慢性阻塞性肺疾病患者血清25-(OH) D3水平与肺功能及免疫功能的相关性研究

目的了解慢阻肺患者中维生素D缺乏情况,同时探讨维生素D水平与慢阻肺肺功能、免疫功能的相关性。方法 122例慢阻肺稳定期患者和117例健康对照组,比较两组血清25-(OH)D3水平及两组维生素D缺乏的患病率。分析慢阻肺稳定期患者肺功能与血清25-(OH)D3水平关系,分析两组免疫功能与血清25-(OH)D3的关系。结果慢阻肺组平均血清25-(OH)D3水平为12.04±5.88 ng/mL,维生素D缺乏患病率为91.80%,维生素D不足占7.38%,足够占0.82%。对照组平均血清25-(OH)D3水平为18.15±6.45 ng/mL,维生素D缺乏患病率为64.10%,维生素D不足占31.63%,足够占4.27%。两组的血清25-(OH)D3水平有差异(P0.01),维生素D缺乏的患病率也存在差异。慢阻肺组患者血清25-(OH)D3水平与FEV_1%、FEV_1/FVC呈正相关(r=0.269/0.299,P=0.013/0.05)。患者血清25-(OH)D3水平与CD4及CD4/CD8值呈正相关(r=0.270/0.259,P=0.012/0.017)。结论慢阻肺患者的血清25-(OH)D3水平较正常人群低。血清25-(OH)D3水平与慢阻肺患者肺功能严重程度相关。与T淋巴细胞分类也具有相关性。     

维生素D对慢阻肺患者免疫调节功能及生活质量的影响

目的探讨慢阻肺患者维生素D缺乏情况及对免疫调节功能和生活质量的影响。方法收集慢阻肺患者106例,随机分为治疗组和对照组,每组53例,对照组给予常规一般治疗,治疗组在对照组的基础上添加维生素D3治疗,10万U每次,连用两周;同时于体检科收集60例作为健康对照组,观察慢阻肺患者与健康对照组的维生素D水平的差异,同时观察慢阻肺患者免疫相关指标的变化及CAT评分情况。结果(1)慢阻肺组在治疗前25-(OH)D平均水平比健康对照组显著降低,差异具有统计学意义(P0.01)。(2)在慢阻肺患者中,治疗组CAT评分显著较对照组低,经比较差异具有统计学意义(P0.05)。(3)免疫相关指标CD_4~+、CD_8~+、CD_4~+/CD_4~+、Ig A、Ig M、Ig G与治疗前比较,各指标均明显上升,差异具有统计学意义(P0.05),但治疗组升高明显优于对照组,差异具有统计学意义(P0.05)。结论慢阻肺患者有较高的维生素D缺乏发病率,添加维生素D辅助治疗,有助于改善慢阻肺患者的免疫调节功能及生活质量。     

初始维生素D水平与初发溃疡性结肠炎患者病情及疗效的相关性研究

目的探讨初始维生素D水平与初发溃疡性结肠炎(UC)患者病情及疗效的相关性和临床意义。方法选取2017年6月至2020年6月在新疆医科大学第一附属医院诊治的114例初发UC患者作为研究对象,分为维生素D正常组(38例)和维生素D缺乏组(76例),另根据初发UC患者的病情严重程度分为轻度组(20例)、中度组(48例)和重度组(46例),均规范治疗12周。比较治疗前维生素D缺乏组与维生素D正常组的初发病情指标,包括白细胞计数(WBC)、红细胞沉降率(ESR)、血红蛋白、血小板计数(PLT)、C反应蛋白(CRP)及改良Mayo评分,并进一步比较各组治疗前后上述指标的变化幅度。结果维生素D正常组治疗前的CRP、ESR、改良Mayo评分均显著低于维生素D缺乏组,血红蛋白显著高于维生素D缺乏组,差异均有统计学意义(P均0.05),而两组治疗前的WBC和PLT差异则均无统计学意义(P均0.05)。对两组初发病情严重程度占比进行分析,结果显示,与维生素D缺乏组相比,维生素D正常组的轻度UC占比升高,重度UC占比降低,差异有统计学意义(P0.05)。维生素D正常组治疗前后的WBC、ESR、血红蛋白、PLT变化幅度均显著大于维生素D缺乏组,差异均有统计学意义(P均0.05),而两组的CRP和改良Mayo评分变化幅度差异则均无统计学意义(P均0.05)。初发病情严重程度轻、中、重度组的初始维生素D水平的差异有统计学意义(P0.01),轻度组的初始维生素D水平高于中度组和重度组,差异有统计学意义(P0.05)。结论初始维生素D水平与UC患者的初发病情严重程度及疗效有关。初始维生素D正常的UC患者经过规范化治疗后,疗效较初始维生素D缺乏的UC患者更好。     

