维生素D受体基因多个位点多态性与绝经后妇女骨密度及骨转换生化标志物的关系

目的：观察维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性与绝经后妇女骨密度及骨转换生化标志物的相关性。 方法：①2007-01/2008-12从福州常住汉族人中随机检测绝经后妇女576例, 年龄48-84(62.17±6.37)岁。受试者均知情同意。②记录年龄、绝经年限、体质量指数和绝经后骨折情况。③双能X射线骨密度仪检测正位第2~4腰椎、左侧股骨颈、大转子和Ward s三角区骨密度。④PCR-RFLP技术检测维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性。⑤用酶联免疫吸附法检测骨转换生化标志物(血清骨钙素、血清骨碱性磷酸酶、尿吡啶啉和尿脱氧吡啶啉)。 结果：561例合格受试者进入结果分析。①维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨密度比较差异无显著性意义(P > 0.05)。②维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨转换生化标志物比较差异无显著性意义(P > 0.05)。③维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨质疏松症发生率比较差异无显著性意义(P > 0.05)。④维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间绝经后骨折发生率比较差异无显著性意义(P > 0.05)。 结论：维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性与绝经后骨质疏松症无明显关联,不能作为福州地区绝经后妇女骨质疏松的遗传标志。     

北京部分汉族男性维生素D受体基因Fok Ⅰ多态性与骨密度的关系

背景：骨质疏松症是受遗传和环境因素共同作用的多因子复杂疾病。维生素D受体基因多态性被认为是调控骨量的重要遗传因素,但在不同种族人群中的研究结果仍存在争议。 目的：观察维生素D受体基因Fok Ⅰ多态性与北京地区部分汉族男性骨密度的关系,以探求北京地区男性骨质疏松症的遗传易感性。 设计、时间及地点：随机对照试验,在2004-09/2007-12在解放军第二炮兵总医院内分泌科和解放军总医院老年病研究所分子生物学实验室共同完成。 对象：筛选2004-09/2006-12长期居住北京地区无血缘关系的20~80岁健康汉族男性230人。 方法：用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析法检测受试者维生素D受体基因Fok Ⅰ基因型,使用双能X射线吸收测定法检测随机抽取的100例受试者腰椎和髋部的骨密度。 主要观察指标：①受试者年龄、身高、体质量。②受试者维生素D受体基因Fok Ⅰ基因型。③受试者L2~4椎体、股骨颈、大转子及Wards三角部位骨密度。 结果：受试者维生素D受体基因Fok Ⅰ的基因型及基因频率的分布为FF 36.96%,Ff 46.96%,ff 16.08%,符合Hardy-Weinberg定律;校正年龄、体质量、身高和体质量指数对骨密度的影响后,40~59岁年龄段男性ff基因型组骨密度较FF,Ff基因型低(P=0.037)。其余各年龄段、各部位ff基因型组骨密度大多低于FF,Ff基因型,但差异无显著性意义(P > 0.05)。 结论：北京地区汉族男性维生素D受体基因Fok Ⅰ多态性分型与骨密度之间可能存在一定关联,该项检测对筛查男性骨质疏松症高危人群的意义需进一步研究。     

骨钙素基因Hind Ⅲ多态性与福州地区汉族绝经后妇女骨密度的相关性*

背景：骨质疏松症是一种多基因遗传病,骨钙素受体基因多态性与骨密度关系存在地域和人群的差异。 目的：观察绝经后妇女骨钙素基因型频率分布及其与骨密度的关系,探讨福州地区汉族绝经后妇女骨质疏松症的遗传易感基因。 方法：用聚合酶链式反应限制性片段长度多态性分析201例汉族绝经后妇女骨钙素基因型,用双能X射线吸收法测定腰椎、股骨颈,大转子和Ward’s三角4个部位骨密度值。 结果与结论：福州地区汉族绝经后妇女骨钙素基因型频率分布符合Hardy-Weinberg定律(χ2=2.29,P > 0.05),基因多态性分布依次为HH 5%、hh 46%、Hh 49%,与福州、北京、广州、台湾地区骨钙素基因Hind Ⅲ位点多态性分布频率差异无显著性意义(P > 0.05)。但是与日本人、白种人差异明显(P < 0.05)。且HH基因型在大转子骨密度明显高于hh型(P < 0.05),但不同基因型在第2~4腰椎、股骨颈、Ward’s三角区的骨密度差异无显著性意义。提示绝经后妇女骨钙素基因型与大转子骨密度可能存在一定关联。     

