维生素D对肌肉功能的影响

维生素D对于钙磷平衡和骨骼健康的意义众所周知,近年来维生素D在骨骼外的作用也逐渐被了解。许多横断面研究发现,维生素D缺乏患者常见肌痛、肌力减低、体能降低、跌倒增加、肌肉形态学改变等。关于维生素D调控肌细胞功能的机制研究从未停止,但仍有不足。虽然开展了大量临床研究,但补充维生素D对于改善肌肉功能、减少跌倒与骨折等的结果并不一致。本文就维生素D对肌肉及其功能的影响做综述。     

补充维生素D对骨质疏松症和骨量减少患者骨密度和骨折风险的影响

目的 :探讨补充维生素D对骨质疏松症和骨量减少患者骨密度(BMD)和骨折风险的影响。方法:在上海市徐汇区湖南路街道社区的居民和我院老年病科及骨质疏松门诊中通过BMD的检查筛选出骨质疏松症及骨量减少的研究对象,询问病史,完成实验室检查。根据血清维生素D的水平分为维生素D缺乏组和维生素D正常组2组,以骨折风险因子评估工具(FRAX)分别估算骨折风险值。对2组患者进行健康教育和生活方式干预,所有研究对象每日补充1粒钙片,缺乏组加用骨化三醇0.25μg/d。随访1年后,复查BMD值及估算骨折风险值。结果:共纳入118例患者,维生素D正常组45例,缺乏组73例。2组在随访前后的年龄、身高差(最高身高-目前身高)、体重、体质量指数(BMI)、BMD、骨折风险值都无统计学差异(均P>0.05)。但比较干预前后,2组的BMD差值(P=0.005)及维生素D缺乏组的骨折风险值(P=0.003)均存在显著性的统计学差异。结论:骨量减少和骨质疏松症患者血清维生素D正常组较维生素D缺乏组在预防骨量进一步减少和降低骨折风险方面获益更多。     

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维生素D缺乏所致的儿童佝偻病和成年后骨软化会促发并加重年老后发生的骨量减少或骨质疏松。因此,充足的维生素D是保证有效预防和治疗骨质疏松的基础。反映体内维生素D水平的最佳指标是血清25-羟维生素D[25(OH)D],其水平与骨密度、骨折风险和跌倒风险呈负相关。最优化的25(OH)D范围为30~50μg/L,20~<30μg/L为不足,低于20μg/L为缺乏。推荐老年人每天补充800~1000 U普通维生素D,骨质疏松患者、肥胖、缺乏日照和吸收不良的人可酌情增加至2000 U。     

维生素D与骨质疏松症

骨质疏松症(osteoporosis,OP)是患病率显著上升、危害严重的骨骼疾病,在其发病机制中,维生素D缺乏是引起负钙平衡、骨丢失加快、继发性甲状旁腺功能亢进、跌倒增加、骨折风险升高的重要危险因素。我国人群中维生素D缺乏广泛存在,建议在OP防治工作中,重视评估患者的维生素D营养状况,并给予患者合理的、个体化的维生素D治疗。     

维生素D及其类似物预防跌倒和降低骨质疏松性骨折的作用

老年人由于下肢神经肌肉功能下降,反应性和平衡能力减低,易发生跌倒,导致骨折。本文阐述了老年人跌倒的相关因素和髋部骨折的危险性,重点分析了维生素D和肌力的关系,补充维生素D能有效减少跌倒的发生。同时综述了维生素D和活性维生素D预防骨质疏松性骨折的作用。     

维生素D及其类似物预防跌倒和降低骨质疏松性骨折的作用

老年人由于下肢神经肌肉功能下降，反应性和平衡能力减低，易发生跌倒，导致骨折。本文阐述了老年人跌倒的相关因素和髋部骨折的危险性，重点分析了维生素D和肌力的关系，补充维生素D能有效减少跌倒的发生。同时综述了维生素D和活性维生素D预防骨质疏松性骨折的作用。     

骨痛-骨折不愈合-血肌酐升高

肾性骨病是慢性肾脏疾病的常见并发症,可显著增加骨折风险。本文对1例以骨痛、骨折不愈合和活动受限为主要表现的老年男性,进行细致病因查询,结果发现患者存在血肌酐水平升高、维生素D严重缺乏、代谢性酸中毒、继发性甲状旁腺功能亢进及骨转换生化指标升高,导致左胫腓骨远端骨折不愈合,影像学检查提示骨质疏松和骨软化。给予钙剂、活性维生素D治疗以及碳酸氢钠纠正代谢性酸中毒后,患者骨痛缓解、骨折愈合,活动能力显著提高。本例患者诊治经验提示肾性骨病可以引起骨折风险增加及骨折不愈合,临床医生应重视对肾性骨病的诊断及治疗。     

