日本两岁男童维生素D缺乏与神经发育问题的相关性研究

维生素D缺乏与神经发育障碍之间的联系已被证实, 但在普通儿童群体中, 关于维生素D水平、神经发育及性别差异的大型研究依旧不足。该研究探索儿童血清中25-羟基维生素D的水平与神经发育问题(NDPs)之间的相关性。     

维生素D与孤独症谱系障碍的关系

孤独症谱系障碍（ASD）是一种复杂的与多个遗传和环境危险因素有关的神经发育障碍。过去几年遗传和环境因素间相互作用已成为研究的热点。最近提出了维生素D缺乏可能是ASD的一个环境危险因素。维生素D在维持大脑内稳态、促进胚胎和神经发育、免疫调节（包括大脑自身的免疫系统）、抗氧化、抗凋亡、影响神经分化及基因调控方面都有独特的作用。多项研究表明ASD患儿血清中维生素D浓度相比健康儿童存在显著降低。因此,母孕期和儿童早期缺乏维生素D可能是引起ASD的环境危险因素之一。     

儿童肥胖与维生素D缺乏

儿童肥胖和维生素D缺乏已成为两大公共卫生问题.近年来大量研究表明肥胖及其相关的代谢性疾病与血清低维生素D水平相关,但维生素D缺乏与肥胖之间的因果关系仍不明确.目前仍没有足够证据证明维生素D补充对改善体重、体块指数及脂肪量有益.肥胖可能导致了低维生素D状态,而维生素D和维生素D受体则可能通过作用于脂肪分化、脂肪细胞凋亡、脂质合成和分解、摄食行为及能量消耗方面影响能量平衡.     

儿童维生素D缺乏的研究进展

研究表明全球50%的人口存在维生素D缺乏的风险.引起维生素D缺乏的主要原因是人们误认为靠日照或通过膳食就可补充足够的维生素D,而忽略了在特殊年龄或特殊季节添加维生素D的重要性.儿童是维生素D缺乏的潜在高危人群,维生素D缺乏町使儿童易患佝偻病,引起生长迟缓和骨骼变形,并可能增加成人后骨质疏松及老年髋部骨折的危险性.维生素D缺乏还与癌症、自身免疫性疾病、内分泌系统疾病、神经系统疾病、高血压及传染病有关.     

晚发性维生素K缺乏症与维生素D缺乏性佝偻病的相关性探讨

目的探讨晚发性维生素K缺乏症与维生素D缺乏性佝偻病的相关性.方法回顾分析42例晚发性维生素K缺乏症患儿的临床表现及辅助检查.结果42例晚发性维生素K缺乏症患儿中39例有颅内出血,3例表现为全身散在出血点,全部病例均伴有维生素D缺乏性佝偻病的早期症状.其中2例维生素D缺乏性手足搐搦症所致惊厥患儿病初头部CT检查未见异常,于惊厥反复发作后始出现颅内出血症状、体征及头部CT异常改变.结论晚发性维生素K缺乏症与维生素D缺乏性佝偻病常同时并存,维生素D缺乏性手足搐搦症所致惊厥可诱发或加重晚发性维生素K缺乏症的颅内出血.     

维生素D与支气管哮喘研究进展

维生素D作为一种免疫调节剂与支气管哮喘的发生、发展关系密切.维生素D参与了胎儿肺和免疫系统的发育;流行病学调查发现,维生素D缺乏和哮喘的发病率上升及哮喘的严重程度有关;维生素D对哮喘的发生有早期干预作用,而且在糖皮质激素耐受性哮喘的治疗和特异性免疫疗法中发挥辅助作用.     

维生素D与过敏性疾病相关性的研究进展

过敏性疾病的患病率在全世界呈上升趋势.流行病学调查结果显示西方发达国家维生素D制剂的使用与过敏性疾病发病率同步增加,早期补充维生素D可能增加患过敏性疾病的风险.近期研究发现维生素D缺乏的地区过敏性疾病发病率也较高,多数学者认为维生素D缺乏与过敏性疾病流行相关.研究发现维生素D参与过敏性疾病的免疫反应,如抑制Th1细胞、树突细胞发育及Th2细胞分化,参与维持肠黏膜上皮细胞屏障完整性,但无证据表明维生素D过量或缺乏可导致过敏性疾病的发生.

Abstract：

The prevalence of allergy diseases is increasing globally. Epidemiological surveies showed that the increased allergy prevalence rates followed the time trend of rickets prophylaxis in western countries. and vitamin D supplement increased the risk of allergy in early stage.Currently,most of investigators think that vltamin D deficiency may be one of the risk factors for allergy diseases.Laboratory investigations showed that vitamin D inhibited Th1、dendritic cell(DC)and Th2 cell proliferating,and keeped on epithelial suIfaces barrier tunction.However,no study has found generating of allergy disease is associated with vitamin D deftciency or excess.     

