维生素D缺乏与Graves病相关性的研究进展

维生素D作为维持机体钙磷代谢平衡的重要激素,对机体骨与矿物质盐代谢起着重要的调节作用。近年来研究发现Graves病患者体内维生素D水平偏低,这可能预示着Graves病患者机体内将出现一系列骨代谢紊乱的发生,测量Graves病患者体内维生素D水平,有助于Graves病相关骨质疏松的治疗和预防。此外,还有研究者发现维生素D缺乏可能参与Graves病的发生发展,而补充维生素D可能有助于Graves病的预防和治疗。本文将对维生素D与Graves病相关性及其可能存在的机制的研究新进展进行综述。     

维生素D与健康研究进展

虽然维生素D营养状况的划分标准还存在一些争议,但近年来许多研究观察到很多国家的居民存在不同程度维生素D缺乏,而适当的维生素D营养状况可对骨量、骨折及其他相关慢性病产生积极的影响。膳食维生素D摄入不足和皮肤合成有限,使部分人群可能需要适当补充维生素D。但上述结论多来自国外研究,需要在中国开展不同人群维生素D及其相关因素疾病的深入研究。     

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。     

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。     

维生素D与原发性甲状旁腺功能亢进症

目的 概述原发性甲状旁腺功能亢进症患者血清维生素D水平的变化及其与临床表现之间的关系,总结可能的致病机制。方法 检索近年来与维生素D及原发性甲状旁腺功能亢进症相关的文献进行综述。结果 原发性甲状旁腺功能亢进症患者存在不同程度的维生素D水平下降。维生素D水平与甲状旁腺腺瘤重量、甲状旁腺素水平及血钙水平呈负相关,与患者骨密度呈正相关。结论 维生素D营养状态影响原发性甲状旁腺功能亢进症患者的疾病严重程度、主要生化指标及临床并发症。引起维生素D水平下降的原因多样,具体致病机制有待进一步研究。对于原发性甲状旁腺功能亢进症患者,在手术前可谨慎适当补充维生素D。     

维生素D受体基因多态性与冠心病的相关性

近年来国内外研究均证实维生素D能够抑制炎症反应程度,从而具有延缓冠状动脉粥样硬化的作用,而维生素D的作用通过维生素D受体来实现,现已知维生素D受体基因存在变异,而这些变异可能影响维生素D的作用。本文拟就维生素D 及其受体基因变异与动脉硬化相关心血管疾病的关系进行综述。     

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的临床研究进展

近年来的研究发现维生素D不仅在骨骼疾病中发挥重要作用,在非骨骼系统疾病中的也起到十分重要的作用。基础研究证实维生素D受体广泛分布于体内各种组织细胞中,越来越多的临床研究发现补充维生素D在预防和治疗骨质疏松症、心脑血管病、肺部疾病、慢性代谢性及肿瘤性疾病中有重要作用。本文就维生素D与上述疾病关系的研究进展进行综述,主要着眼于当前的临床热点研究方面。结果显示观察性研究证据支持维生素D与上述非骨骼系统疾病有很强的相关性,但是尚缺乏大规模和长期的随机临床试验证据,因此,需要更多的研究来探讨补充维生素D在预防和治疗非骨骼系统疾病中的作用。     

活性维生素D3与脂肪组织的相关研究进展

活性维生素D3与脂肪组织的关系密切,参与了脂肪组织在生理、病理过程中诸多功能的调控。为了深入探究活性维生素D3在促进自体脂肪移植再生中应用的科学性,该文作者综述了活性维生素D3与脂肪组织之间的相关作用,特别是活性维生素D3对脂肪生成、细胞凋亡及炎性反应的调控,为临床应用实践拓展了新思路。     

