血液透析患者血清瘦素水平与骨密度和骨代谢的关系研究

目的观察血液透析患者体内血清瘦素水平与骨密度、骨代谢指标之间的关系。方法94名血液透析患者均采用双能X射线骨密度仪检测计算股骨颈和腰椎骨的骨密度。采用酶联免疫法测定血清瘦素,放射免疫检定法测定甲状旁腺素（PTH）,酶联免疫吸附法测定Ⅰ型胶原羧基端肽β特殊序列（β-CTX）,采用全自动生化分析仪检测骨特异性碱性磷酸酶（BAP）。结果女性患者的血清瘦素明显高于男性患者（t=2.44,P＜0.05）,且女性患者血清瘦素和PTH、β-CTX、BAP均呈负相关（r分别=-0.58、-0.23、-0.37,P均＜0.05）,男性患者血清瘦素和PTH、β-CTX呈负相关（r分别=-0.41、-0.45,P均＜0.05）。所有患者的血清瘦素与骨密度相关性不明显（r分别=0.06、0.06,P均＞0.05）。结论血液透析患者女性的血清瘦素水平明显高于男性,女性患者血清瘦素与骨代谢呈负相关;男性患者中血清瘦素与骨代谢中的骨吸收负相关,而与骨形成无关。所有患者的血清瘦素与骨密度相关性均不明显。     

在糖尿病肾病过程中血清骨保护素及骨密度的变化

背景:目前人们对糖尿病肾病过程中所致肾性骨病骨保护素的关系仍不清楚.目的:探索2型糖尿病肾病过程中患者骨密度、血清骨保护素水平的变化及其间的相关性.方法:选择2型糖尿病患者104例,根据肾小球滤过率将患者分为5组:单纯糖尿病组、肾脏轻,中,重度损伤组、肾衰竭组.选择健康体检者20名为对照组.采用双抗体夹心酶联免疫吸附法(ELISA)测定受试者血清骨保护素水平.采用全自动生化分析仪检测血清钙、磷、碱性磷酸酶、肌酐、尿素氮及糖化血红蛋白.采用双能X射线骨密度仪测定正位L_(2～4)的骨密度.观察受试者骨密度、骨保护素水平及其与各指标的多元回归相关分析.结果与结论:糖尿病肾病患者血清骨保护素水平明显高于健康对照人群(P<0.05),肾脏轻,中,重度损伤组、肾衰竭组患者骨密度明显低于健康对照人群(P<0.05,P<0.01,P<0.001).总体来说,肾功能越差,骨保护素水平越高,骨密度越低.糖尿病肾病患者骨保护素水平与骨密度呈负相关(R=-0.497,P<0.01),与糖尿病病程(r=0.566,P<0.01)、血清肌酐水平(r=0.772,P<0.01)、尿素氮水平(r=0.708,P<0.01)、磷水平(r=0.329,P<0.01)、全段甲状旁腺激素水平(r=0.702,P<0.01)呈正相关,与血清钙水平呈负相关(r=-0.505,P<0.01).提示糖尿病肾病过程中随肾脏功能的恶化,骨保护素水平升高,骨密度降低,骨保护素水平与骨密度呈负相关,与糖尿病病程、血清肌酐水平、尿素氮水平、磷水平、全段甲状旁腺激素水平呈正相关,与血清钙水平呈负相关.     

维持性血液透析的CKD合并SHPT患者甲状旁腺次全切除术后骨密度变化

目的 评估合并继发甲状旁腺功能亢进（SHPT）的慢性肾脏病（CKD）维持性血液透析患者甲状旁腺次全切除术后骨密度变化。方法 收集CKD血液透析后因合并SHPT接受甲状旁腺次全切除术的33例患者（手术组）和37例单纯药物治疗的同类患者（药物组）的临床资料。所有患者治疗前后均接受胸部CT扫描,以胸骨为测量位置,观察CT测量的骨钙积分变化,比较2组血钙、血磷、甲状旁腺激素以及骨密度等数据,分析手术与否和骨密度变化的关系。结果 手术组治疗前后血钙、血磷、甲状旁腺激素以及骨密度差异有统计学意义（P均< 0.05）,骨密度升高;药物组治疗前后血钙、血磷、甲状旁腺激素以及骨密度差异无统计学意义（P均> 0.05）。控制了年龄因素后,手术与否和骨密度变化存在相关性（P < 0.05）。结论 对血液透析后出现SHPT的CKD患者实施甲状旁腺次全切除术有助于改善其骨密度。     

