雌激素、维生素D 和骨形态发生蛋白质与骨质疏松症及心脑动脉钙化的发生机制

目的 探讨雌激素、维生素D和骨形态发生蛋白质(BMP)与骨质疏松症及心脑动脉钙化的相关性及其发病机制。方法 在PubMed和中国知网中以雌激素、维生素D、BMP、骨质疏松和动脉钙化斑块为关键词检索1995年1月—2015年9月有关雌激素、维生素D缺乏和骨形成相关蛋白与骨质疏松、心脑动脉钙化斑块的关系等方面的相关文献,对骨质疏松与心脑动脉钙化斑块形成的相关性及发病机制进行分析总结。结果 雌激素缺乏、维生素D缺乏均导致骨质疏松和心脑动脉钙化发生的风险增加。骨保护素、脂联素、BMP、骨桥蛋白等骨形成相关蛋白参与骨质疏松的形成而且是心脑动脉钙化发病的重要调控因子。结论 雌激素、维生素D和骨形成相关蛋白与骨质疏松症及心脑动脉钙化的发生密切相关,并且可能有共同的病理生理机制;该理论对心脑血管疾病和骨质疏松的防治有重要作用。     

维生素D在治疗骨质疏松症中的作用

维生素D主要源于皮肤的合成,目前被认为是一种生理激素,而不是维生素.维生素D缺乏(＜ 50nmol/L)是一个影响人类健康的全球性问题,因其在各种生理系统中起到至关重要的作用.各种研究表明,血清25(OH)D水平高,可降低髋及脊柱骨折的发病率.有关于研究使用治疗剂量维生素D的数据很少,大多数的研究集中在低生理剂量而不是高药理剂量.为了达到75nmol/L的浓度,800～1000IU/天是必需的.未来应该关注将25 (OH) D3维持到75nmol/L,以此增加骨质密度、降低骨折风险,同时在维生素D缺乏的情况下,应用高剂量治疗.根据新的证据表明,维生素D在治疗和补充两个方面需要被重新评估,这需要注意维持血清25(OH)D的水平,为了获得预防骨质疏松症和预期的效果,能够降低骨质疏松性骨折的复发.     

女性高血压患者左心室肥厚相关因素分析及补充维生素D的意义

目的分析女性高血压患者左心室肥厚的相关因素及外源性维生素D补充的意义。方法选择2015年3月至2018年6月在我院就诊的未绝经女性高血压患者443例作为研究对象。根据是否补充外源性维生素D将患者分为补充组(n=239)及未补充组(n=204)。比较两组患者并发左心室肥厚的情况,并采用Logistic回归分析影响女性高血压患者左心室肥厚的相关因素。结果补充组患者左心质量指数明显低于未补充组患者,差异有统计学意义(P <0.05)。单纯性高血压组和左心室肥厚组患者在收缩压、舒张压、肌酐、尿素氮、血红蛋白、尿酸、外源性补充维生素D方面比较,差异具有统计学意义(P<0.05)。结论女性高血压患者血压控制情况与其左心室肥厚相关,外源性维生素D补充是高血压左心室肥厚的独立保护因素。     

帕金森病疲劳的影响因素及补充维生素D的意义

目的:研究血清维生素D水平与帕金森病(Parkinson disease,PD)疲劳的关系,以及补充维生素D后疲劳的改善情况.方法:收集2018年11月至2019年8月在山西医科大学第一医院住院部及门诊就诊的39例PD伴疲劳患者,31例PD非疲劳患者,同时收集39例经相关检查无器质性病变的头晕患者作为对照组.收集3组的...     

