维生素D缺乏与高血压相关研究进展

维生素D是一种脂溶性维生素,目前已知其在调节骨骼代谢、钙盐平衡方面起着重要的作用。近年来,虽然许多研究者发现高血压患者中维生素D缺乏的发生率很高,维生素D缺乏可能导致高血压的发生、发展,但是补充维生素D与高血压的研究结果不一致。因此文章就维生素D缺乏与高血压的相关研究进展作一综述。     

维生素D与心血管疾病关系研究进展

维生素D不仅对人体钙磷代谢和骨质钙化有重要作用,而且对全身各组织细胞都有广泛作用,与各种重要疾病均有密切关系。其中,维生素D缺乏与心血管疾病关系日益受到国际医学界的重视。其可能通过增加甲状旁腺激素、激活肾素-血管紧张素-醛固酮系统、增加胰岛素抵抗等机制对心血管系统产生不良影响,引起高血压、左室肥厚、代谢综合征、系统炎症,从而增加动脉粥样硬化和心血管事件。目前,在我国大多数医院都没有维生素D的检验项目,且缺乏有关维生素D水平的流行病学资料,许多医务人员和科研人员对其认识仅还停留在对钙磷代谢的影响上。本文就维生素D缺乏与心血管疾病的关系以及补充维生素D降低心血管事件等方面临床研究作一系统回顾,以期引起我国学者对维生素D的重视,加强相关研究。     

维生素D缺乏与非骨骼疾病关系的研究进展

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,在非骨骼疾病中也具有非常重要的作用。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;临床研究发现,补充维生素D对预防和治疗代谢综合征及心血管疾病、自身免疫性疾病以及肿瘤有重要作用。本文就维生素D缺乏与上述疾病关系的研究进展进行综述。     

维生素D对心血管疾病影响的研究进展

维生素D参与内分泌、炎症等多种功能。维生素D缺乏与高血压、高血脂症、心肌梗死、中风、慢性肾脏病及2型糖尿病等疾病的发生率升高有关。低维生素D水平会上调肾素-血管紧张素-醛固酮系统，促进炎症并引起内皮功能障碍。本文就维生素D对心血管疾病的影响的研究进展作一综述。     

维生素D和高血压发病的研究进展

维生素D缺乏非常普遍,流行病学和临床研究显示维生素D缺乏可能和高血压发病有关.维生素D可能通过负性调节肾素血管紧张素系统,减少甲状旁腺素分泌,改善胰岛素抵抗及对血管的保护作用降低高血压的发病风险,而且维生素D受体基因多态性也可能和高血压相关.开展维生素D和高血压发病的研究可能对高血压防治提供新的途径.     

维生素D状态与心血管危险

已知维生素D最重要的功能是维持人体钙离子代谢的平衡。近些年来的研究发现维生素D受体广泛存在于人体的多种组织细胞中,因此维生素D是否还具有其他重要的生物学功能成为研究热点,其中维生素D缺乏与心血管风险的关系颇为引人注目。一些研究提示维生素D缺乏可能增加心血管风险,包括高血压、心力衰竭和缺血性心脏病等。但其致病机制和影响程度尚不十分明确。现综述了目前有关维生素D状态与心血管危险间关系的假设机制,并探讨为验证有关假设已进行的一些重要研究。     

血浆（血清）维生素D水平与心率、心脏作功的关系

尽管机制仍不清楚,但越来越多的流行病学证据显示,维生素D缺乏或不足与包括高血压、心肌梗死、脑卒中等心血管疾病发病的高风险密切相关。因此,补充维生素D可能会减少心血管疾病的发生,但维生素D是否会影响心脏功能尚不清楚。本研究旨在评价血清维生素D水平与心率、心脏作功的关系。     

维生素D及其活性代谢物与糖尿病

近年的研究结果显示,维生素D不仅在调节骨和矿物质代谢中起重要作用,而且还与多种慢性疾病密切相关。基础研究发现,维生素D及其活性代谢物参与炎性反应和免疫调节过程。临床研究发现,高血压、肥胖、心血管疾病和糖尿病等现代流行病的发生与发展与维生素D及其活性代谢物有不可分割的联系。本文讨论了维生素D与糖尿病的关系以及维生素D在不同类型糖尿病的预防和治疗中的作用及机制。     

母体维生素D缺乏对妊娠及后代的影响

维生素D不仅与钙、磷代谢以及骨骼运动系统有关,还与免疫调节、细胞分化和凋亡以及神经系统发育有关.妊娠期母体的维生素D水平对孕妇及后代都有重要的影响.目前有研究表明:先兆子痫、妊娠期糖尿病、细菌性阴道炎和早产等与母体维生素D缺乏关系密切,后代的骨营养不良、呼吸道感染、哮喘和其他自身免疫疾病也与母体妊娠期维生素D缺乏相关.妊娠女性维生素D缺乏很常见,因而适当补充维生素D十分必要.     