维生素D在孤独症谱系障碍发病机制中的研究进展

孤独症谱系障碍(ASD)是一组神经发育障碍性疾病,虽然ASD患病率不断上升,但其发病机制至今未明。目前研究提示其可能与遗传因素、免疫因素和环境因素有关。有研究表明维生素D(Vit D)缺乏与ASD患病率存在负相关,补充Vit D可能降低ASD的发病风险。因为Vit D的广泛生理功能,Vit D可作为类固醇激素作用于遗传...     

维生素D及其受体与佝偻病的研究进展

维生素D通过维生素D受体介导,在体内具有广泛的生物学作用,其中对钙磷代谢的调节作用对于正常的骨骼形成与骨矿化有重要影响.佝偻病为常见的儿童骨代谢性疾病,不同类型佝偻病的病因不同,但其病理生理过程、临床表现及治疗均与维生素D及其受体对骨代谢的影响密切相关.     

维生素D与水通道蛋白的研究进展

维生素D是一种脂溶性类固醇激素,通过与维生素D受体(vitamin D receptor,VDR)结合构成1,25 (OH)2D3/VDR信号通路参与调节机体钙磷代谢、糖代谢、脂代谢、水代谢等多种生物功能的调节.水通道蛋白是一类相对分子质量较小的疏水跨膜蛋白,在特殊的组织或细胞中如肾小管、内分泌腺、红细胞等细胞膜上特异表达,参与体内水平衡及代谢的调节.维生素D可以通过抑制肾素-血管紧张素系统在糖尿病肾病等疾病中起积极的作用,而水通道蛋白作为评价肾脏疾病进展及肾脏功能的新指标逐渐走进人们的视线,有研究证实维生素D在参与调节水通道蛋白的表达,维生素D和水通道在肾脏损伤及慢性肾脏疾病发挥着重要作用.     

Vitamin D insufficiency in a boy with obsessive–compulsive disorder

Vitamin D deficiency not only causes low bone mass but also may lead to neuropsychiatric disorders. In the present case, vitamin D supplementation reduced obsessive–compulsive disorder (OCD) symptoms associated with streptococcal infection in a 7‐year‐old boy. Sudden onset of symptoms, including excessive hand washing and fear of touching anything, had occurred 1 month before presentation. Although there are few studies on a possible causal relationship between vitamin D and neuropsychiatric disorders, the present report; together with previous data, suggest an etiological role of vitamin D‐related immune processes.     

维生素D与癫疒间的相关性研究进展

维生素D除参与调节体内钙磷代谢外,其缺乏与全身和神经系统的多种疾病的发病密切相关,如多发性硬化、阿尔茨海默症、帕金森病和脑血管疾病等。近年来研究发现维生素D可能在癫疒间的发病机制中起着重要作用,并可能具有一定的抗惊厥作用。该文对维生素D在癫疒间中的作用,血清维生素D水平及其受体基因的多态性与癫疒间的关系进行了综述,也总结了抗癫疒间药和维生素D之间的相互作用。     

Vitamin D deficiency and insufficiency after pediatric liver transplantation

Vitamin D deficiency and insufficiency are increasingly recognized in the general population, including healthy children. There is also an increasing emphasis on the importance of vitamin D status following pediatric liver transplantation and specifically its relationship to metabolic bone disease and growth retardation. Vitamin D insufficiency has also been associated with multiple immunological and metabolic disorders in adults. To our knowledge, this has not been systematically evaluated in children undergoing liver transplantation to date. Between October 2004 and August 2008, serum 25‐(OH)‐vitamin D levels were measured in 199 children who had undergone liver transplantation at Birmingham Children's Hospital. Potential factors contributing to vitamin D levels were evaluated. Additionally, we evaluated a possible relationship between vitamin D levels and immunological phenomena and metabolic complications. Median 25‐(OH)‐vitamin D level was 19.5 ng/mL (range: 4.4–71.4 ng/mL). A total of 105 children (53%) had insufficient vitamin D levels and 28 children (14%) showed vitamin D deficiency. The only factors found to be associated with vitamin D deficiency were season of sample, ethnicity, and PTH levels. Vitamin D deficiency was more prevalent during the first year after transplantation. We did not find a significant relationship between vitamin D levels and graft function or any other immunological and metabolic complications. Vitamin D insufficiency and deficiency are common in children after liver transplantation, especially in winter and spring and in non‐white patients. Initial post‐transplant period and high PTH are significantly associated with vitamin D deficiency. Vitamin D status should be monitored following pediatric liver transplantation and vitamin D supplementation provided as required.     

