140例移植肾受者骨质丢失原因分析

目的研究调查移植肾受者骨密度并分析其主要影响因素。方法选取移植肾功能正常的受者140例,其中50例患者移植前检测血钙、磷、甲状旁腺激素、骨钙素、活性维生素D、尿钙和尿吡啶啉,双能X线吸收法测定腰椎和股骨近端骨密度。结果移植前患者钙、磷代谢异常明显,移植后血钙、磷、甲状旁腺激素、骨钙素、活性维生素D等均有明显改善,但尿钙／肌酐和尿吡啶啉／肌酐有增高趋势,股骨骨密度明显下降。平均每日激素用量为移植后尿钙／肌酐的主要预测因素。每日环孢素用量、体重指数与移植受者各部位骨密度明显正相关。累计激素用量是肾移植绝经女性病人腰椎和股骨颈骨密度的不良预测因素。结论患者肾移植后骨量减少和骨质疏松的发生率较高。骨质吸收增加可能是其主要原因。激素是移植。肾受者尤其绝经女性骨质吸收增加的主要因素之一。     

绝经后妇女雌激素受体、维生素D受体基因多态性的研究

目的　探讨雌激素受体、维生素D受体基因多态性与绝经后妇女骨密度的关系。方法　选取健康的绝经后妇女共 78例 ,运用双能X线骨吸收法进行骨密度的测量。同时 ,应用分子生物学方法检测其雌激素受体、维生素D受体基因限制性片断长度多态性 (PCR RFLP)。结果　绝经后妇女中 ,雌激素受体基因型仅与腰椎骨密度有显著差异。维生素D受体基因型在股骨颈、大转子部位有差异。PvuⅡ多态性和BsmI多态性共同作用对骨密度影响更大。结论　雌激素受体、维生素D受体基因型分布频率明显不同于西方国家 ,并且与骨密度有一定的关联 ,尤其是基因与基因的共同作用与骨密度的关系更为密切     

系统性红斑狼疮初发患者外周血中维生素D及其受体mRNA的水平和意义

目的 ①检测初发系统性红斑狼疮(SEE)患者外周血中维生素D内分泌系统的水平,探讨维生素D内分泌系统在SLE发病中的作用.②分析维生素D内分泌系统水平与SLE患者骨密度和病情活动程度的关系.方法 选择初发SLE患者43例,健康对照组44名,用酶联免疫吸附试验(ELISA)检测患者外周血浆中25羟基维生素D3(250HD3)和1,25-二羟基D3[1,25(OH)2D3]的水平,利用实时定量反转录-聚合酶链反应(RT-PCR)法检测患者外周血维生素D受体(VDR)表达水平.双能X线分别检测患者腰椎(L1-4)和股骨近端2个部位的骨密度,根据SLE疾病活动指数(SLEDAI)评分评估SLE病情活动程度.采用统计学单因素分析分别检验25OHD3、1,25(OH)2D3和VDR基因mRNA表达水平与SLE患者骨密度和病情活动程度的关系.结果 初发SLE患者25OHD3和1,25(OH)2D3激素水平与健康对照组比较,差异有统计学意义(P均<0.01);初发SLE患者组与健康对照组比较,VDR基因mRNA表达水平的差异有统计学意义(P<0.01);SLE患者2个部位的骨密度均低于健康对照组,且两组间的差异有统计学意义(P<0.05),SLE患者组骨量异常的发生率为35%,骨量异常与骨量健康对照组之间25OHD3、1,25(OH)2D3激素水平及VDR基因mRNA表达水平的差异无统计学意义(P0.05);250HD3、1,25(OH)2D3激素水平和VDR基因mRNA表达水平与SLE患者骨密度的情况不存在相关性(r=0.187,P0.05;r=0.172,P0.05;r=0.287,P0.05),它们与SLE患者的病情活动度之间也不存在相关性(r=0.054,P0.05;r=0.190,P0.05;r=0.046,P0.05).结论 SLE患者维生素D激素的水平及VDR基因的表达异常提示维生素D内分泌系统可能参与了SLE的发病,但与SLE患者骨量异常的发生和SLE病情活动度不存在相关性.     