老年住院患者维生素D的营养状况及其相关因素

目前维生素D缺乏在全球较为普遍,而老年住院患者由于卧床、疾病、用药等因素,维生素D缺乏更为严重.研究表明,季节、性别、年龄、地域、饮食等因素对维生素D缺乏的影响,在老年住院患者和社区老年人中是不一致的;但不论是老年住院患者还是社区老年人,其维生素D缺乏与户外活动时间均显著相关,与肥胖呈负相关,与过度消瘦呈正相关.及时发...     

补充维生素D对伴有维生素D缺乏的青年急性缺血性卒中患者转归的影响

目的 探讨补充维生素D对伴有维生素D缺乏的青年急性缺血性卒中患者转归的影响.方法 采取前瞻性对照研究方法,连续选取青年急性缺血性卒中患者,维生素D缺乏定义为25-羟基维生素D[25-hydroxyvitamin D, 25(OH)D]≤50 nmol/L.按照随机数字表法将伴有维生素D缺乏的患者分为干预组和常规治疗组,常规治疗组不予针对维生素D缺乏的药物干预,干预组给予每日口服阿法骨化醇0.5 μg.治疗1年后再次复查25(OH)D水平,监测用药期间不良反应,并采用改良Rankin量表评估功能转归,0~2分定义为转归良好.结果 在176例青年急性缺血性卒中患者中,94例(53.41%)伴有维生素D缺乏者被随机分为干预组和常规治疗组,每组各47例.随访结束时,干预组转归良好率(82.98%对63.83%;χ2=4.414,P=0.036)和血清25(OH)D水平[(85.83±10.53)nmol/L对(39.10±11.18)nmol/L;t=20.860,P<0.001]均显著高于常规治疗组.随访期间,2组均无失访和死亡事件,干预组仅见2例恶心,1例头昏,不良反应发生率为6.38%.结论 补充维生素D可提高伴有维生素D缺乏的青年急性缺血性卒中患者的维生素D水平,改善功能转归.     

前言——维生素D缺乏与老年常见疾病

正维生素D是人体的一种类固醇激素,其除具有调节钙磷代谢作用外,还有调节神经—内分泌—免疫网络、抗炎、维持免疫稳态等作用。全球范围内均存在着人群不同程度的维生素D水平不足或缺乏的问题,而老年人作为一个特殊群体,体内维生素D缺乏程度往往较年轻人更为严重。研究表明,维生素D不足或缺乏可能与许多老年慢性疾病的发病显著相关,如老年类风湿性关节炎、慢性肾脏病(chronic kidney disease,CKD)、AD、肌少症、高血压、骨质疏松等。随着人们对维生素D缺乏认识的不断深入,维生素D缺乏与老年常见疾病的相关性研究也成为目前医学界研     

重庆老年患者血清25-羟维生素D水平调查

目的调查重庆西南医院老年科住院患者血清25-羟维生素D状况。方法对住院老年患者行问卷调查,测定空腹血清25-羟维生素D含量,采用SPSS13.0软件对所得数据进行统计学处理。结果共调查342例住院患者,血清25-羟维生素D测定值为(14.62±7.96)ng/mL,血清25-羟维生素D水平与性别和年龄无相关性,维生素D缺乏和不足者占住院老年患者的93.27%,维生素D充足者6.72%。补充钙剂组患者血清25-羟维生素D水平均高于未补钙组,差异有统计学意义。补充活性维生素D组患者与未补充活性维生素D组血清25-羟维生素D水平差异无统计学意义。结论重庆市老年住院患者普遍缺乏维生素D,常规监测血清25-羟维生素D含量和积极预防和治疗维生素D缺乏十分必要。     