护骨素基因T245G多态性与老年人骨密度关系的部位及性别差异*☆

背景：作为骨折发生的重要临床预测因子,骨密度在一定程度上由遗传因素决定。护骨素基因是骨质疏松症发病中的重要候选基因。 目的：探讨护骨素基因T245G多态性与骨密度的相关性。 方法：选取2008-09/2010-04在北京大学人民医院进行常规查体的老年人281名,其中男182名,女99名。应用PCR-RFLP结合DNA测序检测护骨素基因T245G多态性,使用双能X射线骨密度测量仪测定受试者腰椎、髋部标准位置及前臂的骨密度。同时收集受试者的生化指标及临床观察项目。应用ANOVA方法分析护骨素基因T245G多态性与各检测指标的关系。 结果与结论：在老年男性及绝经后女性中,T245G基因T,G等位基因频率分布差异无显著性意义(P > 0.05)。在老年男性中,GG和TG基因型具有较高的腰椎骨密度,而TT基因型的腰椎骨密度较低(P < 0.05),Ward’s三角区及前臂骨密度在各基因型间差异无显著性意义(P > 0.05)。在绝经后女性中,T245G多态性与骨密度无关,说明护骨素基因与老年男性腰椎骨密度有关。     

降钙素受体基因多态性与原发性骨质疏松的相关性★

目的：骨质疏松是多基因调控疾病，峰值骨量达到和骨量丢失均受遗传因素影响。观察山东半岛地区汉族人群降钙素受体Alu-Ⅰ基因多态性各基因型频率及其与骨质疏松的关系，探讨原发性骨质疏松症的遗传易感因素。 方法：试验于2005-06/2007-06在青岛大学医学院附属医院中心实验室完成。①试验对象：选取332名长期居住在山东半岛地区无亲缘关系的汉族人群，纳入标准：健康门诊查体人员、原发性骨质疏松症及原发性骨质疏松症所致骨折患者；患者对试验知情同意。排除标准：各种继发性骨质疏松症；影响骨代谢相关疾病史；服用影响骨代谢药物等。其中骨质疏松合并骨折75例作为骨质疏松性骨折组，余257例经过骨密度测定确定骨量，按骨质疏松诊断标准（骨密度测定值比同性别峰值骨密度均值降低2.5个标准差）分为骨量正常组（n =201）及骨质疏松组（n =56）。②试验方法：应用聚合酶链反应限制性片段长度多态性分析技术测定257名山东半岛汉族成年人和75名骨质疏松性骨折患者降钙素受体基因型，用双能X射线吸收法测定腰椎、股骨颈、粗隆间、Ward’s三角和大转子区等部位的骨密度值。 结果：纳入受试者332人，均进入结果分析。①本试验人群降钙素受体基因型频率分布均符合Hardy-Weinberg 定律(χ2=0.47，P =0.493)。基因型频率分布依次为CC型占89.5%，CT型占10.5%，TT型占0%。②年龄与不同部位骨密度值之间呈负相关（P < 0.01），体质量指数与骨密度值之间呈正相关（P < 0.01），在将年龄和体质量指数进行校正后发现女性CC基因型较CT基因型在ward’s三角区有较高的骨密度（P < 0.05)，骨量正常组各基因型与骨质疏松性骨折组之间差异无显著性意义（P > 0.05)。 结论：山东半岛汉族女性降钙素受体基因型与骨密度之间存在一定关联，降钙素受体C1377T基因多态性可能成为胶东半岛汉族女性发生骨质疏松危险性的遗传标志。     

