孕期VD缺乏以及对胎儿的影响

维生素D缺乏是目前社会所面临的严重健康问题。维生素D的主要作用是增加肠钙的吸收,对维持各年龄段骨骼健康矿化都起着非常重要的作用。维生素D缺乏在儿童导致佝偻病;在成年人会发生软骨病和骨质疏松。近年来发现除了传统的骨骼系统的作用外,维生素D缺乏还与多种疾病的发生有关。VD缺乏累及的人群非常广泛,可以发生在各个年龄阶段,特别是孕妇。造成孕期维生素D缺乏的主要原因是多方面的,主要是由于各种原因导致的阳光照射不足以及孕期VD的需求量增加所致。孕妇VD缺乏可能与胎儿及新生儿的多种不良状况有关,如影响胎儿及新生儿骨骼系统和大脑的发育,还可能与心脏疾病和I型糖尿病等的发生有关。因此,合理补充维生素D,预防孕期VD缺乏对提高产科质量以及母婴保健是非常重要的。     

现代社会维生素D缺乏及其预防

维生素D缺乏是目前社会所面临的严重健康问题。维生素D(VD)是人体不可缺少的一种脂溶性维生素,其主要作用是增加肠钙的吸收利用,对维持各年龄段骨骼健康矿化都起着非常重要的作用。维生素D缺乏在儿童导致佝偻病;在成年人会发生软骨病和骨质疏松。此外近年来发现维生素D缺乏还与肿瘤、糖尿病、心血管疾病等多种疾病的发生有关,使其重新引起了人们的关注。造成现代社会维生素D缺乏的原因是多方面的,主要是由于各种原因导致的阳光照射不足。血中的25(OH)D的水平可以作为了解人体内VD状况的指标,多数学者认为25(OH)D的水平低于30ng/mL为维生素D不足,现代社会维生素D缺乏发生率非常高,推测全球可能有10亿人口患有维生素D缺乏。合理补充维生素D对预防维生素D缺乏是非常重要的。     

孕妇血清25羟基维生素D水平与妊娠合并症的关系

维生素D是一种脂溶性类固醇激素,通过其循环活性形式25羟基维生素D(25OHD)在人体中发挥作用。维生素D可调节机体钙磷平衡,维持骨骼健康,对人体免疫调节、葡萄糖代谢、细胞增殖等生理过程均有重要作用。孕期女性血清25OHD的缺乏主要由于日照不足和摄入过少导致。25OHD的水平与妊娠合并症(如妊娠高血压、子痫前期和妊娠糖尿病)密切相关,25OHD的缺乏与妊娠高血压和子痫前期呈显著正相关,与妊娠糖尿病则呈负相关。本文就25OHD与妊娠合并症的关系进行综述。     

中老年男性人群维生素D水平及其与肌力、跌倒风险的研究

目的探讨中老年男性人群维生素D(VD)营养状况及其与肌力、跌倒风险的关系。方法横断面调查,分析某40岁以上查体人群增龄、VD水平与肌力及跌倒风险之间的关系。结果该人群维生素D缺乏占77.41%,其中严重缺乏占7.83%。随增龄,握力、指捏力、下肢肌力逐渐下降,站起步行试验(TGUT)时间、站起试验(CRT)时间及异常率增加,差异有统计学意义。各年龄组维生素D水平在校正摄入奶量、日照时间、运动频率、工作环境等因素后,差异无统计学意义。按维生素D水平分组比较,只有握力及指捏力在严重缺乏组与其他组间差异达到统计学意义。但在校正年龄影响后,血钙水平、握力、指捏力、下肢肌力在组间差异有统计学意义,维生素D严重缺乏组最低。在60岁以上组,CRT时间在维生素D缺乏组最长,组间差异有统计学意义。但TGUT在各年龄亚组,三组维生素D水平组间差异均未达到统计学意义。logistic多元逐步回归显示,增龄、握力减低与维生素D缺乏独立相关,OR值分别为1.37和1.33。结论 40岁以上男性维生素D缺乏比例较高,随增龄肌力下降、跌倒风险增高,增龄、上肢肌力减退是维生素D缺乏的独立影响因素。     

