score (PMS) in patients with IBD. Vitamin D3 was administered in patients with either vitamin D deficiency or insufficiency and CRP, serum vitamin D levels and PMS were re-examined at 6 months of administration. RESULTS: In 88 patients with Crohn's disease (CD), a negative correlation was found between serum vitamin D and CRP. In 178 patients with ulcerative colitis (UC), serum vitamin D showed no association with CRP or PMS. Serum vitamin D increased from 11.08±3.63 to 22.69±6.11 ng/mL in 29 patients with CD and from 11.45±4.10 to 24.20±6.61 ng/mL in 41 patients with UC who received vitamin D3 treatment (P<0.001 and P<0.001, respectively). In patients with CD, median ΔCRP was –0.24 in the normalized vitamin D group and –0.11 in the non-normalized group (P=0.308). In patients with UC, median ΔCRP was −0.01 in the normalized vitamin D group and 0.06 in the non-normalized group (P=0.359). CONCLUSIONS: Although a negative correlation was found between serum vitamin D and CRP levels in patients with CD, administration of vitamin D did not improve the CRP level in patients with CD. In patients with UC, serum vitamin D level was unrelated to CRP or PMS.
C-Reactive Protein ; Calcifediol ; Cholecalciferol ; Colitis, Ulcerative ; Crohn Disease ; Humans ; Inflammatory Bowel Diseases ; Vitamin D Deficiency ; Vitamin D ; Vitamins

OBJECTIVE: To determine the effects of multivitamin vitamin D 300 or 600 units on serum 25 hydroxyvitamin D (25(OH)D) level after 4 weeks of supplementation in postmenopausal women with vitamin D insufficiency. STUDY DESIGN: Randomized double-blind, placebo-controlled trial. METHODS: Postmenopausal women who had vitamin D insufficiency were recruited into the study. The participants were randomized to 3 groups of 4-week treatment period with multivitamin (GPO, Governmental Pharmacy Organization) 2 tablets (contained vitamin D2 amount 600 units), multivitamin 1 tablet (contained vitamin D2 amount 300 units) or placebo. At baseline and after 4 weeks of supplementation, serum 25(OH)D were determined with electrochemilumines-cence immunoassay (Cobas, Roche Diagnostics) and level change of 25(OH)D level were compared among the groups. RESULTS: Out of 144 participants, 49.3% had vitamin D deficiency (<20 ng/ml) and 50.7% had vitamin D insufficiency (<30 ng/ml). However, after 4 weeks of the GPO oral multivitamin, serum 25(OH)D levels significantly increased from 19.4 ± 6.3 ng/ml at baseline to 22.2 ± 5.2 ng/ml (P = 0.01) and from 19.5 ± 5.0 ng/ml to 23.3 ± 5.2 ng/ml (P < 0.01) in the groups receiving vitamin D 300 IU and 600 IU/day, respectively. Approximately, 10% of those who took vitamin D had serum 25(OH)D level above the insufficiency level within 4 weeks. There was no significant changes of serum 25(OH)D after 4 weeks in the placebo group. CONCLUSION: Daily supplementation of the generic multivitamin containing vitamin D2 300 and 600 IU daily for 4 weeks significantly increased mean serum 25(OH)D from baseline up above the deficiency level.
Ergocalciferols ; Female ; Humans ; Immunoassay ; Pharmacy ; Postmenopause ; Tablets ; Vitamin D Deficiency ; Vitamin D* ; Vitamins*