护骨素基因A163G多态性与北京地区老年人群骨密度的关系

背景：护骨素基因是骨质疏松症的候选基因，其基因多态性存在种族差异。 目的：探讨北京地区老年人群中护骨素基因启动子区域A163G位点多态性与骨密度的关系。 方法：选取307名老年受试者，采用双能X射线骨密度吸收仪测定股骨近端、腰椎及前臂骨密度，取其外周血提取DNA，采用多聚酶链反应-限制性片段长度多态性方法测定护骨素基因A163G多态性，并进行基因测序。采用单因素方差分析比较不同基因型对应的骨密度变化，逐步回归法分析骨密度的相关因素。 结果与结论：在绝经后老年女性受试者中，腰椎、股骨Inter区，AA型骨密度高于AG或GG型，老年男性受试者中，各基因型所对应的骨密度，没有明显差异。提示护骨素基因启动区域A613G多态性与绝经后老年女性骨密度有一定关联。     

护骨素基因T950C及A163G多态性与老年2型糖尿病患者的骨密度

背景：2型糖尿病患者发生骨质疏松症的比率较高。 目的：观察老年2型糖尿病患者护骨素基因启动子区域T950C、A163G位点多态性与骨密度的关系。 方法：纳入147例老年2型糖尿病患者,男性100例,女性47例,应用多聚酶链反应-限制性片段长度多态性方法测定患者护骨素基因T950C、A163G的基因型;采用双能X线骨密度吸收仪测定患者腰椎、髋部及前臂的骨密度。 结果与结论：在老年女性2型糖尿病患者中,T950C不同基因型在特定部位具不同骨密度,CC基因型的腰椎L2、L4骨密度高于TC或TT型;在老年男性2型糖尿病患者中,未发现T950C不同基因型与骨密度相关。在老年女性2型糖尿病患者中,A163G不同基因型在特定部位具不同骨密度,AA型的股骨大转子、前臂骨密度高于AG或GG型;在老年男性2型糖尿病患者中AA型的腰椎L3、L4骨密度高于AG或GG型。表明护骨素基因启动子区T950C基因多态性与老年女性2型糖尿病患者的骨密度相关,A163G基因多态性与老年男、女性2型糖尿病患者的骨密度皆相关。     

骨形态发生蛋白7基因变异与新疆维吾尔族肥胖人群的相关性

背景：研究表明骨形态发生蛋白7基因定位的染色体20q13是肥胖的易感区域，功能与基因定位均表明骨形态发生蛋白7基因是肥胖的易感基因。 目的：探讨骨形态发生蛋白7基因变异与新疆维吾尔族肥胖人群的关系。 方法：以流行病学调查为基础的病例-对照研究，选取1 063例维吾尔族人群作为研究对象。先在48例维吾尔族肥胖人群(男/女：24/24)中测序筛查骨形态发生蛋白7基因功能区的变异位点，选取代表性变异位点应用TaqMan-PCR技术在研究人群中进行基因型鉴定并开展病例-对照关联研究。 结果与结论：在骨形态发生蛋白7基因的功能区共发现5个新的和8个已知的变异位点。骨形态发生蛋白7基因的2个代表性变异位点rs60254222和rs17480735均符合Hardy-Weinberg平衡。老年人群中rs60254222变异的AA、AG、GG基因型在肥胖组及正常对照组中的频率分布分别为32.2%，55.7%，12.2%和23.8%，48.3%，27.9%，且两组间频率分布差异有显著性意义(P < 0.01)。老年人群中rs60254222变异不同基因型组间体质量指数、腰围、腰臀比差异有显著性意义(P < 0.05)。Logistic分析提示老年人群中rs60254222变异GG基因型是肥胖的保护性因素(OR=0.578，95%可信区间为0.401~0.833，P=0.003)。结果表明骨形态发生蛋白7基因变异位点rs60254222可能与新疆维吾尔族人群肥胖相关。     