Serum osteoprotegerin levels in patients after liver transplantation and correlation to bone turnover,bone mineral density and fracture status

The aim of this cross sectional study was to evaluate the prevalence of osteoporosis, vertebral fracture status and possible risk factors of bone loss including serum osteoprotegerin, a novel key regulator of osteoclast proliferation and activity in the posttransplantation period. We investigated 15 patients (10 male, 5 female) 20 +/- 6 (SE) months after orthotopic liver transplantation (OLT). All patients received immunosuppressive therapy and non were on calcium and/or vitamin D supplements at the time of admission to our osteoporosis outpatient clinic. Examinations included a bone densitometry measurement at the femoral neck, a standardized spinal X-ray and a morning blood sample. According to WHO criteria, osteoporosis at the femoral neck was present in 67% (10/15) of the patients with a mean T-score of -2.55 +/- 0.35. Vertebral fractures were seen in 33% and the mean number of fractures was 2.4 per patient. Secondary hyperparathyroidism (33%), vitamin D deficiency (53%) as well as impaired renal function (47%) were frequent findings in the patients. Low serum calcium was associated with elevated PTH- (r = -0.75, p = 0.001), serum cross laps- (r = -0.61, p = 0.01), osteocalcin levels (r = -0.49, p = 0.05), was an independent predictor of femoral neck bone mass (r = 0.57, p = 0.02) and accounted for 36% of this variance. Similarly, serum magnesium levels were also independently correlated to femoral neck Z-scores (r = -0.68, p = 0.0005). Two-thirds of the patients had elevated serum cross-laps, osteocalcin and bone specific alkaline phosphatase levels reflecting increased bone turnover. Serum osteoprotegerin (OPG) in liver transplant recipients was not significantly different when compared to healthy, matched controls (84.7 +/- 6.6 vs. 97.3 +/- 9.4 pg/ml, p = 0.50) and similar when fractured/non-fractured or osteoporotic/non-osteoporotic patients were compared. Serum OPG was, however, significantly correlated to serum cross laps (r = 0.71, p = 0.003), osteocalcin (r = 0.63, p = 0.01), serum parathyroid hormone (r = 0.61, p = 0.01) and serum creatinine levels (r = 0.53, p = 0.04) and showed only a weak and non-significant correlation to femoral neck Z-scores (r = -0.38, p = 0.16). Multiple regression analysis revealed that serum OPG was correlated independently of PTH, serum calcium and creatinine to serum cross-laps concentrations (r = 0.63, p = 0.04). In summary, we found a high prevalence of osteoporosis and vertebral fractures in liver transplant recipients with many of the patients showing evidence of vitamin D deficiency, secondary hyperparathyroidism and accelerated bone turnover. We conclude that secondary hyperparathyroidism and possibly serum magnesium seems to contribute significantly to the changes in bone mass during the posttransplantation period. Serum OPG was not correlated to bone mass or fracture status in this cross sectional setting but was elevated together with other bone resorption and -formation markers.     