维生素D在克罗恩病中的作用机制及外源性补充作用北大核心CSCD

维生素D不仅可调节钙磷代谢,还具有免疫调节的作用。克罗恩病(Crohn's disease,CD)患者普遍缺乏维生素D。研究表明维生素D与CD等自身免疫性疾病有关,通过调节肠道免疫、修复肠黏膜屏障、抑制肠纤维化、增强对英夫利西单抗的应答、调节肠道菌群等途径改善CD患者的病情,促进患者的康复。外源性维生素D补充在提高血清维生素D水平的同时可以诱导疾病的缓解。但目前仅有少数随机双盲、安慰剂对照试验研究维生素D在CD中的治疗效果,有关维生素D最佳的补充形式、具体的补充剂量及需要维持的最佳血清浓度尚未明确。该文主要讨论维生素D在CD的作用机制及外源性维生素D补充对CD的有益作用。     

Use of Vitamin D in Various Disorders

Approximately 1 billion people worldwide have been identified as vitamin D deficient in the 21st century, and the number is on the rise; non-classical actions of vitamin D were initially recognized around 30 y ago when receptors for vitamin D were detected in neoplastic cells lines. The aim of this review is to provide a brief overview of the non-classical actions of vitamin D. Reports describing the associations of non skeletal actions of vitamin D, especially pertaining to the immune system, inflammatory disorders, cancers and cardiovascular disease have been summarized in this paper. Reports support a role for the active form of vitamin D in mediating normal function of both the innate and adaptive immune systems. Studies also suggest a link between vitamin D deficiency and autoimmune diseases, such as rheumatoid arthritis, systemic sclerosis, systemic lupus erythematosus and type 1diabetes. There is believed to be an inverse association between serum 25-hydroxyvitamin D concentrations and the incidence of colorectal cancer, sporadic colorectal adenoma and breast cancer. Vitamin D deficiency has been linked with various cardiovascular diseases such as hypertension, myocardial infarction, and stroke. Several epidemiological and genetic studies suggest a strong association between vitamin D and non skeletal acute and chronic disorders. However, currently, robust clinical data are still lacking to support raising intake requirements and target vitamin D plasma levels. Nonetheless, the high prevalence of vitamin D deficiency is alarming and requires implementation of clear supplementation guidelines.     

Bone disease in infants with prolonged obstructive jaundice

Four infants with prolonged cholestasis, of differing aetiologies, developed metabolic bone disease during infancy. Radiologically three distinct patterns of skeletal abnormality were found: classical vitamin D deficiency rickets; axial skeleton demineralization with rib fractures and rickets; and in one patient, long term defective remodelling of tubular bones. Variations in the age of onset of rickets may be related to the baby's gestational maturity at birth, while its severity is probably more closely linked to the interval before vitamin therapy was commenced. In such infants increased supplements of prophylactic vitamin D are recommended.     

Zebrafish as a systems toxicology model for developmental neurotoxicity testing

The developing brain is extremely sensitive to many chemicals. Exposure to neurotoxicants during development has been implicated in various neuropsychiatric and neurological disorders, including autism spectrum disorder, attention deficit hyperactive disorder, schizophrenia, Parkinson's disease, and Alzheimer's disease. Although rodents have been widely used for developmental neurotoxicity testing, experiments using large numbers of rodents are time‐consuming, expensive, and raise ethical concerns. Using alternative non‐mammalian animal models may relieve some of these pressures by allowing testing of large numbers of subjects while reducing expenses and minimizing the use of mammalian subjects. In this review, we discuss some of the advantages of using zebrafish in developmental neurotoxicity testing, focusing on central nervous system development, neurobehavior, toxicokinetics, and toxicodynamics in this species. We also describe some important examples of developmental neurotoxicity testing using zebrafish combined with gene expression profiling, neuroimaging, or neurobehavioral assessment. Zebrafish may be a systems toxicology model that has the potential to reveal the pathways of developmental neurotoxicity and to provide a sound basis for human risk assessments.     

Genetic causes of rickets.

Dietary deficiency of vitamin D, genetic disorders of its bioactivation to 1,25-dihydroxyvitamin D [1,25(OH)2D], or disorders of vitamin D action can cause rickets. The rate-limiting, hormonally-regulated, biologically activating step in the synthesis of 1,25(OH)2D is the 1 alpha-hydroxylation of 25-hydroxyvitamin D, which occurs in kidney and other tissues and is mediated by a mitochondrial cytochrome P450 enzyme, P450c1 alpha. After many years of effort, the cDNA and gene for this enzyme were cloned in late 1997. Mutations in the P450c1 alpha gene, located on chromosome 12, cause 1 alpha-hydroxylase deficiency, also known as vitamin D-dependent rickets type I, an autosomal recessive disease characterized by rickets and impaired growth due to failure of renal synthesis of 1,25(OH)2D. X-linked hypophosphatemic rickets, a dominantly inherited disease, is caused by mutations in the PHEX gene, whose function in regulating renal phosphate and vitamin D metabolism remains to be elucidated.