维生素D缺乏与骨质疏松

维生素D对骨骼最主要的作用之一是为骨质矿化提供合适的微环境。尽管部分食物中强化维生素D,或额外补充维生素D,但人群中维生素D缺乏仍很普遍。维生素D缺乏可导致甲状旁腺功能亢进、骨转换增加和骨丢失,引起骨折风险增加。维生素D和钙剂补充是防治骨质疏松症的基本措施。研究表明补充足量维生素D能增加骨量、肌肉容量,和肌肉协调功能,有助于预防骨质疏松及其骨折。     

维生素D缺乏与肝疾病

一般临床医师对钙磷代谢紊乱引起骨疾病了解较多,但由于维生素D缺乏引起骨疾病了解较少,同时对维生素D引起骨骼外疾病了解甚少。近几年有关维生素D缺乏与慢性肝病相关性研究的报道不断增多,因此有必要重新认识维生素D在肝组织中的生理作用,了解维生素D缺乏时与慢性肝病的相关性和作用,掌握维生素D缺乏的诊断与治疗,     

血清25OHD水平对溃疡性结肠炎患者疾病活动性和生活质量的影响

背景:近年研究发现维生素D具有广泛的生物学效应,参与了包括炎症性肠病在内的多种免疫性疾病的发病过程。目的:研究溃疡性结肠炎(UC)患者血清25羟维生素D(25OHD)水平与疾病活动性和生活质量的关系。方法:收集2015年10月—2016年3月安徽省立医院门诊和住院UC患者50例,同期35名健康体检者作为正常对照组,以电化学发光法检测血清25OHD水平。UC患者同时检测CRP、ESR和PLT,以改良Mayo评分系统评估疾病活动性,以中文版IBD问卷(IBDQ)评估患者生活质量。结果:UC组维生素D缺乏(血清25OHD20 ng/mL)检出率为68.0%,血清25OHD水平显著低于正常对照组[(16.73±8.83)ng/mL对(19.84±4.56)ng/mL,P0.05],并随疾病活动性的升高而逐渐降低(P0.05)。维生素D缺乏组CRP、ESR、PLT均显著高于非维生素D缺乏组(P均0.05),IBDQ总分以及肠道症状、全身症状、情感功能、社会功能四个维度的评分均显著低于非维生素D缺乏组(P均0.05)。Spearman或Pearson相关系数分析显示,UC组血清25OHD水平与Mayo评分和CRP、ESR、PLT呈显著负相关(P均0.05),与IBDQ总分以及四个维度评分呈显著正相关(P均0.05)。结论:UC患者存在较高的维生素D缺乏率,维生素D缺乏可能对患者的疾病活动性和生活质量产生负面影响。     

维生素D缺乏与慢性阻塞性肺疾病

维生素D除了调节钙磷代谢外,近年来大量证据表明它还通过调节炎症因子、氧化应激,以及气道重塑等影响COPD的发展过程。此外,维生素D还能加强呼吸道上皮抗菌肽的表达而产生重要的先天免疫,能够减少病原体负荷和阻塞性肺疾病急性加重的频度。COPD患者的维生素D缺乏经常发生,而且与疾病严重程度相关,因此,严重的COPD患者应该补充维生素D。     

维生素D缺乏与慢性阻塞性肺疾病

维生素D对钙磷代谢具有调节作用,并对骨骼健康会产生影响。但是维生素D及其代谢物广泛的生理作用远不只是对骨骼的生物学效应,许多生理过程都直接或间接受维生素D调节。近年来,维生素D在骨质代谢和钙调节之外的作用越来越受到重视。慢性阻塞性肺疾病（COPD）是一种进行性呼吸功能减退的呼吸道疾病,在老年人群中发病率很高。有研究表明,COPD的严重程度与维生素D缺乏相关。本文的主要目的是提高医务工作者对维生素D与COPD相关性的认识,并评估补充维生素D对减轻COPD患者病情的潜在作用。     