Relationship between bone mineral density and biochemical markers of bone turnover in hemodialysis patients

End-stage renal disease is closely associated with changes in bone and mineral metabolism. In recent times, osteoporosis has become important among hemodialysis (HD) patients. In this study, the investigators sought to evaluate the relationship between bone mineral density (BMD) and biochemical markers of bone turnover among HD patients. A total of 70 uremic patients on a maintenance HD program for at least 1 y were enrolled in the study. All patients were treated with conventional bicarbonated HD for 5 h through the use of low-flux hollow-fiber dialyzers. Bone densitometry was measured by dual energy x-ray absorptiometry in the lumbar spine (LS) and the femoral neck (FN). BMD was classified according to World Health Organization criteria on the basis of BMD T scores. Biochemical bone turnover markers such as calcium, phosphorus, ionized calcium, intact parathyroid hormone, alkaline phosphatase, plasma bicarbonate, blood pH, serum albumin, and hematocrit levels were measured before the HD session in the morning. Male patients (n=37; 52.9%; mean age, 46.2+/-17.0 y) were assigned to a single study group, and female patients (n=33; 47.1%; mean age, 44.0+/-13.1 y) to another. Mean duration of HD treatment was 33.7+/-28.5 mo in females and 33.0+/-26.0 mo in males. Among all patients, BMD T scores in the osteopenia/osteoporosis range were observed at the LS in 58 patients (82.8%) and at the FN in 45 patients (64.3%). According to BMD measurements in FN T score, 10% of patients (n=7) were osteoporotic, 54.3% (n=38), osteopenic, and 35.7% (n=25), normal. On the other hand, in LS T score, the results were 47.1% (n=33) osteoporotic, 35.7% (n=25), osteopenic, and 17.1% (n=12), normal. No statistically significant association was found in osteopenia/osteoporosis between sexes according to FN and LS T score (P=.542, P=.267, respectively). No significant relationship was noted between BMD and biochemical markers of bone turnover. A positive correlation was found between FN T scores of BMD and age (r=.413, P=.000). BMD T scores within the range of scores for osteopenia/osteoporosis were observed in 78.5% of patients at the LS and in 58.5% of patients at the FN. The investigators concluded that no correlation could be found between markers of bone turnover and bone mass measurements in both skeletal regions. LS T score results were worse than FN T score results. Elevated alkaline phosphastase levels combined with high intact parathyroid hormone levels are predictive of renal osteodystrophy but not of adynamic bone disease/osteoporosis.     

Association between bone mineral density and arterial stiffness in hypertensive patients

Hypertension and osteoporosis are two common diseases in the elderly population. Recently, reduced bone mineral density has been found in hypertensive patients compared with healthy controls. Reduced bone mineral density is associated with increased arterial stiffness in chronic dialysis patients and healthy postmenopausal women. However, relationships between bone mineral density and arterial stiffness in hypertensive patients have not been fully assessed. We examined the relationships between bone mineral density and both arterial stiffness and nutritional status in 52 hypertensive patients (27 male and 25 female subjects; mean age 71±8 years) who had been treated with antihypertensive drugs for at least one year. The bone mineral density of the calcaneus was measured with a quantitative ultrasound measurement device, and the stiffness index was determined as a parameter of the bone mineral density. We measured the cardio-ankle vascular index (CAVI) to assess arterial stiffness and used the serum albumin to assess nutritional status. Increased arterial stiffness as assessed with CAVI is associated with reduced bone mineral density (r=-0.289, p=0.038). However, the correlation between CAVI and bone mineral density is not as strong as the correlation between serum albumin and bone mineral density (r=0.501, p<0.001). In conclusion, nutritional status is an important indicator of bone mineral density in hypertensive patients. Moreover, increased arterial stiffness is associated with reduced bone mineral density in hypertensive patients. Therefore, hypertensive patients with increased arterial stiffness may have a high risk of bone fracture due to osteoporosis.     

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水

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。护骨素綦凶是骨质疏松症发病中的晕要候选摹闲。目的：探讨护骨索基因T245G多念性与骨密度的相关性。方法：选取2008-09／2010-04往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测序榆测护骨素基因T245G多态件,使用-烈能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。旨密度。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等化基凶频率分布差异无显苫性意义（P〉0.05）。在老年男性中,GG和TG基凶型具仃较高的腰椎骨密度,而TT基吲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问差异无显著件意义（P〉0.05）。北绝经后女性中,T245G多念性与骨密度无关,说明护骨索基凶与老年男性腰椎骨密度仃关。     

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.     