骨质疏松的遗传因素

骨量峰值和骨丢失速度是骨质疏松及骨折的重要影响因素 ,家系调查显示骨量峰值受遗传控制 ,有腰椎和髋部骨折史的绝经后患者的女儿 (绝经前 )与没有此家族史同年龄的女性相比 ,前者腰椎、股骨颈处的骨密度更低 ,年轻女性(平均年龄 18.6岁 )的骨密度与其母亲的骨密度明显相关〔1〕。双胞胎的研究也提示遗传对中轴骨和外周骨骨量及骨丢失速度有一定影响。各种遗传基因可能也与骨质疏松有一定关系。一、维生素Ｄ受体 (ＶＤＲ)基因在各种可能影响骨密度和骨质疏松危险性的候选基因中 ,维生素Ｄ受体基因是最受人关注和引起争议的。ＶＤＲ基因由 9…     

611例汉族人维生素D受体基因多态性与骨密度关系研究

采用PCR-RFLP分析了611名上海地区汉族人的维生素D受体(VDR)基因型,并测量其骨密度(BMD),统计分析发现男女性VDR基因分布差异存在统计学意义,Bb基因型在男性中的分布频率(26.9%)高于女性(12.7%,P<0.01)。不同基因型的人群BMD差异无统计学意义。     

糖皮质激素所致骨质疏松与维生素D受体基因型相关性的初步研究

目的　利用聚合酶链反应 限制性片段长度多态性方法 (PCR RFLP)研究长期接受糖皮质激素治疗患者的维生素D受体 (VDR)基因型与骨密度 (BMD)之间的关系。方法　收集 71例长期服用糖皮质激素的风湿性疾病患者的临床资料及静脉血 ,双能X线骨密度仪测定其BMD。提取基因组DNA行PCR扩增出约 185 0bp的VDR基因片段 ,用限制性内切酶BsmI进行酶切 ,根据酶切后片段长度不同判定基因型 ,并统计分析基因型与BMD及Z值之间的关系。结果　 71例患者中检测出的基因型为Bb和bb两种 ,分布频率分别为 11 3%、88 7% ,其等位基因分布频率符合遗传平衡定律 (Hardy Weinberg定律 )。两种基因型间年龄、性别比、体重指数 (BMI)、病程、病种构成比、服用激素时间及激素累积量之间差异无显著性 (P >0 0 5 )。Bb及bb基因型患者的骨质疏松发生率分别为 37 5 %和 33 3% ,差异无显著性 (χ2 =0 0 5 ,P =0 8)。两种基因型患者间腰椎、髋部的BMD和Z值有一定的差异 ,但无统计学意义。结论　①我国汉族人群VDR基因型以bb为主 ,Bb其次 ,BB基因型分布频率最低。②长期接受糖皮质激素治疗的患者中 ,Bb和bb两种基因型间骨密度差异无显著性 ,VDR基因型不能预测糖皮质激素相关性骨质疏松发生的危险性 ,但该结论有待于加大样本量后进一步确证     

基因多态性与骨密度的相关性

骨密度受遗传因素影响,骨密度测定是诊断骨质疏松的主要依据.维生素D受体、Ⅰ型胶原、雌激素受体、降钙素受体参与骨形成和骨代谢,其基因多态性决定骨密度.研究发现Wnt蛋白、人类白细胞抗原等基因多态性也与骨密度有关.本文就基因多态性与骨密度的相关性进行论述.     