Role of vitamin D in the pathogenesis of atheromatosis

Background and aimsCardiovascular disease is the main cause of death worldwide, but the collective efforts to prevent this pathological condition are directed exclusively to individuals at higher risk due to hypercholesterolemia, hypertension, obesity, diabetes. Recently, vitamin D deficiency was identified as a risk factor for cardiovascular disease in healthy people, as it predisposes to different vascular dysfunctions that can result in plaque development and fragility. In this scenario, the fundamental aim of the study was to reproduce a disease model inducing vitamin D deficiency and atheromatosis in ApoE^?/- mice and then to evaluate the impact of this vitamin D status on the onset/progression of atheromatosis, focusing on plaque formation and instability.Methods and resultsIn our murine disease model, vitamin D deficiency was achieved by 3 weeks of vitamin D deficient diet along with intraperitoneal paricalcitol injections, while atheromatosis by western-type diet administration. Under these experimental conditions, vitamin D deficient mice developed more unstable atheromatous plaques with reduced or absent fibrotic cap. Since calcium and phosphorus metabolism and also cholesterol and triglycerides systemic concentration were not affected by vitamin D level, our results highlighted the role of vitamin D deficiency in the formation/instability of atheromatous plaque and, although further studies are needed, suggested a possible intervention with vitamin D to prevent or delay the atheromatous disease.ConclusionsThe data obtained open the question about the potential role of the vitamins in the pharmacological treatments of cardiovascular disorders as coadjutant of the primary drugs used for these pathologies.     

Protective links between vitamin D,inflammatory bowel disease and colon cancer

Vitamin D deficiency has been associated with a wide range of diseases and multiple forms of cancer including breast, colon, and prostate cancers. Relatively recent work has demonstrated vitamin D to be critical in immune function and therefore important in inflammatory diseases such as inflammatory bowel disease(IBD). Because vitamin D deficiency or insufficiency is increasingly prevalent around the world, with an estimated 30%-50% of children and adults at risk for vitamin D deficiency worldwide, it could have a significant impact on IBD. Epidemiologic studies suggest that low serum vitamin D levels are a risk factor for IBD and colon cancer, and vitamin D supplementation is associated with decreased colitis disease activity and/or alleviated symptoms. Patients diagnosed with IBD have a higher incidence of colorectal cancer than the general population, which supports the notion that inflammation plays a key role in cancer development and underscores the importance of understanding how vitamin D influences inflammation and its cancer-promoting effects. In addition to human epidemiological data, studies utilizing mouse models of colitis have shown that vitamin D is beneficial in preventing or ameliorating inflammation and clinical disease. The precise role of vitamin D on colitis is unknown; however, vitamin D regulates immune cell trafficking and differentiation, gut barrier function and antimicrobial peptide synthesis, all of which may be protective from IBD and colon cancer. Here we focus on effects of vitamin D on inflammation and inflammation-associated colon cancer and discuss the potential use of vitamin D for protection and treatment of IBD and colon cancer.     

Enfermedad pulmonar obstructiva crónica y osteoporosis

Osteoporosis is one of the systemic effects associated with chronic obstructive pulmonary disease (COPD). Risk factors for bone loss include smoking, skeletal muscle weakness, low bone mass index (BMI), vitamin D deficiency, glucocorticoid use, hypogonadism and systemic inflammation. The most important clinical feature is vertebral fracture, due to its significant morbidity and mortality. The treatment of osteoporosis includes calcium and vitamin D, bisphosphonates, anabolic agents and pulmonary rehabilitation. Prospective studies are required to determine the prevalence of osteoporosis in COPD and to identify which patients are at high risk for osteoporotic fracture. The development of new drugs to control systemic inflammation may contribute to specific treatments for osteoporosis in COPD.     

New insights about vitamin D and cardiovascular disease: a narrative review

The worsening worldwide trend toward nutritional insufficiency and the emerging knowledge of the nonhormonal actions of vitamin D and its metabolites have increased interest in the synthesis, metabolism, and action of vitamin D. Vitamin D deficiency has been linked with hypertension, myocardial infarction, and stroke, as well as other cardiovascular-related diseases, such as diabetes, congestive heart failure, peripheral vascular disease, atherosclerosis, and endothelial dysfunction. This review discusses the physiology and definition of vitamin D deficiency, evaluates the worldwide prevalence of vitamin D deficiency, and discusses recent evidence for the association between hypovitaminosis D and cardiovascular disease. Few randomized, controlled trials have evaluated the effect of vitamin D replacement on cardiovascular outcomes, and the results have been inconclusive or contradictory. Carefully designed randomized, controlled trials are essential to evaluate the role of vitamin D supplementation in reducing cardiovascular disease.     