河北健康汉族人群GSTO2基因多态性研究

目的探讨河北汉族人群谷胱甘肽硫-转移酶O2(GSTO2)基因多态性的分布情况。方法应用聚合酶链式反应-限制性酶切片段长度多态性(PCR-RFLP)方法对210例河北汉族正常人进行GSTO2N142D和GSTO2 A183G基因多态性分析。结果河北汉族人群GSTO2 N142D和GSTO2 A183G基因多态性符合Hardy-Weinberg遗传平衡定律。河北汉族人群GSTO2 N142D基因型频率分布和等位基因频率分布与贵州汉族人群、台湾地区人群、泰国人群、伊朗人群、意大利人群、美国人群有显著差异(P0.05)。河北汉族人群GSTO2 A183G基因型频率分布与台湾地区人群、德国人群、美国人群有显著差异(P0.05),而与日本人群无显著差异(P0.05);但其等位基因频率与台湾地区人群、日本人群、德国人群、美国人群有显著差异(P0.05)。结论河北汉族人群GSTO2基因存在多态性,具有特异性。     

福州地区老年男性雌激素受体α基因多态性与骨密度关系：150例数据分析

背景：关于男性骨质疏松症候选基因的研究,不同国家和地区的学者针对不同的种族和人群,得出的结论并不一致。 目的：分析福州地区汉族老年男性雌激素受体α基因XbaⅠ及PvuⅡ多态性分布,进一步研究其与骨密度的关系。 设计、时间及地点：骨密度及基因型相关性分析,于2007-02/2008-09在福建省中医药研究院门诊部及中医药管理局经络三级实验室完成。 对象：福州地区60岁以上汉族男性150例,年龄(68.92±5.33)岁,体质量(66.47±9.08) kg,体质量指数(24.23±3.12) kg/m2。 方法：双能X射线骨密度仪检测受试者正位L2~4、左侧股骨颈、大转子和Ward’s区骨密度,应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)检测雌激素受体α基因XbaI及PvuⅡ多态性。 主要观察指标：骨密度;雌激素受体α基因型;年龄;身高;体质量。 结果：150例受试对象中,雌激素受体α XbaI基因型分别为XX型10例(占6.7%)、Xx型56例(占37.3%),xx型84例(占56.0%),X等位基因频率为25.3% 、x等位基因频率为74.7% ;PvuⅡ基因型分别为PP型18例(占12.0%)、Pp型78例(占52.0%),pp型54例(占36.0%),P等位基因频率为38.0% 、p等位基因频率为62.0% ;基因型分布均符合Hardy-Weinberg定律。分析基因型与骨密度的关系显示：与XX基因型相比,xx基因型人群在Ward’s区、大转子具有较高骨密度值,差异具有显著性 (P 分别为0.0192及0.087);xx基因型人群在大转子比Xx基因型具有较高骨密度值 (P < 0.05);PvuⅡ多态性各基因型间骨密度值均无差异。 结论：雌激素受体α基因XbaⅠ多态性与福州地区汉族老年男性骨密度相关,x基因是骨密度保护因素。     

