Vitamin D supplementation: a potential booster for urticaria therapy

Chronic urticaria is a common skin condition whereby the etiology remains largely idiopathic and the mainstay therapy is symptomatic control with antihistamines. There have been a limited number of small studies suggesting a potential role for vitamin D in chronic urticaria, and this this editorial review will discuss the current supporting evidence. Associations for decreased serum vitamin 25 hydroxyvitamin D levels in subjects with chronic urticaria have been reported. In addition to observational reports, there has been a randomized, prospective, blinded trial demonstrating symptom improvement when high vitamin D3 supplementation was utilized as an add-on therapy for urticarial management. More research is needed to address mechanisms of action and to investigate vitamin D supplementation in larger and longer duration human trials.     

Vitamin D supplementation attenuates asthma development following traffic-related particulate matter exposure

1. Download high-res image (150KB)
2. Download full-size image

     

Vitamin D supplementation does not increase immunogenicity of seasonal influenza vaccine in HIV-infected adults

The influence of vitamin D on influenza vaccine immunogenicity in HIV was assessed using data from a phase 3, randomized trial conducted during the 2008-2009 influ-enza season. Thirty-three percent of participants were on supplemental vitamin D at baseline. Neither seroconversion nor seroprotection were predicted by vitamin D use for any of the 3 vaccine strains. There is no evidence of improved influenza vaccine immunogenicity with vitamin D supplementation in this HIV-positive population.     

Vitamin D supplementation during exercise training does not alter inflammatory biomarkers in overweight and obese subjects

The purpose of this study was to examine the effects of vitamin D supplementation on inflammatory biomarkers in overweight and obese adults participating in a progressive resistance exercise training program. Twenty-three (26.1 ± 4.7 years) overweight and obese (BMI 31.3 ± 3.2 kg/m2) adults were randomized into a double-blind vitamin D supplementation (Vit D 4,000 IU/day; female 5, male 5) or placebo (PL, female 7; male 6) intervention trial. Both groups performed 12 weeks (3 days/week) of progressive resistance exercise training (three sets of eight exercises) at 70-80% of one repetition maximum. Whole-blood lipopolysaccharide (LPS)-stimulated tumor necrosis factor (TNF) α production as well as circulating C-reactive protein (CRP), TNFα, interleukin 6 (IL-6), and alanine aminotransferase (ALT) were assessed at baseline and after the 12-week intervention. No main effects of group or time were detected for circulating CRP, TNFα, IL-6, and ALT. As expected, when PL and Vit D groups were combined, there was a significant correlation between percent body fat and CRP at baseline (r = 0.45, P = 0.04), and between serum 25OHD and CRP at 12 weeks (r = 0.49, P = 0.03). The PL group had a significant increase in 25 μg/ml LPS + polymixin B-stimulated TNFα production (P = 0.04), and both groups had a significant reduction in unstimulated TNFα production (P < 0.05) after the 12-week intervention. Vitamin D supplementation in healthy, overweight, and obese adults participating in a resistance training intervention did not augment exercise-induced changes in inflammatory biomarkers.     

维生素D与免疫

随着研究的不断深入,人们对维生素D的认识不再局限于钙、磷以及骨代谢.在各种免疫细胞中均存在维生素D受体及代谢相关的酶.维生素D与免疫的关系愈来愈受到重视.维生素D在免疫细胞的作用机制也逐步明确.越来越多的临床随机对照试验显示,维生素D有利于免疫功能,尤其在自身免疫性疾病、抗感染等方面发挥着重要作用.目前,维生素D介导下的免疫耐受作用机制探究正在成为新的研究热点.     

Vitamin E supplementation and lifespan in model organisms

We have conducted a comprehensive literature review regarding the effect of vitamin E on lifespan in model organisms including single-cell organisms, rotifers, Caenorhabditis elegans, Drosophila melanogaster and laboratory rodents. We searched Pubmed and ISI Web of knowledge for studies up to 2011 using the terms “tocopherols”, “tocotrienols”, “lifespan” and “longevity” in the above mentioned model organisms. Twenty-four studies were included in the final analysis. While some studies suggest an increase in lifespan due to vitamin E, other studies did not observe any vitamin E-mediated changes in lifespan in model organisms. Furthermore there are several studies reporting a decrease in lifespan in response to vitamin E supplementation. Different outcomes between studies may be partly related to species-specific differences, differences in vitamin E concentrations and the vitamin E congeners administered. The findings of our literature review suggest that there is no consistent beneficial effect of vitamin E on lifespan in model organisms which is consistent with reports in human intervention studies.     

Vitamin D and spondyloarthritis

In cross-sectional studies, vitamin D deficiency is frequent in spondyloarthritic patients and associated with increased spondyloarthritis (SpA) activity and structural damage. Experimental studies also show that vitamin D interferes with molecular pathways critically involved in SpA, especially regarding entheseal inflammation and ossification (involving cytokines such as IL-23 and sclerostin). Vitamin D deficiency might also affect the course of the disease through periodontal and gut inflammation, leading to increased functional impairment. Therefore, Vitamin D receptor selective agonists could represent a promising therapeutic pathway in this pathology. Randomised-controlled intervention studies are required in order to further elucidate complex relationships between vitamin D deficiency and SpA.     