Association Between Vitamin D Status and COPD Phenotypes

Background

It has been suggested that identifying phenotypes in chronic obstructive pulmonary disease (COPD) might improve treatment outcome and the accuracy of prediction of prognosis. In observational studies vitamin D deficiency has been associated with decreased pulmonary function, presence of emphysema and osteoporosis, upper respiratory tract infections, and systemic inflammation. This could indicate a relationship between vitamin D status and COPD phenotypes. The aim of this study was to assess the association between vitamin D levels and COPD phenotypes. In addition, seasonality of vitamin D levels was examined.

Methods

A total of 91 patients from a Danish subpopulation of the “Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points” cohort took part in a biomarker substudy. Vitamin D concentration was measured from blood samples taken at two visits, approximately 6 months apart. The participants were 40–75-year-old patients with COPD and had a smoking history of >10 pack-years.

Results

Fifty-six patients had 25-hydroxyvitamin D measured from blood samples from both visits. In the final model of the multivariate analyses, the factors that were associated with vitamin D deficiency at the first visit were age (OR: 0.89, p = 0.02) and summer season (OR: 3.3, p = 0.03). Factors associated with vitamin D level also at the first visit were age (B: 0.9, p = 0.02) and 6 min walking distance (B: 0.05, p = 0.01).

Conclusion

Vitamin D was not associated with COPD phenotypes and season did not seem to be a determinant of vitamin D levels in patients with moderate to severe COPD.     

Vitamin D and the Pathogenesis of Inflammatory Bowel Disease

Vitamin D has traditionally been known for its role in bone metabolism, but emerging evidence has suggested a broader role for vitamin D in immune regulation. Vitamin D deficiency has been associated with the pathogenesis of diverse autoimmune disorders and has similarly been implicated as a contributor to inflammatory bowel disease. In this review, we discuss animal, in vitro, genetic, and epidemiologic studies that have linked vitamin D deficiency with inflammatory bowel disease pathogenesis or severity. Nonetheless, we present the caveat in interpreting these studies in the context of reverse causation: Does vitamin D deficiency lead to gastrointestinal disease, or does gastrointestinal disease (with related changes in dietary choices, intestinal absorption, nutritional status, lifestyle) lead to vitamin D deficiency?     

Vitamin D: A new player in non-alcoholic fatty liver disease?

Vitamin D through its active form 1a-25-dihydroxyvtamin D[1,25(OH)2D]is a secosteroid hormone that plays a key role in mineral metabolism.Recent years have witnessed a significant scientific interest on vitamin D and expanded its actions to include immune modulation,cell differentiation and proliferation and inflammation regulation.As our understanding of the many functions of vitamin D has grown,the presence of vitamin D deficiency has become one of the most prevalent micronutrient deficiencies worldwide.Concomitantly,non-alcoholic fatty liver disease(NAFLD)has become the most common form of chronic liver disease in western countries.NAFLD and vitamin D deficiency often coexist and epidemiologic evidence has shown that both of these conditions share several cardiometabolic risk factors.In this article we provide an overview of the epidemiology and pathophysiology linking NAFLD and vitamin D deficiency,as well as the available evidence on the clinical utility of vitamin D supplementation in NAFLD.     

Progression of osteoporosis in patients with COPD: a 3-year follow up study

Currently, our knowledge on the progression of osteoporosis and its determinants is limited in patients with chronic obstructive pulmonary disease (COPD). Bone mineral density generally remains stable in patients with COPD over a period of 3 years. Nevertheless, the progression of vertebral fractures was not assessed, while an increase of vertebral fractures over time may be reasonable. Aims of the current study were to determine the percentage of newly diagnosed osteoporotic patients after a follow up of 3 years and to identify baseline risk factors for the progression of osteoporosis in COPD. Clinically stable COPD outpatients were included. Lung function parameters, body composition measures, six minute walk distance, DXA-scan and X-spine were assessed at baseline and repeated after 3 years. Prevalence of osteoporosis in COPD patients increased from 47% to 61% in 3 years mostly due to an increase of vertebral fractures. Lower baseline T-score at the trochanter independently increased the risk for the development of osteoporosis. Additionally, baseline vitamin D deficiency increased this risk 7.5-fold. In conclusion, the prevalence of osteoporosis increased over a 3-year period in patients with COPD. Baseline risk factors for the development of osteoporosis are osteopenia at the trochanter and vitamin D deficiency.