女性型脱发患者的血清维生素D水平及与雄激素的相关性研究

目的：探究女性型脱发的血清维生素D水平以及与雄激素的相关性,为女性型脱发的发病机制及治疗选择提供新的线索。方法：分析皮肤科门诊就诊的70例女性型脱发患者与体检中心招募的65例健康人的血清维生素D,分析其与严重程度、人口学特征、生活习惯以及雄激素的相关性。结果：女性型脱发患者的平均维生素D水平（13.59±5.82）ng/ml,健康人群的平均维生素D水平为（15.94±6.89）ng/ml(P<0.05)。女性型脱发患者维生素D水平与性激素结合球蛋白呈正相关,与游离睾酮呈负相关（P<0.05）。性激素结合球蛋白降低或游离睾酮升高的患者维生素D水平明显降低（P<0.05）。但暂未发现女性型脱发患者的维生素D水平与严重程度、人口学特征、生活习惯的相关性。结论：女性型脱发较健康人群维生素D水平明显降低,提示维生素D降低可能是女性型脱发的发病因素之一。性激素结合球蛋白降低、游离睾酮升高与维生素D水平降低存在的相关性,可能是维生素D缺乏导致女性型脱发的机制之一,有待进一步研究验证。     

The dualistic role of vitamin D in vascular calcifications

Vitamin D is a multifunctional hormone that can affect many essential biological functions, ranging from the immune regulation to mineral ion metabolism. A close association between altered activity of vitamin D and vascular calcification has been reported in various human diseases, including in patients with atherosclerosis, osteoporosis, and chronic kidney disease (CKD). Vascular calcification is a progressive disorder and is a major determinant of morbidity and mortality of the affected patients. Experimental studies have shown that excessive vitamin D activities can induce vascular calcification, and such vascular pathology can be reversed by reducing vitamin D activities. The human relevance of these experimental studies is not clear, as vitamin D toxicity is relatively rare in the general population. Contrary to the relationship between vitamin D and vascular calcification, in experimental uremic models, low levels of vitamin D were shown to be associated with extensive vascular calcification, a phenomenon that is very similar to the vascular pathology seen in patients with CKD. The current treatment approach of providing vitamin D analogs to patients with CKD often poses a dilemma, as studies linked vitamin D treatment to subsequent vascular calcification. Recent genetic studies, however, have shown that vascular calcification can be prevented by reducing serum phosphate levels, even in the presence of extremely high serum 1,25-dihydroxyvitamin D and calcium levels. This article will briefly summarize the dual effects of vitamin D in vascular calcification and will provide evidence of vitamin D-dependent and -independent vascular calcification.     

Parathyroid hormone, vitamin D, and cardiovascular disease in chronic renal failure.

BACKGROUND: Parathyroid hormone and vitamin D have been shown to influence cardiac and vascular growth and function experimentally in human subjects with normal renal function. Because of the increased prevalence of hyperparathyroidism and altered vitamin D status in chronic renal failure, these alterations have been considered to contribute to the increased prevalence of cardiovascular disease and hypertension seen in this patient population. Methods and Results. In this article, we review experimental and clinical literature on the cardiovascular effects of parathyroid hormone and vitamin D and relate them to the development of cardiac and vascular dysfunction in uremia, such as: cardiomyopathy, myocardial hypertrophy, and fibrosis, as well as to myocardial ischemia; uremic glucose intolerance, dyslipidemia, and atherosclerosis; hypertension; and vascular and cardiac calcifications. CONCLUSIONS: The hyperparathyroid state and altered vitamin D status found in uremia contribute to the cardiovascular pathology seen clinically in uremia and also to the excess mortality from cardiovascular causes found in this patient group. The therapeutic implications of these observations are also discussed.     