维生素D缺乏相关性疾病研究进展

维生素D是人体必需的一种脂溶性维生素,它通过维生素D受体发挥其主要作用。近10年人们对于维生素D的关注度越来越高。根据流行病学调查,目前全球近10亿人处于维生素D不足或缺乏状态,我国人群维生素D不足现象也较为普遍。由于1,25-羟维生素D半衰期非常短,最近维生素D水平已用血清25-羟维生素D水平来描述。多种证据表明,维生素D缺乏不仅造成骨骼疾病(包括营养性佝偻病、软骨病、骨质疏松),还与多种骨骼外疾病密切相关,包括全因死亡率、心血管疾病及心血管病死亡率、代谢综合征(肥胖、糖耐量减低/糖尿病、脂代谢紊乱、高血压)、恶性肿瘤、感染、过敏性疾病及哮喘、精神及神经疾病、自身免疫性疾病、慢性肾病等。虽然使用维生素D治疗骨骼疾病已经得到广泛认可,但是治疗骨骼外疾病的疗效及远期效果还不明确。维生素D缺乏已成为全世界的公共健康问题。本文综述了近年来对维生素D缺乏相关性疾病的研究进展。     

维生素D的代谢及调控研究新进展

维生素D是前激素（prohormone）,它的发现及其在临床上的成功应用,为治愈佝偻病和成人软骨症开辟了有效途径。维生素D的主要作用是参与调节人体内钙、磷代谢及骨的形成,并有抑制细胞生长、调节免疫作用的功能,尤其对骨质疏松症、自身免疫疾病、肿瘤等多种疾病有防治的功效。正因如此,人们对维生素D的健康效能有着广泛的期待,可是摄入维生素D的同时又担心因过量而引起毒副作用。本文从维生素D的代谢和调控两方面来讨论维生素D激素系统的作用及自我保护功能。     

维生素D缺乏对骨和骨外作用研究进展

维生素D缺乏作为一种在人群中发病率较高的疾病,日益受到人们的广泛关注。维生素D缺乏的主要诊断指标是血清25-羟维生素D水平。大量研究表明,维生素D缺乏不仅可以引起体内钙磷代谢障碍、佝偻病、软骨病和骨质疏松性骨折等骨骼系统疾病,而且还可能引起癌症、免疫系统疾病、心血管疾病、代谢性疾病(2型糖尿病和肥胖症)、肌肉功能障碍和跌倒等其他骨外系统疾病。维生素D缺乏对骨骼系统的作用,目前学术界已形成共识,然而维生素D缺乏对骨外系统的作用,目前学术界存在较大争议。笔者就维生素D缺乏对骨和骨外作用的研究进展进行全面介绍,探讨维生素D具有广泛作用的可能机理。初步阐述维生素D缺乏对骨和骨外系统的作用,不仅为研究维生素D缺乏对骨和骨外作用及可能机理提供新的研究思路,而且为防治维生素D缺乏的相关疾病提供新的临床思路。尽管目前对维生素D缺乏的骨外作用观点不一,但有充分证据表明补充适量的维生素D有助于身体健康。     

骨质疏松症治疗中维生素D的最佳水平及补充剂量的研究进展

人们普遍认为维生素D(vitamin D,VD)是骨骼系统中的积极调节因子。近年来,骨质疏松症发病率的增加,VD不足及缺乏现象明显,国内外越来越多研究发现骨密度与VD状态之间存在不一致表现,高水平VD状态对提高骨密度及降低骨折风险并没有起到积极作用,VD最佳水平和在骨质疏松症治疗时如何补充VD仍有争议。笔者综述了近年来的研究成果,进一步探讨VD最佳水平、高水平VD的补充对骨密度及骨折的影响,并提出目标25-羟维生素D[25-hydroxyvitamin D,25(OH)D]浓度为20 ng/mL(50 nmol/L),每日VD补充剂量为400~800 IU,超过这一水平增加VD补充剂量是不必要的,甚至可能存在潜在危险。     

维生素D分子机制及其与成纤维生长因子23、Klotho 相关性的新进展

维生素D（ VD）的经典作用为调节钙磷和骨代谢,同时还与免疫系统、细胞增殖和分化等有重要联系。1α,25－羟基维生素D（1,25（OH）D）配体结合维生素D受体（VDR）引发VDR与维甲酸X受体（RXR）紧密结合,且配体结合的VDR－RXR异二聚体识别VD调控基因序列中的维生素D应答元件（VDREs）。虽然1,25（OH）D－VDR可通过非基因机制快速发挥作用,但1,25（OH）D－VDR主要通过基因机制实现功能。1,25（OH）D－VDR可控制基因转录,VD配体、VDRE的DNA序列以及招募的共激活因子／共阻遏因子都能影响基因表达。1,25（OH）D－VDR调节基因的VDREs具有重要功能。通过推测RANKL基因染色质成环模型表明DNA成环和染色质的结构在VD调节基因表达的作用中发挥主要作用。1,25（OH）D－VDR调节基因表达可以延缓衰老和老年性疾病,比如癌症、2型糖尿病和心血管疾病。针对VD在磷酸盐代谢与衰老方面的关系已有了新的认识,认为1,25（OH）D－VDR诱导的骨骼中FGF23和肾脏中Klotho蛋白在该代谢途径中发挥重要作用,VD调节磷酸盐稳态可能是延缓衰老及相关慢性疾病的机制。     