维生素D受体基因多态性与骨质疏松

骨质疏松的发生与多种因素有关 ,除运动、营养、绝经等因素外 ,遗传因素也具有十分重要的作用。澳大利亚学者Morrison等首先发现维生素 D受体 (VDR)基因多态性与骨钙素水平相关 ,并可以预测骨密度。此后 ,各国就 VDR基因多态性对骨密度、骨丢失和骨质疏松性骨折的影响开展了广泛研究。1　VDR基因的结构VDR基因位于 12号染色体 (12 q13- 14 ) ,长约 75 kb,由 11个外显子组成。其中 IA、IB和 IC为非编码区 ,外显子 II- IX编码维生素 D受体。到目前为止 ,使用 Fok I、Bsm I、Apa I和 Taq I酶已发现 VDR基因四种酶切位点多态性 (…     

中老年人骨质疏松性骨折流行病学特点及相关因素

目的探讨中老年人骨质疏松性骨折的流行病学特点及其影响因素。方法 2012年7月至2015年8月该院收治的中老年骨质疏松患者493例,采用问卷调查方式调查患者基线资料、相关生化指标及骨密度,采用多因素Logistics回归分析探究骨质疏松患者发生骨折的影响因素。结果 493例骨质疏松患者中男184例,女309例,发生骨折181例(36.71%),随着年龄的增加骨质疏松患者骨折的发生率越大(χ2=14.694,P=0.002);多因素Logistics回归显示年龄(OR=1.031,P0.05)、腰椎骨密度(OR=11.337,P0.05)、腰椎骨密度T值(OR=3.121,P0.05)、股骨颈骨密度T值(OR=8.913,P0.05)是骨质疏松患者发生骨折的危险因素,男性(OR=0.552,P0.05)、血清维生素D(OR=0.873,P0.05)是骨质疏松患者发生骨折的保护因素。结论随着年龄增长中老年人骨质疏松性骨折的发生率逐渐升高,应当对中老年人进行运动、饮食的干预,增加骨密度,以预防骨质疏松及骨质疏松性骨折的发生,提高中老年人生命质量。     

老年人维生素D受体基因启动子中Cdx-2结合位点多态性与骨密度的关系

目的 探讨老年人维生素D受体基因启动子中Cdx-2结合位点多态性的分布规律及与骨密度的相关性。方法 60岁以上的汉族老年人174例，用特异等位基因多重聚合酶链反应法检测维生素D受体基因启动子中Cdx-2结合位点多态性分布。用DPX-L双能X线吸收仪（Lunar，USA）测定髋部骨密度（g／cm^2）。结果 该人群维生素D受体基因启动子中Cdx-2结合位点基因型分布为AA：21．3％、AG：52．8％、GG：25．9％，以年龄、身高、体重作校正，各基因型间股骨颈、大转子和Wardg区的骨密度无显著性差别。结论 该人群维生素D受体基因启动子中Cdx-2结合位点多态性与髋部骨密度无明显相关性。     

Bone mineral density in premenopausal women with systemic lupus erythematosus

OBJECTIVE: To study bone mineral density (BMD) in premenopausal women with systemic lupus erythematosus (SLE) and to evaluate the influence of disease activity and use of corticosteroids. METHODS: A cross-sectional study on BMD of 118 premenopausal women with SLE. Patients were divided into 2 groups, 74 who had been treated with corticosteroids and 44 who had not. BMD at lumbar spine, femoral neck, and trochanter was measured. RESULTS: BMD in patients without and with corticosteroid treatment was 1.13 +/- 0.13 vs 1.05 +/- 0.14 g/cm2 (p = 0.005) at lumbar spine, 0.92 +/- 0.12 vs 0.86 +/- 0.12 g/cm2 (p = 0.005) at femoral neck, and 0.78 +/- 0.13 vs 0.72 +/- 0.12 g/cm2 (p = 0.014) at trochanter, respectively. Stepwise multilinear regression analysis showed that corticosteroid exposure was independently associated with decreased BMD in the corticosteroid treated patients (r2 = 7% for lumbar and 6.6% for trochanter model). No significant difference in BMD in corticosteroid treated patients appeared when they were subgrouped according to whether they were taking calcium supplements. Prevalence of osteoporosis at lumbar spine in corticosteroid treated patients was 1.4%, and was lower than reported for age and sex matched Caucasians. CONCLUSION: BMD measurements were significantly lower in premenopausal SLE patients who had had corticosteroid treatment than those who had not. There was a negative correlation between BMD and corticosteroid therapy, but not disease activity. Prevalence of osteoporosis, based on lumbar spine BMD, was lower than that reported in Caucasians.     