北京地区汉族妇女绝经前后护骨素基因多态性与骨密度的关系

背景：原发性骨质疏松症是多基因遗传性疾病，但是调节骨量的基因需进一步研究。目的：探讨护骨素基因启动子区基因多态性与中国北京地区绝经前后妇女骨密度之间的关系。设计：前瞻性调查研究。单位：北京协和医院。对象：选择2002—07在北京协和医院健康体检的495名北京地区无亲缘关系的汉族妇女，其中绝经前妇女为306名，年龄20-39岁，绝经后妇女（指自然停经1年以上者）为189名，年龄50-84岁。所有受试对象均对检测项目知情同意。方法：①骨密度测量：应用双能X线骨密度测量方法，观察对象均采取仰卧位，采用骨密度仪测量其后前位第1-4腰椎及股骨近端，包括股骨颈、ward’s三角和大转子部位的骨密度值。②基因分型：提取两组受试对象外周血DNA，初步确定护骨素基因分型。并取部分PCR产物送上海博亚有限公司测序，验证基因型，观察两组受试对象护骨素基因型的分布频率及其与骨密度的关系，并用Logistic回归作病因学进一步分析观察绝经后妇女护骨素基因多态性与骨质疏松的关系。主要观察指标：①两组受试对象护骨素基因型的分布频率，及其与骨密度的关系。②绝经后妇女护骨素基因多态性与骨质疏松的关系。结果：纳入受试对象495名，全部进入结果分析。①两组受试对象OPG基因型和等位基因分布频率无明显差异，两组总体基因型分布频率依次为163A→G位点，AA型为70．1％，AG型为26．9％，GG型为3．0％；245T→G位点TT型为71．3％，TG型为25．9％，GG型为2．8％。绝经前妇女在163A→G位点，AA组在L2-4股骨颈、ward’s三角和大转子的骨密度低于GG＋AG组，在245T→G位点，TT组与GG＋TG组相比各部位的骨密度也低，但均无统计学差异（P〉0．05）。绝经后妇女163位点AG＋GG组在L2-4股骨颈、Ward’s三角和大转子的骨密度均显著低于AA组（P〈0．05）；245位点TG＋GG组在股骨颈、Ward’s三角和大转子的骨密度显著低于TT组（P〈0．05）。②绝经后妇女163位点AG＋GG组在L2-4、Ward’s三角是骨质疏松的危险因素（OR=2．045，2．956，P〈0．05，95％可信限1．05—6．7），245位点TG＋GG组在L2-4、Ward’s三角、大转子是骨质疏松的危险因素（OR=2．059，2．859，2．123，P〈0．05，95％可信限1．04—6．5）。结论：北京地区绝经后妇女护骨素基因启动子区的163和245位点为变异型G等位基因时，股骨颈、Ward’s三角和大转子的骨密度较低，变异型G等位基因与绝经后妇女骨密度降低相关。     