维生素D与心房颤动的研究进展

维生素D参与骨骼的发育及骨骼外组织的代谢,维生素D缺乏与心血管疾病发生发展密切相关,维生素D缺乏与心房颤动的关系也日益受到研究者的关注。目前国内外研究提示,维生素D缺乏参与心房颤动的发生。笔者就维生素D缺乏和心房颤动的关系进行简要综述。     

Role of vitamin D in diabetes mellitus and chronic kidney disease

Approximately 30%-50% of people are recognized to have low levels of vitamin D,and insufficiency and deficiency of vitamin D are recognized as global health problems worldwide.Although the presence of hypovitamin D increases the risk of rickets and fractures,low vitamin D levels are also associated with hypertension,cancer,and cardiovascular disease.In addition,diabetes mellitus(DM) and chronic kidney disease(CKD) are also related to vitamin D levels.Vitamin D deficiency has been linked to onset and progression of DM.Although in patients with DM the relationship between vitamin D and insulin secretion,insulin resistance,and β-cell dysfunction are pointed out,evidence regarding vitamin D levels and DM is contradictory,and well controlled studies are needed.In addition,vitamin D influences the renin-angiotensin system,inflammation,and mineral bone disease,which may be associated with the cause and progression CKD.There is increasing evidence that vitamin D deficiency may be a risk factor for DM and CKD;however,it remains uncertain whether vitamin D deficiency also predisposes to death from DM and CKD.Although at this time,supplementation with vitamin D has not been shown to improve glycemic control or prevent incident DM,clinical trials with sufficient sample size,study periods,and optimal doses of vitamin D supplementation are still needed.This review focuses on the mechanism of vitamin D insufficiency and deficiency in DM or CKD,and discusses the current evidence regarding supplementation with vitamin D in patients with these diseases.     

Vitamin D for skeletal and non-skeletal health: What we should know

Vitamin D plays an essential role in regulating calcium and phosphate metabolism and maintaining a healthy mineralized skeleton. Humans obtain vitamin D from sunlight exposure, dietary foods and supplements. There are two forms of vitamin D: vitamin D₃ and vitamin D₂. Vitamin D₃ is synthesized endogenously in the skin and found naturally in oily fish and cod liver oil. Vitamin D₂ is synthesized from ergosterol and found in yeast and mushrooms. Once vitamin D enters the circulation it is converted by 25-hydroxylase in the liver to 25-hydroxyvitamin D [25(OH)D], which is further converted by the 25-hydroxyvitamin D-1α-hydroxylase in the kidneys to the active form, 1,25-dihydroxyvitamin D [1,25(OH)₂D]. 1,25(OH)₂D binds to its nuclear vitamin D receptor to exert its physiologic functions. These functions include: promotion of intestinal calcium and phosphate absorption, renal tubular calcium reabsorption, and calcium mobilization from bone. The Endocrine Society's Clinical Practice Guideline defines vitamin D deficiency, insufficiency, and sufficiency as serum concentrations of 25(OH)D of <20 ng/mL, 21–29 ng/mL, and 30–100 ng/mL, respectively. Vitamin D deficiency is a major global public health problem in all age groups. It is estimated that 1 billion people worldwide have vitamin D deficiency or insufficiency. This pandemic of vitamin D deficiency and insufficiency is attributed to a modern lifestyle and environmental factors that restrict sunlight exposure, which is essential for endogenous synthesis of vitamin D in the skin. Vitamin D deficiency is the most common cause of rickets and osteomalacia, and can exacerbate osteoporosis. It is also associated with chronic musculoskeletal pain, muscle weakness, and an increased risk of falling. In addition, several observational studies observed the association between robust levels of serum 25(OH)D in the range of 40–60 ng/mL with decreased mortality and risk of development of several types of chronic diseases. Therefore, vitamin D-deficient patients should be treated with vitamin D₂ or vitamin D₃ supplementation to achieve an optimal level of serum 25(OH)D. Screening of vitamin D deficiency by measuring serum 25(OH)D is recommended in individuals at risk such as patients with diseases affecting vitamin D metabolism and absorption, osteoporosis, and older adults with a history of falls or nontraumatic fracture. It is important to know if a laboratory assay measures total 25(OH)D or only 25(OH)D₃. Using assays that measure only 25(OH)D₃ could underestimate total levels of 25(OH)D and may mislead physicians who treat patients with vitamin D₂ supplementation.     