补充维生素D和钙预防老年人骨折受质疑

通常认为老年人维生素D缺乏是导致跌倒和骨折的重要原因之一,以往的研究也表明,补充维生素D和钙可以降低老年人骨折的风险。在美国,医师建议50岁的人每天服用200IU（国际单位）维生素D,51～70岁的人服用4加IU,超过70岁则建议服用600IU。维生素D有助于钙的吸收,50岁以上的成人钙摄取量每天应达到1200mg。但是英国科学家的两项最新研究也许将要改变人们这一固有的思维模式,因为他们的研究结果显示,补充维生素D和钙似乎并不能预防高风险的老年人骨折。     

炎症性肠病患者25-羟基维生素D季节变化的临床意义

炎症性肠病(IBD)是一类原因不明的自身免疫性慢性炎症性疾病,近年来研究表明,炎症性肠病有不断增加的趋势[1].IBD患者因肠道功能较差,抵抗力和免疫力均会受到影响,也容易出现感染和骨质疏松等并发症.近年来研究发现,Vit D不仅参与钙、磷代谢[2],它还是癌症和其它慢性疾病风险的独立预示因子,而且还具有明显的抵抗感染作用[3].25-羟基维生素D是Vit D在人体血液循环的主要代谢形式,为常用的检测患者体内Vit D水平的指标[3-4].Vit D与25-羟基维生素D两者有区别,但检测25-羟基维生素D能反映Vit D的情况.本文探讨IBD患者25-羟基维生素D水平与季节变化的关系,为指导临床预防和治疗提供依据,现报告如下.     

外周维生素D结合蛋白、25-羟维生素D和原发性肝细胞癌风险的关系

目的 25-羟维生素D[25(OH) D)]已被证明与原发性肝细胞癌(HCC)的发生有关,但对于维生素D结合蛋白(VDBP)在原发性肝细胞癌发生中的作用却知之甚少.作者检测了25(OH)D的主要载体维生素D结合蛋白(VDBP),研究其在25(OH)D与原发性肝细胞癌风险中的作用.方法 收集146例HCC患者和249名对照组的血样,检测血浆VDBP和25(OH)D的浓度.采用logistic回归计算比值比(OR)和95％可信区间(CI),评估外周血VDBP、25(OH)D与原发性肝细胞癌的发生风险之间的关系.结果 血浆VDBP浓度与HCC风险之间呈负相关;血浆25(OH)D与HCC风险呈正相关.只有在25(OH)D浓度高于中位数的人群中,VDBP升高显著,降低了HCC风险.在VDBP浓度低于中位数的人群中,高浓度的25(OH)D显著提高了HCC风险.结论 高浓度的VDBP可结合更多的25(OH)D,减少游离25(OH)D的生物利用度,同时检测VDBP和25(OH)D水平对于确定维生素D与HCC风险的相关性非常重要.     

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.     

维生素D与妊娠糖尿病

维生素D具有广泛的生理作用,近期动物以及人体研究提示维生素D能够改善胰岛素抵抗及胰岛β细胞功能。本文总结了孕期维生素D的代谢状况及其在糖代谢中的作用机制,并综述维生素D与妊娠糖尿病相关性的研究结果。但现有研究结果并不一致,还需要设计良好的随机对照试验探索补充维生素D能否降低妊娠糖尿病的发生率或改善孕期糖代谢。     