北京地区汉族妇女绝经前后护骨素基因多态性与骨密度的关系

背景:原发性骨质疏松症是多基因遗传性疾病,但是调节骨量的基因需进一步研究。目的:探讨护骨素基因启动子区基因多态性与中国北京地区绝经前后妇女骨密度之间的关系。设计:前瞻性调查研究。单位:北京协和医院。对象:选择2002-07在北京协和医院健康体检的495名北京地区无亲缘关系的汉族妇女,其中绝经前妇女为306名,年龄20～39岁,绝经后妇女(指自然停经1年以上者)为189名,年龄50～84岁。所有受试对象均对检测项目知情同意。方法:①骨密度测量:应用双能X线骨密度测量方法,观察对象均采取仰卧位,采用骨密度仪测量其后前位第1～4腰椎及股骨近端,包括股骨颈、Ward’s三角和大转子部位的骨密度值。②基因分型:提取两组受试对象外周血DNA,初步确定护骨素基因分型。并取部分PCR产物送上海博亚有限公司测序,验证基因型,观察两组受试对象护骨素基因型的分布频率及其与骨密度的关系,并用Logistic回归作病因学进一步分析观察绝经后妇女护骨素基因多态性与骨质疏松的关系。主要观察指标:①两组受试对象护骨素基因型的分布频率,及其与骨密度的关系。②绝经后妇女护骨素基因多态性与骨质疏松的关系。结果:纳入受试对象495名,全部进入结果分析。①两组受试对象OPG基因型和等位基因分布频率无明显差异,两组总体基因型分布频率依次为163A→G位点,AA型为70.1%,AG型为26.9%,GG型为3.0%;245T→G位点TT型为71.3%,TG型为25.9%,GG型为2.8%。绝经前妇女在163A→G位点,AA组在L2-4、股骨颈、Ward’s三角和大转子的骨密度低于GG AG组,在245T→G位点,TT组与GG TG组相比各部位的骨密度也低,但均无统计学差异(P>0.05)。绝经后妇女163位点AG GG组在L2-4、股骨颈、Ward’s三角和大转子的骨密度均显著低于AA组(P<0.05);245位点TG GG组在股骨颈、Ward’s三角和大转子的骨密度显著低于TT组(P<0.05)。②绝经后妇女163位点AG GG组在L2-4、Ward’s三角是骨质疏松的危险因素(OR=2.045,2.956,P<0.05,95%可信限1.05-6.7),245位点TG GG组在L2-4、Ward’s三角、大转子是骨质疏松的危险因素(OR=2.059,2.859,2.123,P<0.05,95%可信限1.04-6.5)。结论:北京地区绝经后妇女护骨素基因启动子区的163和245位点为变异型G等位基因时,股骨颈、Ward’s三角和大转子的骨密度较低,变异型G等位基因与绝经后妇女骨密度降低相关。     

老年维持性血液透析患者骨密度改变临床研究

目的:探讨老年维持性血液透析患者骨密度变化特点。方法:维持性血液透析老年患者40例为透析组,同期老年健康体检者40例为对照组。采用双能X线骨密度仪测量2组腰椎(L1-4)及左侧股骨骨密度,同时检测2组血钙、血磷及透析组甲状旁腺素等指标。结果:血液透析患者股骨颈骨密度及股骨大转子密度均低于对照组(P<0.05),而腰椎骨密度比较差异无统计学意义(P>0.05);透析组血钙及血磷浓度以及及骨折发生率均高于对照组(P<0.05);透析组中骨质疏松患者透析时间较非骨质疏松患者长(P<0.05),血钙、血磷高于非骨质疏松者(P<0.05),甲状旁腺素水平较非骨质疏松者低(P<0.05)。结论:老年维持性血液透析患者骨密度下降以皮质骨明显,多不伴有低钙血症但甲状旁腺素水平偏低。     

老年维持性血液透析患者骨密度改变临床研究

目的:探讨老年维持性血液透析患者骨密度变化特点.方法:维持性血液透析老年患者40例为透析组,同期老年健康体检者40例为对照组.采用双能X线骨密度仪测量2组腰椎(L1-4)及左侧股骨骨密度,同时检测2组血钙、血磷及透析组甲状旁腺素等指标.结果:血液透析患者股骨颈骨密度及股骨大转子密度均低于对照组(P<0.05),而腰椎骨密度比较差异无统计学意叉(P>0.05);透析组血钙及血磷浓度以及及骨折发生率均高于对照组(P<0.05);透析组中骨质疏松患者透析时间较非骨质疏松患者长(P<0.05),血钙、血磷高于非骨质疏松者(P<0.05),甲状旁腺素水平较非骨质疏松者低(P<0.05).结论:老年维持性血液透析患者骨密度下降以皮质骨明显,多不伴有低钙血症但甲状旁腺素水平偏低.     