维生素D缺乏继发甲状旁腺功能亢进症患者的临床特点

目的分析3例严重维生素D缺乏继发甲状旁腺功能亢进症患者的临床特点及治疗策略。方法收集确诊为维生素D缺乏继发甲状旁腺功能亢进患者3例,对其进行详细的病史采集和体格检查,生物化学指标测定及影像学检查。结果患者1、2起病隐匿,临床症状不典型;患者3有长期双下肢乏力,全身疼痛,进行性加重的活动障碍及身高变矮。实验室检查结果:血25羟维生素D (25 hydroxyvitamin D,25OHD)低于检测值下限(8. 0μg/L),甲状旁腺素(parathyroid hormone,PTH)水平升高,碱性磷酸酶(alkaline phosohatase,ALP)及Ⅰ型胶原C端肽(C-terminal telopeptide of type 1 collagen,β-CTX)升高。双能X线吸收检测仪(dual energy X-ray absorptiometry,DXA)检测骨密度,提示骨密度显著降低。给予维生素D联合钙剂治疗3个月后,患者临床症状好转,随着25OHD水平升高,血PTH及骨转换标志物水平均下降,骨密度检查可见骨量增加。结论维生素D缺乏在人群中普遍存在,由于早期缺乏临床症状易被忽视,但当其引起继发性甲状旁腺功能亢进时,会对骨骼产生严重影响,导致骨转换增加,骨量流失加快,摔倒及骨折风险增加等。因此,应重视维生素D缺乏的早期防治,避免发生继发性甲状旁腺功能亢进。     

以低钙血症抽搐表现的严重维生素D缺乏性骨软化症一例

维生素D缺乏可引起成年患者骨软化症,出现疼痛、骨骼畸形、活动障碍等。严重缺乏者可出现低钙血症、抽搐。本文报道1例罕见的维生素D严重缺乏老年女性患者,以长期骨痛,近期出现抽搐、呼吸困难为主要临床表现就诊。实验室检查提示血钙降低,血碱性磷酸酶(alkaline phosphatase,ALP)升高,血甲状旁腺素(parathyroid hormone,PTH)升高,血25羟维生素D(25-hydroxy vitamin D,25OHD)水平低于检测值下限,影像学检查提示腰椎压缩性骨折。给予钙剂、活性维生素D制剂后血钙恢复正常,抽搐症状消失。长期予维生素D补充治疗,骨痛症状缓解。本文同时对维生素D缺乏引起低钙抽搐的病例报告文献进行复习和总结。     

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。     

Active vitamin D metabolite and prevention of falls

Recently, vitamin D metabolites have been internationally recognized to be effective for osteoporosis. The beneficial trend of the drugs for osteoporosis has been more in the prevention of fracture than in the increase of bone mineral density, and more in the prevention of fractures of four extremities compared to spinal fractures. The reason to reduce the fracture frequency of four extremities is due to increase the muscle power, the decrease of body sway and the reduction of falls by the action of the vitamin D. In the study of Japanese, it was declared that administration of active vitamin D significantly reduced the frequency of femoral neck fracture.     

The effect of vitamin D on bone and osteoporosis

The main effect of the active vitamin D metabolite 1,25(OH)2D is to stimulate the absorption of calcium from the gut. The consequences of vitamin D deficiency are secondary hyperparathyroidism and bone loss, leading to osteoporosis and fractures, mineralization defects, which may lead to osteomalacia in the long term, and muscle weakness, causing falls and fractures. Vitamin D status is related to bone mineral density and bone turnover. Vitamin D supplementation may decrease bone turnover and increase bone mineral density. Several randomized placebo-controlled trials with vitamin D and calcium showed a significant decrease in fracture incidence. However, very high doses of vitamin D once per year may have adverse effects. When patients with osteoporosis are treated with a bisphosphonate, they should receive a vitamin D and calcium supplement unless the patient is vitamin D replete. These subjects are discussed in detail in this review. Finally, the knowledge gaps and research agenda are discussed.     

The genes related to the effects of vitamin D on muscle and bone

Vitamin D is most frequently used as a drug for osteoporosis in Japan, and its effects on the maintenance of bone mineral density and inhibition of fracture risk have been shown. Recently, the actions of vitamin D on muscle have been elaborated, and its prevention of falls is noted. Active vitamin D modulates several genes in muscle and bones. The studies using vitamin D receptor deletion mice revealed that active vitamin D modulates the genes related to muscle differentiation and bone resorption.     

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.     

Drug therapy for osteoporosis associated with rheumatoid arthritis (vitamin D)

A various factors are related to osteoporosis with Rheumatoid Arthritis (RA) complicatedly. Improvement of bone decrease does not become only the bone fracture prevention and leads to the prevention of joint destruction. Osteoporosis in RA causes by increase of bone resorption. However, the decrease of bone formation has been found to osteoporosis in many RA patients containing steroid induced osteoporosis. The treatment for osteoporosis in RA with vitamin D may be letting the bone formation decreased in RA normalize by regulatory of immunity. The vitamin D would become the useful drug for promoting the bone formation by examination of new agents, method and dosage of treatment for osteoporosis in RA patients.     