Antiepileptic drug-induced bone loss in young male patients who have seizures

BACKGROUND: Long-term antiepileptic drug (AED) therapy is a known risk factor for bone loss and fractures. Vitamin D deficiency is frequently cited as a cause for bone loss in patients who have seizures. OBJECTIVE: To determine whether men who have seizures, but who are otherwise healthy, suffer substantial bone loss in the hip while taking AEDs. PATIENTS AND METHODS: We prospectively examined femoral neck bone mineral density (BMD) by dual-energy x-ray absorptiometry in 81 consecutive men, aged between 25 and 54 years old (mean age, 45 years), who were attending an outpatient seizure clinic. Low BMD values were analyzed for known risk factors for bone loss. Dual-energy x-ray absorptiometry scans were repeated in 54 patients, 12 to 29 months later (mean, 19 months), to assess the rate of change in BMD over time. RESULTS: Multivariate linear regression analysis revealed that age (P<.001) and time receiving AEDs (P<.003) were the 2 important risk factors associated with low femoral neck BMD. Neither vitamin D deficiency, hypogonadism, cigarette smoking, nor excess alcohol intake were associated with low BMD after correcting for age and time on AEDs. Longitudinal analysis of femoral neck BMD revealed that only those in the youngest age group (25-44 years) showed significant declines in femoral neck BMD (1.8% annualized loss; 95% confidence interval, -3.1 to -0.9; P<.003) while receiving AED therapy. There was no evidence that a specific type of AED was more causally related to bone loss in this group although most patients were taking phenytoin sodium or carbamazepine during the longitudinal assessment. CONCLUSIONS: Long-term AED therapy in young male patients who have seizures causes significant bone loss at the hip in the absence of vitamin D deficiency. Dual-energy x-ray absorptiometry scanning of the hip is useful in identifying patients who are particularly susceptible to rapid bone loss while taking AEDs.     

中国北方地区老年人冬季维生素D缺乏与骨量丢失**☆

背景：中国北方地区老年人维生素D营养状态存在季节变化,冬春季维生素D缺乏严重。 目的：分析沈阳市老年人冬季维生素D缺乏对骨量丢失的影响。 方法：随机选择沈阳市60岁以上汉族健康老年人100名,于2000-03检测受试者血浆中25羟维生素D、甲状旁腺激素、钙和磷,清晨空腹2 h尿中脱氧吡啶、钙、磷、肌酐,2000-03/2005-03两次检测髋部骨密度。 结果与结论：基线时,血浆25羟维生素D浓度为(31.0±12.30) nmol/L,40%受试者低于25 nmol/L;血浆甲状旁腺激素水平为(29.4±11.5) ng/L,血浆25羟维生素D浓度低于25 nmol/L者甲状旁腺激素水平为(34.6±13.5) ng/L,血浆25羟维生素D浓度与甲状旁腺激素呈负相关(r=-0.479,P < 0.000 1)。5年后股骨颈骨丢失率为(3.05±4.07)%,大转子为(1.46±5.02)%,经体质量和身高变化率校正后,股骨颈骨丢失率与基线血浆25羟维生素D浓度呈负相关(r=-2.3,P=0.02),股骨颈骨丢失率基线血浆25羟维生素D浓度≤ 25 nmol/L者高于浓度>25 nmol/L者103%( F=7.206 2,P=0.008 5)。其他检测指标与骨丢失无显著相关性。说明老年人群冬季维生素D缺乏严重,维生素D缺乏促进骨量丢失,影响骨健康。     

Bone status in multiple sclerosis: beyond corticosteroids

The aim of this study was to determine the possible factors affecting bone mineral density (BMD) in multiple sclerosis (MS). In this cross-sectional study, 65 clinically definite MS patients and 72 comparable controls were prospectively evaluated. To assess bone mineral metabolism in MS, the BMD of the lumbar spine and hip (femoral neck, trochanter and total) was measured by dual-energy X-ray absorptiometry, and serum vitamin D and parathyroid hormone levels and biochemical markers of bone turnover were also evaluated. MS patients had significantly lower BMD values than the control group at all measurement sites. There was a significant correlation between the disease duration and BMD values at the trochanter in women with MS. A correlation between femoral BMD values and functional status in women was also detected. There was no relationship between bone biochemical markers and BMD, except a negative correlation between bone alkaline phosphatase and trochanter BMD. Both disability and disease duration have an influence on BMD of the MS patients, whereas no significant correlation between glucocorticoid use and BMD was observed.     