Vitamin D supplementation ameliorates arthritis but does not alleviates renal injury in pristane-induced lupus model

Systemic lupus erythematosus (SLE) is a multifactorial and autoimmune inflammatory disease with pleomorphic clinical manifestations involving different organs and tissues. The study of different murine models has provided a better understanding of these autoimmune phenomena. Pristane-induced lupus represents a suitable model to study factors that could influence the induction and/or progression of SLE, including genetic factors. The objective of the present study was to evaluate the development and evolution of SLE after vitamin D supplementation in PIL model. Here, we evaluated the effects of vitamin D supplementation in model of pristane-induced SLE in female BALB/c mice. The animals were randomly divided into three groups: control group (CO), pristane-induced lupus group (PIL) and pristane-induced lupus group plus vitamin D (VD). Lupus was induced in PIL and VD groups using pristane. PIL group showed arthritis and kidney injury, characterized by increased proteinuria, glomerular mesangial expansion and inflammation. Moreover, PIL model showed increased levels of IL-6, TNF-α and IFN-γ in serum. We observed that treatment with vitamin D improved arthritis through reduced of incidence and arthritis clinical score and edema, but does not influenced renal injury. Treatment with vitamin D was not able to reduce proteinuria levels, decrease mesangial hypercellularity or IgG and IgM deposition in the kidney. Vitamin D supplementation did not alter IL-6, TNF-α, IL-2 and IL-4, but reduce IFN-γ. These results support that the role of vitamin D may be different depending on acting site, what could explain different responses according clinical phenotype. Therefore, further investigations of vitamin D are needed to explore the supplement dosage, timing, and the molecular basis in SLE.     

Vitamin D supplementation does not improve human skeletal muscle contractile properties in insufficient young males

Purpose

Vitamin D may be a regulator of skeletal muscle function, although human trials investigating this hypothesis are limited to predominantly elderly populations. We aimed to assess the effect of oral vitamin D₃ in healthy young males upon skeletal muscle function.

Methods

Participants (n = 29) received an oral dose of 10,000 IU day^?1 vitamin D₃ (VITD) or a visually identical placebo (PLB) for 3 months. Serum 25[OH]D and intact parathyroid hormone (iPTH) were measured at baseline and at week 4, 8 and 12. Muscle function was assessed in n = 22 participants by isokinetic dynamometry and percutaneous isometric electromyostimulation at baseline and at week 6 and 12.

Results

Baseline mean total serum 25[OH]D was 40 ± 17 and 41 ± 20 nmol L^?1 for PLB and VITD, respectively. VITD showed a significant improvement in total 25[OH]D at week 4 (150 ± 31 nmol L^?1) that remained elevated throughout the trial (P < 0.005). Contrastingly, PLB showed a significant decrease in 25[OH]D at week 12 (25 ± 15 nmol L^?1) compared with baseline. Despite marked increases in total serum 25[OH]D in VITD and a decrease in PLB, there were no significant changes in any of the muscle function outcome measures at week 6 or 12 for either group (P > 0.05).

Conclusions

Elevating total serum 25[OH]D to concentrations > 120 nmol L^?1 has no effect on skeletal muscle function. We postulate that skeletal muscle function is only perturbed in conditions of severe deficiency (<12.5 nmol L^?1).     

Vitamin D status and bone density in steroid-treated children with glomerulopathies: effect of cholecalciferol and calcium supplementation

PurposeThe aim of this study was to assess vitamin D status and bone density in steroid-treated children with glomerulopathies and to evaluate the effect of prophylactic vitamin D and calcium supplementation.Material and MethodsRetrospective analysis was performed on 55 children aged 4–18 yrs with glomerulopathies. The following data were analyzed: antropometrical parameters, bone densitometries, parathormone, 25-hydroxyvitamin D (25-OHD), urinary calcium excretion and medications received for prevention of low bone mass.ResultsA significant number of children (38%) had decreased spinal bone mineral density (BMD z-score < ?2.0) and the majority of them (89%) had hypovitaminosis D (25-OHD < 30ng/ml), 75% were vitamin D insufficient (25-OHD < 20ng/ml) and 16% were vitamin D deficient (25-OHD < 10ng/ml). The mean serum 25-OHD concentration was comparable to that of controls (19.32±12.87 vs. 15.05±8.52 ng/ml). Nearly all patients (82%) were receiving preparations of calcium and/or vitamin D to improve bone health. Patients on cholecalciferol had higher mean concentration of 25-OHD compared to those who were not receiving it (p=0.027) and to the controls (p=0.047). In 23 children on vitamin D and calcium supplementation for an average 6-month time, we observed an increase in the mean BMD values (p=0.004), however, mean BMD z-score and 25-OHD concentrations did not significantly change over time.ConclusionsVitamin D and bone density deficits are remarkably common in steroid-treated children with glomerulopathies, despite vitamin D and calcium repletion. In order to enhance the effectiveness of vitamin D supplementation for improvement of bone density, we suggest regular assessment of serum concentration of 25-OHD that can guide subsequent dose adjustment of vitamin D.