老年患者骨密度与血尿酸相关性分析

目的研究老年患者骨密度与血尿酸的相关性。方法回顾性研究136例老年医学科住院患者,采用双能X线吸收检测法(DXA)进行骨密度(BMD)检测。根据骨密度结果分为:骨质疏松组60例,骨量减少组56例,骨量正常组20例。并检测所有患者血尿酸(UA)水平。结果三组骨密度水平差异有统计学意义(F=106.567,P<0.001);三组血尿酸水平差异有统计学意义(F=5.821,P=0.004);骨质疏松组、骨量减少组及骨量正常组血尿酸水平依次升高,骨密度与血尿酸水平呈现正相关(r=0.273,P=0.001)。结论较高的血尿酸水平可能对老年人骨密度具有保护作用。     

去势大鼠血清血管内皮生长因子水平和骨密度的相关性*

背景：血管内皮生长因子在促进骨质疏松性骨折愈合中发挥重要作用,而它是否影响骨密度变化还没明确。目的：观察去势大鼠血清血管内皮生长因子水平和骨密度及成骨细胞变化的相关性。方法：SD 雌性大鼠40只随机数字表法均分为去势组和对照组,3个月后测大鼠全身、腰椎及股骨骨密度。大鼠 ELISA 试剂盒测血清中血管内皮生长因子的水平,同时两组大鼠股骨干骺端固定,脱钙,脱水、石蜡包埋、切片,苏木精-伊红染色,每切张片随意取5个视野(10×40)行股骨远侧干骺端成骨细胞计数在光学显微镜。结果与结论：去势3个月后大鼠体质量明显增加(P <0.05),去势组全身、腰椎及股骨骨密度较对照组全身、腰椎及股骨骨密度降低(P <0.05),表明骨质疏松的模型建立。而去势大鼠和对照大鼠血管内皮生长因子水平比较差异无显著性意义(P >0.05),去势组及对照组的成骨细胞数量无明显差异(P >0.05),去势组及对照组骨密度与成骨细胞数及血清血管内皮生子水平无相关性。提示去势大鼠的骨密度下降,体质量升高,而去势大鼠骨密度的降低与血清血管内皮生长因子变化可能无关。     

Increased levels of osteoprotegerin in hemodialysis patients.

Recently identified soluble circulating osteoprotegerin (OPG), a member of tumor necrosis factor receptor family, is the osteoclastogenesis inhibitory factor (OCIF). It acts as a "decoy" receptor for receptor activator of NF-kappaB ligand (RANKL) and antagonises RANKL/RANK activity. This way OPG exerts the protective effect on bone, which is also important in hyperparathyroidism. The studies measuring OPG levels in secondary hyperparathyroidism have shown contradictory results and inconsistent conclusions. The aim of our work was to evaluate OPG levels in hemodialysis patients and their correlation with the intensity of bone turnover, bone formation and bone resorption. Serum OPG levels, bone alkaline phosphatase activity (bALP) and beta-CrossLaps (CTx) were measured in a control group (n = 20, age 30+/-6.7 years) and in two groups of dialysis patients: the first group with serum intact parathyroid hormone (iPTH) concentration below 200 pg/ml (n = 28, age 62.6+/-14.8 years) and the second group with iPTH concentration above 200 pg/ml (n = 16, age 63.7+/-14.8 years). Compared to controls, serum OPG levels were 6.4-fold higher in dialysis patients. OPG levels in patients with high PTH were approximately 1.2-fold higher than in the low-PTH group. OPG correlated weakly with bALP (r = 0.277, p = 0.153), as well as with CTx (r = 0.018, p = 0.929) in the low-PTH group, and there was an insignificant negative correlation in the high-PTH group (r = -0.145, p = 0.593 and r = -0.219, p = 0.416, respectively). In conclusion, 6.4-fold increase in OPG might protect bone against intensive bone loss in hemodialysis patients, but this increase is probably not mediated by the increased bone formation; rather, it seems to be the consequence of the imbalance of bone kinetics in renal disease. The precise role of OPG in the pathogenesis of renal osteodystrophy remains unknown and establishing it requires further studies.     

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。     

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.     