Vitamin D and cardiovascular risk

Vitamin D deficiency results in abnormal mineralization of bones and has resulted in prevention programs for children with supplementation when they are breast fed. Further activities of vitamin D relate to defence of microbial infections, e.g. tuberculosis, prevention of cancer, contractility of muscle cells and counteraction of congestive heart failure. Given early reports in the 1960s on deleterious effects of vitamin D supplementation in rodents, that is ectopic media ossification of arterial vessels, a pro-atherogenic function had been anticipated for humans as well. However, cross-sectional studies reveal that vitamin D deficiency in humans is associated with elevated blood pressure and propagation of atherogenesis. These contradictory findings on the progression of atherosclerosis may be reconciled by dissecting the activation mechanism(s) of vitamin D in rodents versus humans. Notably, novel findings convincingly indicate that vitamin D exerts anti-inflammatory effects. In conclusion, vitamin D supplementation in adults may be regarded as simple means with few potential side effects to prevent atherogenesis or halt its progression and combat arterial hypertension. Adjustment of vitamin D dosing regimens is required in patients with chronic kidney disease; however, prospective clinical trials are urgently needed to guide these recommendations with evidence.     

Vitamin D, the renin-angiotensin system, and insulin resistance

Insulin resistance is characterized by the systemic impairment of insulin action and is usually the result of aging, obesity, chronic inflammation, or another factor that may contribute to the inhibition of the insulin signaling pathway. Insulin resistance is accompanied by defects in lipid metabolism and blood coagulation, hypertension, obesity, and vascular inflammation in a syndrome called syndrome X or metabolic syndrome. Metabolic syndrome is involved in the development of atherosclerosis with consequent cardiovascular complications including acute myocardial infarction, stroke, and vascular disease. Recent data have shown that vitamin D acts as a negative regulator of the renin gene and that vitamin D deficiency is followed by increased renin-angiotensin II expression. The link between the insulin signaling pathway/insulin resistance and the renin-angiotensin system has been well documented in previous studies. The present review focuses on disorders characterized by a reduction in vitamin D concentration or its receptor function and the development of insulin resistance or metabolic syndrome, and discusses also possible therapeutic interventions.     

维生素D与骨关节炎

骨关节炎(OA)是一类以渐进性软骨磨损、骨赘形成为主要特征的退行性疾病。最近的研究认为,OA的发生与进展是多因素的,涉及软骨、关节下骨、滑膜组织、神经肌肉组织等多方面。OA的确切病因和发病机制仍不清楚,尚无法从根本上阻止和治疗。在世界范围内,维生素D缺乏的状况愈发严峻,越来越多的证据显示维生素D与骨关节炎的发病和进展存在密切的联系。本文回顾性地总结与分析维生素D与骨关节炎的相关文献,展示维生素D缺乏的现状,探讨维生素D与骨关节炎之间的关系及其相应的作用机制。     

Vitamin D and its analogues: do they protect against cardiovascular disease in patients with kidney disease?

BACKGROUND: Patients with chronic kidney disease (CKD) are at high risk for cardiovascular disease, and despite recent advances in hypertension control, anemia management, and dialysis adequacy, mortality remains high. Improved understanding of nontraditional risk factors, including those present at early phases in CKD, may lead to novel therapeutic strategies. CKD has been demonstrated to be an independent risk factor for cardiovascular disease in the general population, but data are lacking as to the associated potential abnormalities that occur in association with reduced glomerular filtration rate (GFR), which may contribute to this increased risk. Data are accumulating regarding the role of abnormalities of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) in cardiovascular disease. Vitamin D deficiency is present even in the early stages of CKD. Vitamin D plays a central role in calcium-phosphorus homeostasis, regulation of PTH, and formation and maintenance of bone. However, until recently, vitamin D has not been considered to have a biologic role in CKD beyond mineral regulation, or has been considered as a negative factor contributing to soft tissue and cardiovascular calcification. In light of recent observational studies showing an association of vitamin D therapy and survival benefit in hemodialysis patients, the effects of vitamin D on cardiovascular system have become a heavily debated issue. METHODS: A Medline search was performed to identify relevant literature describing the role of vitamin D in the pathogenesis of cardiovascular disease. Both the experimental and clinical literatures in English were reviewed. RESULTS: The accumulating published data demonstrate both associative relationships and mechanisms for biologic plausibility. The following three potential mechanisms may be important for the protective effects of vitamin D against cardiovascular disease mortality: vitamin D can inhibit various aspects of inflammation, which have been established as a key pathogenic mechanism in atherosclerosis; vitamin D exerts an antiproliferative effect on myocardial cell hypertrophy and proliferation, which underlies the pathogenesis of congestive heart failure; and vitamin D acts as a negative endocrine regulator for the renin-angiotensin system, which itself plays an important independent role in hypertension and cardiovascular health. CONCLUSION: Vitamin D deficiency might be an underestimated nonclassical risk factor for cardiovascular disease in CKD. Based on a review of the evidence, from both basic science and clinical studies, this article supports the possible protective role of vitamin D beyond its effect on mineral metabolism, and suggests the need for ongoing evaluation of the role of vitamin D in cardiovascular health in the CKD population.     