维生素D与多囊卵巢综合征相关性的研究进展

维生素D缺乏在多囊卵巢综合征(PCOS)妇女中常见,它与PCOS妇女的胰岛素抵抗、高雄激素表现、心血管疾病危险及生育功能下降有关。适当补充维生素D可减轻PCOS的危险因素,改善PCOS妇女的健康。     

Vitamin D deficiency in mothers of rachitic infants

Summary The existence of nutritional deficiency rickets among infants in sunny Riyadh was confirmed radiologically. Most of the rachitic infants were breast-fed, some received unsupplemented infant feeding formulae, and all live in an environment that is devoid of sunlight. Their mean age at the time of onset was 10.5 months. 25-Hydroxyvitamin D (25OHD) levels were found to be low in mothers of the rachitic infants. This maternal deficiency as a factor in pathogenesis of rickets in the infant is discussed. Proposals are made to prevent the occurrence of rickets on this scale.     

25(OH) Vitamin D3 in patients with chronic kidney disease and those on dialysis: rediscovering its importance

In terms of both exogenous sources (diet), and endogenous production (activation through exposure to ultraviolet light), vitamin D is unique. Few foods naturally contain vitamin D and only a few are fortified with vitamin D. Most people get more than 90% of their vitamin D requirements from exposure to sunlight. Those who protect their skin from ultraviolet-B radiation with clothing or sunscreen, the elderly, and dark-skinned individuals have limited capacity to produce vitamin D. Vitamin D deficiency is common in the general population and even more common in patients with chronic renal failure (CKD). Increased use of sun-blocking agents and decreased exposure to sunlight, to reduce the risk of skin cancer, attributed to exposure to UV radiation, may contribute to the increase in vitamin D deficiency in the population. These issues are particularly important in the dialysis population who are at particular risk because these, mostly elderly, individuals have an inactive life style and have reduced exposure to sunshine and UV light, thus limiting the actinic synthesis of vitamin D. The nephrology community seems to have overlooked the importance of vitamin D for overall health and well being in patients with CKD. Recently however, several authors have called attention to the role of plasma 25(OH)D₃ levels in mineral metabolism dysregulation in patients with chronic kidney diseases, and those on dialysis. Vitamin D not only contributes to skeletal health but also plays a major role in the health of a wide variety of other organ systems. It seems that vitamin D supplementation is the most effective way of preventing vitamin D deficiency.     

Vitamin D and skeletal health in infancy and childhood

During growth, severe vitamin D deficiency in childhood can result in symptomatic hypocalcaemia and rickets. Despite the suggestion from some studies of a secular increase in the incidence of rickets, this observation may be driven more by changes in population demographics than a true alteration to age, sex and ethnicity-specific incidence rates; indeed, rickets remains uncommon overall and is rarely seen in fair-skinned children. Additionally, the impact of less severe vitamin D deficiency and insufficiency has received much interest in recent years, and in this review, we consider the evidence relating vitamin D status to fracture risk and bone mineral density (BMD) in childhood and adolescence. We conclude that there is insufficient evidence to support the suggestion that low serum 25-hydroxyvitamin D [25(OH)D] increases childhood fracture risk. Overall, the relationship between 25(OH)D and BMD is inconsistent across studies and across skeletal sites within the same study; however, there is evidence to suggest that vitamin D supplementation in children with the lowest levels of 25(OH)D might improve BMD. High-quality randomised trials are now required to confirm this benefit.     

女性血清维生素D浓度对体外受精-胚胎移植妊娠结局的影响

维生素D是人体内维持钙磷代谢的脂溶性维生素,全世界各个地区有大量人群存在维生素D缺乏的现象,其中很大一部分是年轻的育龄期妇女。近年来,血清维生素D的浓度和女性生殖的关系,以及对体外受精-胚胎移植(IVF-ET)助孕结局的影响越来越引起人们的关注。本文对维生素D与IVF妊娠结局关系的研究进行综述,以期为今后的深入研究提供帮助。     

减重代谢外科中的维生素D缺乏及其影响

维生素D在钙、磷代谢及细胞生长分化中发挥重要作用,随着研究深入,维生素D在人体营养代谢,特别是糖脂代谢中的重要作用越来越受到重视.减重代谢手术是治疗肥胖症、2型糖尿病和其他相关合并症的有效方法.接受减重代谢手术的患者在术前及术后常出现维生素D的缺乏.本文试综述维生素D在减重代谢手术术前、围手术期、术后的水平及其影响,分析维生素D缺乏原因、对代谢性疾病的影响、对减重代谢手术治疗效果的影响,并探讨减重代谢手术对体内维生素D水平的影响及及补充措施.