维生素D与心血管疾病危险因素

人们过去一直认为维生素D的作用就是调节钙、磷代谢及骨重建,然而最近研究发现维生素D还有其他功能,其中维生素D缺乏与糖尿病、高血压、低度炎症反应及血脂异常等心血管疾病危险因素之间的研究成为目前研究的热点。在维生素D缺乏的人群中,心血管疾病危险因素发生率明显升高,补充维生素D后能够防止或延缓心血管疾病危险因素的发生。故以维生素D作为新的切入点深入研究,将会对未来预防和治疗心血管疾病有重要意义。     

Interplay of vitamin D and metabolic syndrome: A review

Vitamin D deficiency is a worldwide public health problem. Vitamin D deficiency plays key role in the pathophysiology of risk factors of metabolic syndrome which affect cardiovascular system, increase insulin resistance and obesity, stimulate rennin–angiotensin–aldosterone system that cause hypertension. The discovery of vitamin D receptor expressed ubiquitously in almost all body cells such as immune, vascular and myocardial cells, pancreatic beta cells, neurons and osteoblasts suggests an involvement of vitamin D mediated effects on metabolic syndrome. Moreover vitamin D deficiency as well as cardiovascular diseases and related risk factors frequently co-occur. This underlines the importance of understanding the role of vitamin D in the context of metabolic syndrome. The paper provides an insight into the physiology of vitamin D and relationship of vitamin D deficiency with risk factors of metabolic syndrome through observational and supplementation studies.     

Potential pathophysiological role for the vitamin D deficiency in essentialhypertension

Vitamin D deficiency has been indicated as a pandemicemerging public health problem. In addition to the well-known role on calcium-phosphorus homeostasis in thebone, vitamin D-mediated processes have been recentlyinvestigated on other diseases, such as infections, can-cer and cardiovascular diseases. Recently, both the dis-covery of paracrine actions of vitamin D(recognized as"local vitamin D system") and the link of vitamin D with renin-angiotensin-aldosterone system and the fibroblast growth factor 23/klotho pathways highlighted its ac-tive cardiovascular activity. Focusing on hypertension, this review summarizes the more recent experimental evidence involving the vitamin D system and deficiency in the cardiovascular pathophysiology. In particular, we updated the vascular synthesis/catabolism of vitamin D and its complex interactions between the various endocrine networks involved in the regulation of blood pressure in humans. On the other hand, the conflicting results emerged from the comparison between obser-vational and interventional studies emphasize the frag-mentary nature of our knowledge in the field of vitamin D and hypertension, strongly suggesting the need of further researches in this field.     

Food allergy is linked to season of birth,sun exposure,and vitamin D deficiency

The season of birth and ultraviolet B exposure have been related to the occurrence of food allergy. The levels of vitamin D produced from skin by ultraviolet B exposure might reflect this relationship. Vitamin D is known to induce antimicrobial peptides, protect intestinal flora, enhance the gut epithelial barrier, suppress mast cell activation and IgE synthesis from B cells, and increase the number of tolerogenic dendritic cells and IL-10-producing regulatory T cells. Vitamin D deficiency has been shown to exacerbate sensitization and allergic symptoms in a murine model of food allergy. However, in clinical situations, contradictory observations have been reported regarding the relationship between food allergy and vitamin D deficiency/supplementation. In this review, we have explored the links between food allergy and vitamin D levels. One explanation for the discrepant findings is confounding factors such as race, age, residency, skin color, and epigenetic changes that contribute to vitamin D levels. In addition, the season of birth influences the development of atopic dermatitis, which could lead to food sensitization. Finally, ultraviolet radiation could lead to regulatory T cell expansion and immunosuppression, irrespective of vitamin D status. Based on our current understanding, we believe that correction of vitamin D deficiency by supplementation, appropriate skin care, and sufficient ultraviolet radiation exposure could alter the prognosis of food allergy. To identify potential treatment strategies for food allergy, it is essential to gain a better understanding of the appropriate levels of vitamin D and ultraviolet radiation exposure.     