The Role of Vitamin D in Chronic Obstructive Pulmonary Disease,Asthma and Other Respiratory Diseases

There has been a growing interest in recent years in the extraosseous effects of vitamin D.In this article, we review the physiology of vitamin D, the physiopathological effects associated with vitamin D deficit and the available evidence on its etiopathogenic role in respiratory diseases. Given the pleiotropic actions of vitamin D, it is biologically plausible that the deficit of this vitamin could play a pathogenic role in the development of various respiratory diseases. However, the many epidemiological studies that have shown an association between low vitamin D levels and a higher risk of developing various respiratory diseases, or a poorer prognosis if they do appear, were unable to show causality. Post hoc analyses of some clinical trials, particularly in chronic obstructive pulmonary disease (COPD) and asthma, appear to suggest that some patient subtypes may benefit from correction of a vitamin D deficit. In this respect, it would be interesting to determine if the interindividual differences found in the effect of vitamin D deficit and responses to correcting this deficit could be explained by the genetic variants involved in vitamin D metabolism. Ultimately, only appropriately designed clinical trials will determine whether 25-OH D supplements can prevent or improve the course of the various respiratory diseases in which an epidemiological association between prognosis and vitamin D deficit has been described.     

Nutritional vitamin D supplementation in haemodialysis: A potential vascular benefit?

Aim: Vitamin D deficiency is highly prevalent in end‐stage renal disease and has been associated with atherosclerosis, endothelial dysfunction and left ventricular hypertrophy. Although activated vitamin D has shown to be cardioprotective, the cardiovascular benefits of nutritional vitamin D (i.e. ergocalciferol or cholecalciferol) have not been explored in the dialysis population. The aim of this investigation was to evaluate the effect of ergocalciferol therapy on vascular adhesion molecules, markers of inflammation and atherosclerosis among haemodialysis patients. Methods: This was a pilot study of matched haemodialysis patients. For every patient enrolled taking ergocalciferol, an age and race matched control was recruited. Predialysis blood samples were collected and assayed for adhesion molecules (soluble vascular cell adhesion molecule‐1 (sVCAM‐1), soluble intercellular adhesion molecule‐1 (sICAM‐1), E‐selectin and P‐selectin), inflammatory cytokines (interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α)), oxLDL‐β₂GPI and IgG anticardiolipin. Results: A total of 40 haemodialysis patients were studied (20 on ergocalciferol therapy, 20 not receiving ergocalciferol therapy). Patients taking ergocalciferol had higher 25‐hydroxyvitamin D levels compared with those not taking ergocalciferol. Even though doxercalciferol usage and dosing was similar between groups, plasma sVCAM‐1, sICAM‐1 and P‐selectin concentrations were lower among ergocalciferol treated patients. No significant differences in E‐selectin, IL‐6, TNF‐α, oxLDL‐β₂GPI or anticardiolipin antibody levels were observed. Conclusion: Patients receiving ergocalciferol had lower plasma levels of vascular adhesion molecules despite equivalent use of activated vitamin D therapy. Future investigations should confirm the role of nutritional vitamin D therapy, in addition to activated D therapy, in haemodialysis patients and the potential vascular benefits of these agents.