The cutaneous synthesis of vitamin D in response to ultraviolet radiation exposure is the most important factor in maintaining vitamin D balance in Man. The skin is not only the site of vitamin D synthesis, but also a target organ for calcitriol(1, 25-dihydroxy-vitamin D) which is naturally occuriag, hormonally active form of vitamin E. It is now known that calcitriol inhibits the proliferation of epidermal cells and induces her differentiation. In this study, epidermal keratinocytes and melanocytes were isilated from the neonatal foreskin, and were culturod using a MCDB 153 and modified TIC media, respectively. And then various concentratioris of calcipotriol(MC 903), a synthetic aralogue of calcitriol, were added to each culture. The effects of calcipotriol on the growth of human keratinocytes and melanocytes were investigated. The results were as follows : 1. The addition of calopotriol to human keratinocyte and melalocyte cultures inhibited their proliferation in a dosdependent manner. 2. Calcipotriol had no effects on the melanization process of the melanocyte. 3. Calcipotriol was found to inhibit the proliferation, however it induced the terminal differentiation of cultured keratinocytes, as judged by morphologicai changes. The decreased density of kerationcytes, The formation of cornified cells, and the cellular destruction in a concentration of 10 M of calcipotriol were observed. 4. By using the light atid the electron microscope, we observed that the epidermal thickness was decreased and terminal differentiation was facilitateir. Living Skin Equivalent (LSE) according to the increasing concentration of calcipotriol. A]i)parent cytotoxic effects were observed in 10 M, 10 M of calcipotriol. In summary, the above results indicate that the addition of calcipotriol to the in vitro culture system of human keratinocyte and melanocyte induces the biologic process of terminal differentiation of keratinocytes and inhibits proliferation of keratinoytes and melanocytes in a dose-dependent manner.
Calcitriol ; Cholecalciferol* ; Foreskin ; Humans* ; Keratinocytes* ; Melanocytes* ; Skin ; Tics ; Vitamin D ; Vitamin E ; Vitamins*

Vitamin D, also known as cholecalciferol, is the precursor to the active steroid hormone 1, 25-dihydroxyvitamin D3 (calcitriol; 1, 25(OH)2D3). The main physiological role for 1, 25(OH)2D3 is to regulate calcium and inorganic phosphate homeostasis for bone health. More recently, vitamin D has been investigated for its effects in the prevention and treatment of a variety of diseases such as cancer, autoimmune disorders, and cardiovascular disease. Preclinical data strongly support a role for vitamin D in the prevention of cancer through its anti-proliferative, pro-apoptotic, and anti-angiogenic effects on cells. Epidemiologic and clinical studies have shown mixed data on the correlation between serum vitamin D levels and cancer risk. This report seeks to outline results from the most recent preclinical and clinical studies investigating the potential role of vitamin D in cancer prevention.
Calcitriol ; blood ; Cholecalciferol ; blood ; Humans ; Neoplasms ; blood ; etiology ; prevention & control ; Vitamin D ; blood ; Vitamin D Deficiency ; blood ; complications

BACKGROUND: It is still unclear the ideal vitamin D dosage once the deficiency and insufficiency is treated. Once deficiency was corrected we prospectively treated patients with 2,000 IU of vitamin D3 to check whether this dosage is enough to keep them above the 30 ng/mL of 25-hydroxy-vitamin D (25[OH]D). METHODS: One hundred and thirty-five Saudi Arabian men and women treatment naïve for the vitamin D deficiency and insufficiency were part of this study. History and clinical examination were done to rule out any metabolic bone disease. Weight and height was taken to calculate the body mass index (BMI). Patients who were vitamin D deficient (≥30 ng/mL), a standard treatment of 50,000 IU of vitamin D3 weekly for 3 months, a blood test for the vitamin D levels at the end of 3 months, maintenance dose of 2,000 IU of vitamin D3 for 3 months and a third blood sample after 3 months. RESULTS: The data for 128 patients was available for analysis. The average age was 44.95±12.97 years with the mean BMI of 29.60±2.59 kg/m2. The baseline 25(OH)D level was 13.16±3.30 ng/mL. The increase in the level of 25(OH)D on 50,000 IU weekly was significant from 13.16±3.3 ng/mL to 36.97±4.67 ng/mL (P < 0.001) and then 2,000 IU daily for next 3 months, the level of 25(OH)D dropped top 20.38±5.42 ng/mL (P < 0.001). CONCLUSIONS: Our study indicates that the maintenance dose of 2,000 IU of vitamin D is not enough for patients to keep the 25(OH)D levels above 30 ng/mL.
Body Mass Index ; Bone Diseases, Metabolic ; Calcifediol ; Cholecalciferol ; Dietary Supplements ; Female ; Hematologic Tests ; Humans ; Male ; Prospective Studies ; Vitamin D Deficiency ; Vitamin D* ; Vitamins*