有氧运动联合左旋甲状腺素与维生素D3改善亚临床甲减大鼠骨质疏松的作用

文题释义：亚临床甲减：是指轻度甲状腺功能衰竭的表现，其临床表现为促甲状腺激素(TSH)升高而游离的甲状腺激素T3、T4基本正常，是一种内分泌代谢性疾病，是甲状腺功能障碍的早期阶段。亚临床甲减是一种系统性疾病，可以引起机体各器官功能状态变化，包括引起骨密度降低、骨质疏松等。抗酒石酸酸性磷酸酶(tartrate resistant acid phosphatase，TRACP)：为最近发现的骨吸收和破骨细胞活性的良好标志物，测定血清中抗酒石酸酸性磷酸酶尤其是抗酒石酸酸性磷酸酶5 b的浓度，有助于了解生理条件和各种病理条件下的骨代谢状况。抗酒石酸酸性磷酸酶缺乏和过度表达的大鼠模型分别表现为骨硬化和骨质疏松。背景：左旋甲状腺素可以显著改善亚临床甲减的症状，也有研究指出左旋甲状腺素可部分改善实验大鼠的骨代谢异常，但其对于亚临床甲减性骨质疏松的治疗作用却鲜有研究。 目的：在亚临床甲减大鼠模型上观察有氧运动联合左旋甲状腺素与维生素D3对骨质疏松症状的改善作用。方法：将Wistar大鼠分为空白对照组、假手术组、模型组进行造模，并检测大鼠甲功指标，此为造模阶段；造模成功后将模型组分为无处理组、运动组、左旋甲状腺素组、维生素D3组、运动+左旋甲状腺素组、运动+维生素D3组、左旋甲状腺素+维生素D3组、运动+左旋甲状腺素+维生素D3组，另设置一组正常对照组，其中正常对照组不作任何处理，其余各组分别接受相应的单一因素或者联合因素处理，共52 d，此为处理阶段。随后，检测大鼠血清中骨吸收标志物(β-Ⅰ型胶原羧基端肽和血清抗酒石酸酸性磷酸酶5b)、骨形成标志物(骨型碱性磷酸酶、Ⅰ型前胶原氨基端前肽和血清骨钙素)等骨代谢指标，并对大鼠头骨、脊柱、上肢和下肢进行骨密度扫描，测量各组大鼠血清中钙和磷及右股骨组织中Cathepsin K的蛋白水平，对各组大鼠股骨头行苏木精-伊红染色。 结果与结论：①在造模阶段，相对于空白对照组与假手术组，模型组大鼠血清中促甲状腺素水平显著增加(P < 0.05)，而血清FT3、FT4无明显变化，说明亚临床甲减大鼠造模成功。②进行干预后，与其他无甲状腺素处理的各组大鼠相比，4个补充左旋甲状腺素组大鼠的血清促甲状腺素水平明显降低(P < 0.05)，而T3、T4无明显变化，但其骨代谢指标和骨密度则显著升高(P < 0.05)，且以运动+左旋甲状腺素+维生素D3组改善最为显著(P < 0.05)。左旋甲状腺素+维生素D3组及运动+左旋甲状腺素+维生素D3组大鼠中的血清钙和磷水平显著高于其他无维生素D3处理组(P < 0.05)；4个补充左旋甲状腺素组大鼠的股骨组织中Cathepsin K蛋白表达水平低于其他各组(P < 0.05)，且其骨小梁组织形态比其他各组大鼠得到明显改善。③提示：亚临床甲减可诱发骨质疏松，而补充左旋甲状腺素是至关重要的一环；补充维生素D3通过增加血清钙和磷的水平起到改善骨质疏松的作用；有氧运动能显著增加左旋甲状腺素及维生素D3对亚临床甲减性骨质疏松的改善作用；亚临床甲减性骨质疏松的治疗中，应重视甲状腺素、维生素D3及有氧运动的综合性治疗手段。 ORCID: 0000-0002-9466-9885(武青梅) 中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程     

维生素D及其受体与毛发的关系

背景：越来越多的研究发现,维生素D及其受体与毛发有一定关系。 目的：全面阐述维生素D及其受体与毛囊干细胞、毛发生长周期、信号转导以及脱发性疾病等的关系。 方法：应用计算机以“维生素D、维生素D受体、毛发、脱发、基因多态性”或“vitamin D,vitamin D receptor,hair,alopecia,gene polymorphism”为检索词检索PubMed和CNKI数据库1990/2011-11发表的关于维生素D及其受体与毛发关系的文章,同一领域选择近期发表或发表在权威杂志上的文章。 结果与结论：初检得到152篇文献,根据纳入排除标准选择30篇文章进行综述。目前研究显示,维生素D及其受体在毛发中扮演重要角色,其异常可导致脱发等疾病的产生,为预防和治疗脱发性疾病提供新的可能,并有望在未来广泛应用。关键词：维生素D;维生素D受体;毛发;脱发;基因多态性;毛囊干细胞 doi:10.3969/j.issn.1673-8225.2012.14.035     