Reduced bone mineral density in Japanese premenopausal women with systemic lupus erythematosus treated with glucocorticoids

We evaluated bone mineral density (BMD) in Japanese female patients with systemic lupus erythematosus (SLE) and assessed the influence of the use of glucocorticoids. Lumbar BMD was measured by dual x-ray absorptiometry (DXA) in 60 premenopausal females who previously had been receiving glucocorticoid therapy. Therapeutic- and disease-related variables for SLE were analyzed and bone resorption or formation markers were measured. Osteoporosis was defined as a T-score below 2.5 SD by DXA; 12 patients (20%) showed osteoporosis, and 30 (50%) had osteopenia. Compared with the nonosteoporotic group (n = 48), the osteoporotic group (n = 12) had a significantly longer duration of glucocorticoid treatment (P = 0.01), a cumulative prednisolone dose (P = 0.002), and an SLE damage index (SLICC/ACR). There was no difference in the incidence of osteoporosis either with or without the previous use of methyl-prednisolone pulse or immunosuppressive drugs. There was a significant positive correlation between urinary type I collagen cross-linked N-telopeptides (NTx) and serum bone-specific alkaline phosphatase (BAP) (r = 0.404, P = 0.002), but these bone metabolic markers showed no difference between the osteoporotic and nonosteoporotic groups. A good significant negative correlation was shown between BMD and the cumulative glucocorticoid dose (r = −0.351, P = 0.007). Stepwise logistic regression analysis showed that the cumulative glucocorticoid intake was independently associated with osteoporosis. Glucocorticoid-induced osteoporosis was frequently observed in Japanese SLE patients, as in Caucasian populations. The cumulative glucocorticoid dose was associated with an increased risk for osteoporosis. Bone metabolic markers such as NTx and BAP were not influenced by glucocorticoid treatment and could not predict current osteoporosis in SLE patients. Received: October 18, 2001 / Accepted: April 8, 2002 Correspondence to:S. Banno     

Prevalence and etiology of low bone mineral density in juvenile systemic lupus erythematosus

OBJECTIVE: Studies of adults with systemic lupus erythematosus (SLE) have frequently demonstrated the presence of decreased bone mineral density (BMD). However, there have been few investigations in pediatric patients to date. This study was undertaken to determine the prevalence of low BMD in patients with juvenile SLE and to identify associated risk factors. METHODS: We studied 64 consecutive patients with juvenile SLE in whom routine dual x-ray absorptiometry (DXA) scanning was performed. Lumbar spine osteopenia was defined as a BMD Z score of < -1 and > or = -2.5, and osteoporosis as a BMD Z score of < -2.5. Decreased hip BMD was defined as a value of < 80%. Data on disease activity, quality of life, disease-related damage, sex, ethnicity, body mass index, age at diagnosis, age at DXA, medication use and duration, clinical features, and puberty status were collected at the time of DXA. RESULTS: Lumbar spine osteopenia was seen in 24 patients (37.5%) and osteoporosis in 13 (20.3%). Decreased hip BMD was present in 12 patients (18.8%). By univariate analysis, osteopenia was significantly correlated with age, disease duration, duration of corticosteroid use, cumulative corticosteroid dose, azathioprine use, cyclophosphamide use, lupus nephritis, and damage. Two additional variables, mycophenolate mofetil use and class III-IV nephritis, were associated with osteoporosis. Abnormal hip BMD was associated with disease duration, duration of corticosteroid use, and cumulative corticosteroid dose. By multivariate analysis, only disease duration remained in the model for osteoporosis and abnormal hip BMD, while cumulative corticosteroid dose was the variable associated with osteopenia. CONCLUSION: These results indicate that osteopenia and osteoporosis are common in juvenile SLE and are associated more closely with increased disease duration than with cumulative corticosteroid dose.     