Vitamin D deficiency and osteoporosis

Osteoporosis is a disease of disequilibrium between bone formation and bone loss, and vitamin D is one of the key hormones in the regulation of bone metabolism, the major role of which is to provide the proper micro‐environment for bone mineralization. Vitamin D deficiency which has been defined by most experts as circulating 25‐hydroxyvitamin D levels of less than 20 ng/mL (50 nmol/L) is widespread all over the world. As shown by the results of recent studies, vitamin D deficiency could increase the risk of low bone mineral density or osteoporosis, muscle disorders, falls, and as a matter of course, fractures due to both osteoporosis and falls. Long‐term supplementation of vitamin D and calcium are good prevention measures for osteoporosis, falls and fractures. At the same time, they are essential components of osteoporosis management. Many studies show that sufficient vitamin D intake could increase bone mass, and decrease the risk of falls and fractures.     

Glucocorticoid-induced osteoporosis

Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Glucocorticoids cause a rapid bone loss in the first few months of use, but the most important effect of the drug is suppression of bone formation. The administration of oral glucocorticoid is associated with an increased risk of fractures at the spine and hip. The risk is related to the dose, but even small doses can increase the risk. Patients on glucocorticoid therapy lose more trabecular than cortical bone and the fractures are more frequent at the spine than at the hip. Calcium, vitamin D and activated forms of vitamin D can prevent bone loss and antiresorptive agents are effective for prevention and treatment of bone loss and to decrease fracture risk. Despite the known effects of glucocorticoids on bone, only a few patients are advised to take preventive measures and treat glucocorticoid-induced osteoporosis.     

华法林引发骨质疏松症的发病机制及治疗策略

骨质疏松症是一种以骨矿物质含量低下、骨微结构损坏、骨强度降低、骨脆性增加、易发生骨折为主要特征的全身性骨代谢障碍性疾病。华法林可拮抗维生素K,使骨钙素的羧化受抑制,减少骨钙沉积,抑制骨矿化,从而干扰骨代谢,导致骨质疏松症或骨折,对于老年患者的影响尤其明显。长期服用华法林导致骨质疏松症的风险可能与用药剂量和时间相关。目前预防和治疗华法林引起的骨质疏松症主要依据原发性骨质疏松症的治疗原则,对于长期服用华法林的患者应补充钙剂和维生素D以预防骨质疏松症,对于已出现骨质疏松症的患者根据具体病情选择用双膦酸盐、降钙素、雌激素和甲状旁腺类似物治疗。本文对华法林引发骨质疏松症的发病机制、研究进展和治疗策略进行综述。     

REVIEW ARTICLE: Reducing fracture risk with calcium and vitamin D

Studies of vitamin D and calcium for fracture prevention have produced inconsistent results, as a result of different vitamin D status and calcium intake at baseline, different doses and poor to adequate compliance. This study tries to define the types of patients, both at risk of osteoporosis and with established disease, who may benefit from calcium and vitamin D supplementation. The importance of adequate compliance in these individuals is also discussed. Calcium and vitamin D therapy has been recommended for older persons, either frail and institutionalized or independent, with key risk factors including decreased bone mineral density (BMD), osteoporotic fractures, increased bone remodelling as a result of secondary hyperparathyroidism and increased propensity to falls. In addition, treatment of osteoporosis with a bisphosphonate was less effective in patients with vitamin D deficiency. Calcium and vitamin D supplementation is a key component of prevention and treatment of osteoporosis unless calcium intake and vitamin D status are optimal. For primary disease prevention, supplementation should be targeted to those with dietary insufficiencies. Several serum 25‐hydroxyvitamin D (25(OH)D) cut‐offs have been proposed to define vitamin D insufficiency (as opposed to adequate vitamin D status), ranging from 30 to 100 nmol/l. Based on the relationship between serum 25(OH)D, BMD, bone turnover, lower extremity function and falls, we suggest that 50 nmol/l is the appropriate serum 25(OH)D threshold to define vitamin D insufficiency. Supplementation should therefore generally aim to increase 25(OH)D levels within the 50–75 nmol/l range. This level can be achieved with a dose of 800 IU/day vitamin D, the dose that was used in succesfull fracture prevention studies to date; a randomized clinical trial assessing whether higher vitamin D doses achieve a greater reduction of fracture incidence would be of considerable interest. As calcium balance is not only affected by vitamin D status but also by calcium intake, recommendations for adequate calcium intake should also be met. The findings of community‐based clinical trials with vitamin D and calcium supplementation in which compliance was moderate or less have often been negative, whereas studies in institutionalized patients in whom medication administration was supervised ensuring adequate compliance demonstrated significant benefits.     

Osteoporosis in patients with inflammatory bowel disease: risk factors, prevention, and treatment

Patients with inflammatory bowel disease (IBD) are at increased risk for osteoporotic fracture. Bone density testing and osteoporosis management are recommended for IBD patients at greater risk for fracture (ie, postmenopausal women, men aged . 60 years, and those with low body mass indices, glucocorticoid use, family history of osteoporosis, and malabsorption). Patient management includes modification of osteoporosis risk factors, such as calcium and vitamin D supplementation, hormone deficiency correction, and smoking cessation. When indicated, bisphosphonates, such as risedronate and alendronate, have been shown to increase bone mass and reduce fracture risk in patients with glucocorticoid-induced osteoporosis. Infliximab, an anti-tumor necrosis factor a antibody, increases bone mineral density, but this effect has not as yet translated into reduced fracture risk.