Mucosal vitamin D signaling in inflammatory bowel disease

Epidemiological studies have identified vitamin D (25(OH)D) deficiency to be highly prevalent among patients with inflammatory bowel disease (IBD), and low serum levels correlate with a higher disease activity and a more complicated disease course. The link to IBD pathogenesis has been subject of investigations, primarily due to the distinct immunological functions of vitamin D signaling, including anti-inflammatory and anti-fibrotic actions. Vitamin D is a pleiotropic hormone that executes its actions on cells through the vitamin D receptor (VDR). A leaky gut, i.e. an insufficient intestinal epithelial barrier, is thought to be central for the pathogenesis of IBD, and emerging data support the concept that vitamin D/VDR signaling in intestinal epithelial cells (IECs) has an important role in controlling barrier integrity. Here we review the latest evidence on how vitamin D promotes the interplay between IECs, the gut microbiome, and immune cells and thereby regulate the intestinal immune response. On the cellular level, vitamin D signaling regulates tight junctional complexes, apoptosis, and autophagy, leading to increased epithelial barrier integrity, and promotes expression of antimicrobial peptides as part of its immunomodulating functions. Further, intestinal VDR expression is inversely correlated with the severity of inflammation in patients with IBD, which might compromise the positive effects of vitamin D signaling in patients with flaring disease. Efforts to reveal the role of vitamin D in the pathophysiology of IBD will pave the road for the invention of more rational treatment strategies of this debilitating disease in the future.     

Pathology consultation on vitamin D testing

The last decade has seen a substantial increase in clinical interest in vitamin D deficiency and of laboratory testing for vitamin D status. Many clinical laboratories in the United States have seen requests for vitamin D testing increase 100% or more in the last 5 years. The most common laboratory test to assess vitamin D nutritional status is total 25-hydroxyvitamin D serum concentrations. Laboratory professionals are often confronted with challenges related to vitamin D testing, including controversy over optimal and target vitamin D concentrations, variable reference ranges across marketed assays and reference laboratories, lack of standardization of vitamin D assays, and misordering of 1,25-dihydroxyvitamin D testing. This article presents a common clinical case scenario regarding vitamin D and an up-to-date discussion and review of the literature on vitamin D testing.     

The role of vitamin D in perinatology. An up-to-date review

The role of vitamin D in perinatology is a subject of major interest in current medicine. There is growing evidence about the role of maternal vitamin D levels in pregnancy outcomes. The aim of this review is to summarize the current literature about the role of vitamin D in perinatology. Evidence from this review suggests associations between low levels of maternal vitamin D and higher risk of certain obstetrical complications. Vitamin D has been found to be related to preeclampsia, gestational diabetes mellitus, low birth weight, and preterm birth. The current literature supports vitamin D supplementation in pregnant women, but more high-quality data are necessary. The problem that remains is how to achieve an optimal 25-hydroxyvitamin D level. To determine the real benefits of vitamin D supplementation in pregnancy, we need high-quality trials in larger groups.     

Relevance of vitamin D in reproduction

The steroid hormone vitamin D is historically recognized for its relevance to bone health and calcium homeostasis. Recent years have witnessed a shift in focus to non-skeletal benefits of vitamin D; in this latter context, an accruing body of literature attests to a relevance of vitamin D to reproductive physiology. This article reviews the existing data about the diverse and previously underappreciated roles for vitamin D in reproductive health. A large body of available literature suggests that vitamin D deficiency may be detrimental to reproductive biology. However, given that our appreciation of vitamin D's role in reproductive physiology is almost entirely shaped by 'associative' studies and that data based on prospective interventional trials are limited, these concepts remain predominantly conjectural. Exact mechanisms whereby vitamin D may participate in the regulation of reproductive physiology remain far from clear. This review underscores a need for appropriately designed intervention trials to address the existing knowledge gaps and to delineate the specific roles of vitamin D signaling in reproductive biology.     

Vitamin D toxicity redefined: vitamin K and the molecular mechanism

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.     