广西壮、汉族绝经后妇女维生素D 受体基因型与骨密度、骨代谢的关系

目的探讨维生素D受体基因(VDR)型在壮、汉族绝经后妇女中的分布及其与骨密度、骨代谢的关系.方法在广西居住20年以上的绝经后汉族妇女116名,壮族妇女82名.记录年龄、绝经年龄,测量身高、体重.采用双能X线吸收法测定骨密度(BMD);用聚合酶链反应-限制性片段长度多态性(PCR -RFLP)法测定受试者的VDR基因型;测定血清骨钙素(osteocalcin,OC)、尿脱氧吡啶啉(deoxypyridinoline,DPD)和尿肌酐(creatinine,Cr).结果壮、汉族妇女年龄、绝经年限、体重、体重指数、BMD、VDR基因型频率分布无显著性差异(P>0.05);BB、Bb、bb基因型检出率分别为6.57%、66.16%和27.27%;BB基因型组第2腰椎(L2)BMD比bb基因型组低10.03%,第4腰椎(L4)BMD分别较bb、Bb基因型组低9.63%和12.44%(P<0.05);BB基因型组骨质疏松发生率最高(46.15%),Bb基因型组次之(19.85%),bb基因型组最低(14.81%)(P<0.05);BB基因型组OC最低,与Bb、bb 基因型组比较也有显著性差异(P<0.05);三组间尿DPD排泄率(DPD/Cr)差异无统计学意义.结论 VDR基因型可作为预测广西壮、汉族绝经后妇女骨质疏松危险性的遗传学标志.     

Risks factors for low bone mineral density in pre-menopausal Mexican women with systemic lupus erythematosus

The aim of this study was to determine the prevalence and risk factors for low bone mineral density (BMD) in women with systemic lupus erythematosus (SLE). A cross-sectional study was conducted among 100 pre-menopausal patients with SLE. Patients were evaluated using a questionnaire about the following variables: age, disease duration, disease activity, chronic disease damage, cumulative corticosteroid dose, and history of fracture. Lumbar spine and hip measurements of BMD were performed by dual absorptiometry. Univariate and multivariate statistical analyses were used to assess the relationship between risk factors and BMD. The mean age was 32.8 ± 8.7 years, and the median duration of SLE was 73.2 ± 65 months. The mean cumulative corticosteroid dose was 20.0 ± 21.3 g. The mean BMD was 1.09 ± .18 g/cm² in the lumbar spine and 1.0 ± .14 g/cm² in the hip. Osteopenia was present in 40% of patients and osteoporosis in 5%. In the multiple regression analysis, low BMD in the lumbar spine was associated with chronic disease damage and low body mass index (BMI). Low BMD in the hip was associated with cumulative corticosteroid dose and low BMI. Chronic disease damage, low BMI, and cumulative corticosteroid dose are risks factors for low BMD in pre-menopausal SLE patients. Osteopenia was found in 40% of patients, while osteoporosis was found in only 5%.     

Body composition in systemic lupus erythematosus

The objectives were to determine the body composition, and the effects of disease and corticosteroid therapy on body composition, in a population of female patients with systemic lupus erythematosus (SLE). All female SLE patients managed through a single centre were invited to participate in a cross-sectional study of body composition. Data were collected by standardized interview and examination, and review of medical records. Body composition was assessed by dual-energy X-ray absorptiometry (DXA). Eighty-two subjects were evaluated, 30 of whom were post-menopausal. Univariate linear regression analysis revealed a significant association of reduced fat-free mass with SLE severity [as measured by the Systemic Lupus International Collaborative Clinics (SLICC)] (P = 0.020), a history of corticosteroid exposure (P = 0.043) and age (P = 0.048). Reduced total body bone mineral density (BMD) was also significantly associated with SLICC (P < 0.001) and corticosteroid exposure (P = 0.017), and with age (P < 0.001), post-menopausal status (P = 0.003) and the duration of menopause (P < 0.001). Stepwise multiple linear regression analysis revealed a significant association between fat-free mass and total body, lumbar spine and femoral neck BMD (P = 0.007, P = 0.025, P = 0.003, respectively). Fat mass was significantly associated only with lumbar spine BMD (P = 0.008). In this SLE population, disease severity and corticosteroid exposure were independently associated with a negative effect both on total body BMD and on fat-free mass. Fat-free mass was a significant predictor of lumbar spine, femoral neck and total body BMD.      