维生素D与代谢综合征

维生素D是人体必需的营养物质,其功能主要是通过维生素D受体来介导的.近年来研究发现,维生素D对胰岛具有保护作用,并且是维持正常胰岛素分泌和糖耐昔所必需的物质.临床及动物模型研究已证实维生素D对保证胰岛素正常释放以及维持糖耐量正常是必不可少的.维生素D受体基因多态性可能影响脂肪形成以及胰岛素敏感性.维生素D缺乏不仅与胰岛素抵抗和高血压的发生直接相关,而且可显著增加代谢综合征的发病风险.     

维生素D缺乏与糖尿病周围神经病变

糖尿病周围神经病变（DPN）患者中普遍存在维生素D缺乏的现象.1,25（OH）2D3作为维生素D的活性形式,通过与细胞内的维生素D受体（VDR）结合发挥生物学作用.已有研究证明DPN与维生素D缺乏之间具有相关性.维生素D缺乏导致DPN的机制尚不完全清楚,但有资料证实维生素D缺乏可导致神经系统发育障碍、神经损伤及神经变性性疾病,减弱抗炎作用,促进动脉粥样硬化发展,损害胰岛β细胞功能及上调基质金属蛋白酶水平,进一步导致DPN的发生和发展.     

The association of serum vitamin D levels with several cardiometabolic risk and aortic pulse wave velocity in elderly persons

Recent studies have shown that vitamin D, an important factor for bone health, can also play a role in reducing the risk for several other diseases. Its deficiency seems to be associated with cardiovascular disease. Arterial stiffness, a well-known predictor of hypertension, morbidity and mortality, increases with advancing age. We evaluated the relationship between serum 25-hydroxyvitamin D levels and arterial pulse wave velocity (aPWV) in an aging population. In randomly selected 876 subjects we studied the association between the vitamin D level and arterial stiffness. We used a Sphygmocor device to measure the aortic pulse velocity (PWV) to evaluate the arterial stiffness. There was a clearly negative trend in aortic PWV among 25-OH-D tertiles. The association between 25-0H-D and aortic PWV remained significant after adjustment for age, gender and other potential confounders; subjects in the first 25-OH-D tertile had adjusted odds ratio 1.9 (1.2–3.0) for having aortic PWV top tertile in multiple regression. Vitamin D levels are inversely associated with increased arterial stiffness in a normative aging population, irrespective of traditional risk factors burden. Further research is needed to clarify the role of vitamin D on arterial stiffness and whether supplemental vitamin D may play a role in prevention of cardiovascular disease or not.     

Vitamin D deficiency and secondary hyperparathyroidism: clinical and biochemical associations in older non-institutionalised Southern Tasmanians

Aim : To determine the prevalence and associations of vitamin D (25-OHD) deficiency in a sample of older Tasmanian subjects.
Methods : A cross-sectional survey of: 109 patients with a mean age of 79 years (range 60–101 years) consecutively admitted to a short stay geriatric rehabilitation ward; 52 community dwelling subjects with a mean age of 75 years (range 64–88 years). Subjects answered a questionnaire, had anthropometric measurements and underwent venepuncture.
Results : The main outcome measure was 25 hydroxy vitamin D (25-OHD) level with deficiency defined as < 28 nmol/L. Vitamin D deficiency was found in 67% and secondary hyperparathyroidism in 49% of the hospitalised group. Vitamin D deficiency was also found in 17% of the community group, in particular one in three residents of Independent Living Units was deficient. Subjects who were deficient were older (80 years vs 76 years [ p <0.001]), had lower body mass index (23.7 kg/m² vs 25.9 kg/m² [ p <0.001]) and had a lower serum albumin (35 gm/L vs 39 gm/L [ p <0.001]). Deficient subjects had poorer physical functional status ( p =0.02) and lower activity levels ( p <0.001) and reported less habitual sun exposure ( p <0.001). Biochemical measures such as parathyroid hormone, alkaline phosphatase and calcium were weakly predictive of vitamin D levels. By stepwise multiple regression analysis, the only significant predictors of vitamin D levels were the Frenchay Activity Index, albumin and calcium.
Conclusion : Vitamin D deficiency and secondary hyperparathyroidism is common in community living older people who are hospitalised in Southern Tasmania and is associated with increasing age, poor physical function and activity and low reported sun exposure.