Autism and vitamin D

Any theory of autism's etiology must take into account its strong genetic basis while explaining its striking epidemiology. The apparent increase in the prevalence of autism over the last 20 years corresponds with increasing medical advice to avoid the sun, advice that has probably lowered vitamin D levels and would theoretically greatly lower activated vitamin D (calcitriol) levels in developing brains. Animal data has repeatedly shown that severe vitamin D deficiency during gestation dysregulates dozens of proteins involved in brain development and leads to rat pups with increased brain size and enlarged ventricles, abnormalities similar to those found in autistic children. Children with the Williams Syndrome, who can have greatly elevated calcitriol levels in early infancy, usually have phenotypes that are the opposite of autism. Children with vitamin D deficient rickets have several autistic markers that apparently disappear with high-dose vitamin D treatment. Estrogen and testosterone have very different effects on calcitriol's metabolism, differences that may explain the striking male/female sex ratios in autism. Calcitriol down-regulates production of inflammatory cytokines in the brain, cytokines that have been associated with autism. Consumption of vitamin D containing fish during pregnancy reduces autistic symptoms in offspring. Autism is more common in areas of impaired UVB penetration such as poleward latitudes, urban areas, areas with high air pollution, and areas of high precipitation. Autism is more common in dark-skinned persons and severe maternal vitamin D deficiency is exceptionally common the dark-skinned. Conclusion: simple Gaussian distributions of the enzyme that activates neural calcitriol combined with widespread gestational and/or early childhood vitamin D deficiency may explain both the genetics and epidemiology of autism. If so, much of the disease is iatrogenic, brought on by medical advice to avoid the sun. Several types of studies could easily test the theory.     

A review of vitamin D and Parkinson's disease

The role of vitamin D in bone health has been known for over a century. More recent research has suggested that vitamin D may play a role in the muscular, immune, endocrine, and central nervous systems. Animal research suggests that vitamin D may have some protective effects against toxic insults that are known to damage dopamine cells, the primary cells to degenerate in PD. Persons with PD tend to have lower vitamin D levels than persons of similar ages without PD. Vitamin D levels are generally associated with bone mineral density (BMD) in persons with PD, but simply giving vitamin D does not appear to improve BMD. Results of genetic studies examining polymorphism of the vitamin D receptor and PD risk, severity, or age at onset have shown variable results, with FokI CC seeming to possibly carry some increased risk of PD. Amount of sun exposure and vitamin D levels in earlier life may influence the risk of developing PD. Cross-sectional research suggests a relationship between vitamin D levels and severity of PD symptoms. A single intervention study did show some improvement in PD with vitamin D supplementation. Vitamin D may have effects on PD symptoms and perhaps even on the risk of disease development or disease progression. More well designed intervention studies are needed to confirm the effect of vitamin D on PD symptoms. Human neuroprotection studies are needed, but probably not feasible until better biomarkers are established.     

Dietary vitamin D intake and vitamin D related genetic polymorphisms are not associated with gastric cancer in a hospital-based case-control study in Korea

There have been few studies on the association between vitamin D levels and gastric cancer in Asian populations, but no studies have been performed on the interactions between vitamin D intake and polymorphisms in the vitamin D pathway. The effects of vitamin D intake, vitamin D related genetic polymorphisms, and their association with the incidence of gastric cancer were investigated in a hospital case-control study, including 715 pairs of newly diagnosed gastric cancer patients and controls matched for age and sex. Correlations between vitamin D intake and plasma vitamin D concentrations were also assessed in a subset of subjects. No statistically significant difference was observed in the dietary intake of vitamin D between the patients and controls, nor were there any evident associations between vitamin D intake and risk of gastric cancer in multivariate analyses. Vitamin D intake significantly correlated with the circulating 25-hydroxyvitamin D levels, but not with the active form of the vitamin, 1,25-dihydroxyvitamin D. There were no statistically significant interactions between vitamin D intake, and VDR or TXNIP polymorphisms. This study suggests that dietary vitamin D intake is not associated with gastric cancer risk, and the genetic polymorphisms of vitamin D-related genes do not modulate the effect of vitamin D with respect to gastric carcinogenesis.