Determinants of bone mass in systemic lupus erythematosus: a cross sectional study on premenopausal women.

OBJECTIVE: To evaluate bone mineral density (BMD) in young ambulatory female patients with systemic lupus erythematosus (SLE) and to assess the influence of disease related variables and use of corticosteroids. METHODS: Lumbar and femoral BMD were measured by dual x-ray absorptiometry (DXA) in 84 premenopausal patients with SLE (age 30.5+/-7.5 years). All patients were receiving corticosteroids at the time of the study. Variables evaluated were: disease duration, clinical pattern, disease activity (SLEDAI), cumulative damage index (SLICC/ACR), current and cumulative prednisone dose, duration of steroid treatment, and use of immunosuppressive agents. Osteoporosis was defined as a t score below 2.5 SD compared to a reference population of healthy women in at least one region of measurement. RESULTS: Vertebral and femoral BMD were significantly lower in patients with SLE than in age matched controls. Osteoporosis was detected in 22.6% of patients. No significant differences in BMD were detected between patients according to clinical pattern or activity index, whereas patients with damage index > 0 (n = 46) had a significantly lower BMD at both the lumbar (p = 0.008) and the femoral (p = 0.05) level. Compared with non-osteoporotic patients with SLE, women with osteoporosis had similar age, lower body mass index, significantly longer disease duration (p < 0.0001), higher cumulative steroid intake (p < 0.006), and higher SLICC/ACR score (p < 0.01). Stepwise logistic regression analysis showed that disease duration is independently associated with osteoporosis (OR 1.2 for each year of disease, 95% CI 1.07-1.33). Since disease duration and duration of steroid treatment were highly correlated, a new stepwise logistic model was run without disease duration, which revealed that prednisone was associated with an increased risk for osteoporosis (OR 1.16 for each year of treatment, 95% CI 1.05-1.29). CONCLUSION: Osteoporosis is a frequent feature in young patients with SLE. Disease duration is associated with an increased risk for osteoporosis, but the role of glucocorticoid treatment seems to be crucial. Steroid exposure was the only treatment related variable exerting an influence on the development of osteoporosis.     

Bone mineral density, biochemical markers of bone turnover, and hormonal status in men with systemic lupus erythematosus

The aim of this study was to evaluate bone mineral density (BMD), biochemical markers of bone turnover, and hormone levels in men with systemic lupus erythematosus (SLE). BMD at L2-L4 lumbar vertebrae (LS), left proximal femur neck, and radius at the ultradistal and mid-33% region was measured by dual-energy X-ray absorptiometry in 23 men with SLE (mean age, disease duration, and cumulative corticosteroid dose were 45.6 years, 11.9 years, and 33.410 g, respectively) and 40 healthy, age- and sex-matched controls. Biochemical markers of bone turnover, parathyroid hormone and 25-hydroxyvitamin D (25-OH-D), testosterone, and dehydroepiandrosterone sulfate (DHEAS) levels were measured. There was no difference in BMD between the SLE and control group. The prevalence of osteoporosis was 17.4% (4 out of 23), found at LS. Biochemical markers of bone turnover were within the reference range. There was a high prevalence of hypovitaminosis D (65.2%), hypotestosteronism (62.5%), and hypodehydroepiandrosterone sulfate (100%). There was no correlation between BMD and duration of disease, corticosteroid doses, SLE Disease Activity Index (SLEDAI), SLE Collaboration Clinics/American College of Rheumatology (SLICC/ARC) damage index, or markers of bone turnover. Bone-specific alkaline phosphatase (BSAP) (r, -0.500; P=0.018) and DHEAS (r, -0.511; P=0.013) correlated with the daily corticosteroid dose. Despite corticosteroid therapy, bone mass in men with SLE was not decreased.     