Bone mineral density and vitamin D status in Parkinson’s disease patients

Bone loss is more common in Parkinson’s disease (PD) than in the general population. Several factors may be involved in the development of bone loss, including malnutrition, immobilization, low body mass index, decreased muscle strength, vitamin D deficiency and medication use. This study investigates the prevalence of osteoporosis and possible risk factors associated with bone loss in early stage PD. In 186 PD patients (Hoehn and Yahr stage 1–2.5, mean age 64.1 years, 71 % men) bone mineral density (BMD) measurements were performed with DEXA. T- and Z-scores were calculated. Univariate linear regression analysis was performed to identify variables that contributed to BMD. 25-OH-vitamin D status of PD patients was compared with 802 controls (mean age 63.3 years, 50 % men) using linear regression analysis. Osteoporosis (11.8 %) and osteopenia (41.4 %) were common in PD patients. Mean Z-score for the hip was 0.24 (SD 0.93), and for the lumbar spine 0.72 (SD 1.91). Female gender, low weight, and low 25-OH-vitamin D were significantly correlated with BMD of the hip and lumbar spine. PD patients had lower 25(OH)D serum levels than controls (B = ?10, p = 0.000). More than half of the patients with early stage PD had an abnormal BMD. Female gender, low weight, and low vitamin D concentration were associated with bone loss. Furthermore, vitamin D concentrations were reduced in PD patients. These results underscore the importance of proactive screening for bone loss and vitamin D deficiency, even in early stages of PD.     

BsmI vitamin D receptor’s polymorphism and bone mineral density in men and premenopausal women on long‐term antiepileptic therapy

Background: Utilization of antiepileptic drugs (AEDs) has long been associated with bone deleterious effects. Furthermore, the BsmI restriction fragment polymorphism of the vitamin D receptor (VDR) has been associated with reduced bone mineral density (BMD), mostly in postmenopausal women. This study evaluates the association between bone metabolism of patients with epilepsy and the BsmI VDR’s polymorphism in chronic users of AEDs. Methods: This study evaluated 73 long‐term users of antiepileptic drug monotherapy, in a cross‐sectional design. Fasting blood samples were obtained to estimate the circulating serum levels of calcium, magnesium, phosphorus, parathormone, 25hydroxyvitamin D as well as the VDR’s genotype. Bone mineral density at the lumbar spine was measured with Dual Energy X‐Ray Absorptiometry. Results: Bone mineral density was significantly associated with the genotype of VDR (mean BMD: Bb genotype 1.056 ± 0.126 g/cm²; BB genotype 1.059 ± 0.113 g/cm²; bb genotype 1.179 ± 0.120 g/cm²; P < 0.05). Additionally, the presence of at least one B allele was significantly associated with lower bone mineral density (B allele present: BMD = 1.057 ± 0.12 g/cm², B allele absent: BMD = 1.179 ± 0.119 g/cm²; P < 0.01). Patients with at least one B allele had lower serum levels of 25hydroxyvitamin D when compared with bb patients (22.61 ng/ml vs. 33.27 ng/ml, P < 0.05), whilst they tended to have higher levels of parathyroid hormone. Discussion: Vitamin D receptor polymorphism is associated with lower bone mass in patients with epilepsy. This effect might be mediated through the vitamin D‐parathormone pathway.     

The association between BsmI polymorphism and bone mineral density in young patients with epilepsy who are taking phenytoin