瘦素水平与绝经后2型糖尿病患者骨密度的关系

目的:分析绝经后2型糖尿病患者瘦素水平与骨代谢变化的关系。方法:选取2004-01/2006-01上海市杨浦区中心医院收治的80例2型糖尿病住院患者,符合WHO1999年糖尿病诊断标准,均为绝经后女性,年龄60～80岁,对本实验知情同意。排除标准:雌激素替代治疗者、使用糖皮质激素及影响钙磷代谢药物者、有胃肠手术史者、其他内分泌疾病患者。记录患者年龄、糖尿病病程、绝经年限、体质量指数。氧化酶法测定空腹血糖,微柱亲和层析法测定糖化血红蛋白。ELISA法测定瘦素水平。采用法国UPIS3000型定量骨超声测定仪将专用探头置于被检者右足跟部,测定其跟骨超声传导速度、振幅衰减,计算骨硬度指数。骨硬度指数=0.67×振幅衰减 0.28×跟骨超声传导速度-383。对跟骨定量超声指标、一般指标、瘦素水平进行直线相关分析。结果:80例绝经后2型糖尿病患者全部进入结果分析。振幅衰减、跟骨超声传导速度、骨硬度指数与患者年龄(r=-0.342～-0.298,P均<0.01)、病程(r=-0.341～-0.309,P均<0.01)、绝经年限(r=-0.318～-0.289,P均<0.01)、糖化血红蛋白(r=-0.308～-0.273,P<0.05或0.01)呈显著负相关;与瘦素水平(r=0.336～0.528,P均<0.01)、体质量指数(r=0.302～0.353,P均<0.01)呈显著正相关。校正年龄、病程、绝经年限、体质量指数等影响因素后,振幅衰减、跟骨超声传导速度、骨硬度指数仍与瘦素水平呈显著正相关(R2=0.498～0.546,P均<0.01)。结论:2型糖尿病患者糖代谢异常与其骨质疏松发生有关,高瘦素水平和高体质指数对骨代谢有明显的保护作用。     

降钙素受体基因多态性与骨密度的相关性

目的:就近几年对降钙素受体基因多态性与骨密度相关性方面的研究进行综述。详细地分析了降钙素受体基因突变对骨密度的影响,从而为鉴定骨质疏松高危人群提供依据。资料来源:应用计算机检索Medline、springerlink和ScienceDirect Online数据库1980-01/2007-01期间的相关文章,检索词为"降钙素受体、基因多态性、骨质疏松、骨密度、候选基因"限定文章语言种类为英文。同时计算机检索中国期刊全文数据库1990-01/2007-01期间的相关文章,检索词为"降钙素受体,基因多态性,骨质疏松,骨密度",限定文章语言种类为中文。资料选择:对资料进行初审,选择关于降钙素受体基因多态性与骨密度相关性文献79篇,筛除明显缺少对照的实验研究,并对剩余原文查找全文,排除综述类和重复研究。资料提炼:选择其中有代表性的31篇进行综述,涉及到降钙素和降钙素受体的作用机制及基因多态性、降钙素受体基因多态性与骨密度相关性方面的研究。47篇被排除的文章中,44篇缺少随机对照或重复研究,另3篇是综述。资料综合:对所选文章内容进行总结。对降钙素受体基因多态性与骨密度相关性方面的资料进行概括和评价,对降钙素受体基因型在正常与骨质疏松组进行比较。计算不同基因型在人体测量指标、脊柱及股骨骨密度等方面的差异。通过这些数据分析,降钙素基因多态性在预测骨质疏松方面的潜在价值仍很有争议。结论:分析降钙素受体基因多态性与骨质疏松相关性有很重要的临床价值。对骨量的基因调控方面的研究有几个潜在的价值:通过认证哪些基因对骨质疏松的发病有作用,可能会改善治疗方法,实际上一些候选基因本身成为新治疗的靶点;分子标志在认证个体在骨质疏松发病风险方面的潜在价值同样很重要。降钙素受体基因多态性与骨质疏松相关性的基因研究方面的重要成果会对认证这种疾病的高危人群起到促进作用。