Loss of bone mineral density in Chinese pre-menopausal women with systemic lupus erythematosus treated with corticosteroids

The adverse effect of disease and chronic corticosteroid therapy on bone mineral density (BMD) in patients with systemic lupus erythematosus (SLE) has been reported in several studies of Caucasian populations. As the factors controlling bone homeostasis may be different in Asian populations, we measured BMD in 52 pre-menopausal Chinese women (mean age 34.1 +/- 8.0 yr) with SLE (mean disease duration 6.4 +/- 4.5 yr) treated with prednisone (mean daily dose 11.4 +/- 10.8 mg/day). Lumbar spine, hip (total and subregions) and total body BMDs were measured in the SLE patients using dual-energy X-ray absorptiometry (DEXA), and compared with those from healthy controls matched for age, sex and body mass index. Compared to controls, SLE patients were found to have lower BMD (g/cm2) at several sites: the lumbar spine (0.98 vs 0.90, P = 0.001), Ward's triangle (0.72 vs 0.67, P = 0.03), total body (1.04 vs 1.01, P = 0.04) and total hip (0.87 vs 0.82, P = 0.05). There was no correlation between BMD at any region and duration of disease, activity of disease or prednisone therapy (mean daily dose, cumulative dose or treatment duration). When BMDs were compared between controls and SLE patients, subgrouped according to those not on calcium and those arbitrarily receiving calcium supplements (1 g/day), significantly lower BMDs were found in those not on calcium compared to both controls and SLE patients on calcium. BMDs in SLE patients on calcium were not different from those in controls. The low prevalence of osteoporosis in our SLE patients (4-6%) suggests significant loss of BMD in Chinese SLE patients on corticosteroid therapy is less than that reported in Caucasians (12-18%).      

Vitamin D receptor gene start codon polymorphism (FokI) and bone mineral density in healthy male subjects

OBJECTIVE: The genetic factors determining peak bone mineral density (BMD) in men are not well characterized. Recent studies have investigated the relationship between the start codon polymorphism (SCP) of the vitamin D receptor (VDR) gene and BMD in different populations. We have now examined the relationship between SCP of the VDR gene and BMD in a group of healthy Caucasian men from the north-east of England. SUBJECTS: Ninety-six healthy men (median age 50, range 40.0-77.0 years). MEASUREMENTS: Analysis of the FokI genotypes of SCP of the VDR and measurements of BMD at the femoral neck and lumbar spine were performed. RESULTS: FF, Ff and ff VDR FokI genotypes were found to have the highest, intermediate and the lowest lumbar spine BMD, respectively (Mean +/- SD, for FF 1.07 +/- 0.14, Ff 1.05 +/- 0.16 and ff 0.95 +/- 0.10 g/cm2). There was a significant difference in spine BMD between FF and ff genotypes (P < 0.05, analysis of variance [ANOVA]), but no such difference was apparent between Ff and ff (P > 0.05, ANOVA). Interestingly, there was no association between FokI polymorphism and femoral neck BMD (Mean +/- SD, for FF 0.85 +/- 0.12, Ff 0.87 +/- 0.15 and ff 0.83 +/- 0.15 g/cm2). The distribution of FokI VDR genotypes approached Hardy-Weinberg equilibrium and was similar to that reported for women from different ethnic groups, as the prevalence of FF and ff genotypes was 44% and 16%, respectively. CONCLUSION: The study shows that in this population of healthy men there is a weak association between lumbar spine bone mineral density and FokI restriction fragment length polymorphism at the translation initiation site of the vitamin D receptor gene.