Purpose: This study sought to determine the association between BsmI polymorphism and bone mineral density, 25‐hydroxyvitamin D, and parathyroid hormone levels in patients with epilepsy. Methods: We recruited ambulatory young adults with epilepsy who were taking phenytoin. Data regarding demographics, basic laboratory studies, history of clinical epilepsy, parathyroid hormone, and vitamin D levels, as well as BsmI polymorphism of the vitamin D receptor (VDR) gene, were obtained. The bone mineral density (BMD) of the lumbar spine and left femur were measured using dual‐energy x‐ray absorptiometry. Key Findings: Ninety‐four patients were included in the study. BsmI polymorphism had a statistically significant lower T‐score of the lumbar spine and left femoral neck than patients with wild‐type VDR gene (p < 0.01 and p < 0.01, respectively). In addition, patients with BsmI polymorphism had a statistically significant lower z‐score of the lumbar spine and left femoral neck than patients with wild‐type VDR gene (p < 0.01 and p < 0.01, respectively). The 25‐hydroxyvitamin D level in patients with wild‐type genes was higher than in epileptic patients with BsmI polymorphism (p < 0.01 and p < 0.01, respectively). Parathyroid hormone level in patients with wild‐type VDR gene or patients having BsmI polymorphism was not correlated with BMD at either site. Significance: In patients with epilepsy taking phenytoin, having BsmI polymorphism was associated with lower BMD.     

Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: a randomized controlled trial.

Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization-induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2-year follow-up period was studied. At baseline, both groups of patients had low BMD with high levels of serum-ionized calcium and urinary deoxypyridinoline (D-Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10-0.85). The number of hip fracture per 1,000 patient-years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D-Pyr levels decreased significantly during the follow-up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures.     

Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in Parkinson's disease

A high incidence of fractures, particularly of the hip, represents an important problem in patients with Parkinson's disease (PD), who are prone to falls and have osteoporosis. We previously showed that 25-hydroxyvitamin D (25-OHD) deficiency due to sunlight deprivation with compensatory hyperparathyroidism causes reduced bone mineral density (BMD) in elderly patients with PD. The present study was undertaken to address the possibility that sunlight exposure may maintain BMD and reduce the incidence of hip fracture in elderly patients with PD. In a prospective study, PD patients were assigned to regular sunlight exposure (n=162) or usual lifestyle (n=162), and followed for 2 years. BMD of the second metacarpal bone was measured using a computed X-ray densitometer. Incidence of hip fracture in the two patient groups during the 2 year follow-up period was assessed. At baseline, patients of both groups showed vitamin D deficiency due to sunlight deprivation with compensatory hyperparathyroidism. The exposed group patients were exposed to sunlight (3231 min/year). BMD increased by 3.8% in the sunlight-exposed group and decreased by 2.6% in the usual lifestyle group (p<.0001). Serum 25-OHD level increased from 27 nmol/L to 52 nmol/L in the sunlight-exposed group. Eleven patients sustained hip fracture in the normal lifestyle group, and 3 fractures occurred among the sunlight-exposed group (p=.03; odds ratio=2.4). Sunlight exposure can increase the BMD of vitamin D deficient bone by increasing 25-OHD concentration and leads to the prevention of hip fracture.     

Reduced bone density and major hormones regulating calcium metabolism in anorexia nervosa.

Bone density of lumbar vertebrae (L2 to L4) and the whole body in 29 patients with anorexia nervosa were measured by dual photon absorptiometry, and the results were compared with those of 10 age-matched normal controls. The patients had significantly lower bone mineral density (BMD) in L3 and L2-4 than controls. However, there was no difference in whole-body BMD. L3 and L2-4 BMD was positively correlated with body weight and was negatively correlated with duration of illness and amenorrhea. Patients who had been more active 6 months before the time of the study had significantly higher L3 BMD than the less active patients. Most patients had an abnormally low serum estrogen level, whereas the mean serum levels of thyroid hormone (T3, T4), cortisol, calcitonin, parathyroid hormone and vitamin D were within the normal range. No correlation was found between L3 or L2-4 BMD and the levels of these hormones. These results suggest that severe weight loss, low physical activity, longer duration of amenorrhea and deficiency of estrogen contribute to bone loss in patients with anorexia nervosa, whereas calcium-regulating hormones such as parathyroid hormone, calcitonin and vitamin D are unlikely to be a primary contributor to bone loss.