中老年高血压患者使用培哚普利治疗3年对骨密度及骨代谢指标的影响

目的探索中老年高血压患者使用培哚普利治疗3年对骨密度及骨代谢指标的影响。方法 138例老年高血压并骨质疏松患者随机分为治疗组(n=69)和对照组(n=69)。治疗组患者给予培哚普利治疗,对照组给予苯磺酸左旋氯氨地平片治疗。治疗3年,测定治疗前及治疗后36个月的血清Ⅰ型胶原交联C末端肽(CTX),抗酒石酸酸性磷酸酶(TRAP)和骨特异性碱性磷酸酶(BALP)和骨密度值(腰椎L_(1-4)及股骨粗隆、左侧股骨颈、Ward三角区)的水平。结果治疗后3年后,两组BALP及腰椎L_(1-4)及股骨粗隆、左侧股骨颈、Ward三角区BMD水平显著升高,而CTX和TRAP水平显著降低(P0. 05);而治疗组治疗后BALP、s-CTX、TRAPL及腰椎L_(1-4)及股骨粗隆、左侧股骨颈、Ward三角区BMD水平改变显著优于对照组(P0. 05)。结论长期培哚普利治疗对高血压合并骨质疏松患者的骨密度和骨代谢有一定的疗效。     

Ward三角区再研究

目的深入研究Ward三角区骨密度的临床意义。方法采用美国Norland XR-600双能X线骨密度仪,通过测定1189例病人的左股骨近端骨密度,评估计算机自动生成的Ward三角区的特点;通过测定30例志愿者左右股骨近端骨密度,评估不同肢体侧别的骨密度是否存在差异;通过对72例随访病人3~6月内进行左股骨近端骨密度测定,观察Ward三角区骨密度在较短时间内随时间的变化规律及临床特点。结果 1Ward三角区由计算机根据骨密度最低值自动搜索形成,大部分受试者(86.7%)Ward三角区位于股骨颈底边附近,少部分受试者(5.2%)位于股骨颈外,以大粗隆最为常见,与解剖位置不完全对应;2部分受试者(8.7%)Ward三角区骨密度并非股骨上段最低值,最低值出现在大粗隆。3计算机自动生成的Ward三角区小方块前后两次位置无明显变化。4Ward三角区骨密度值的精确度误差(2.27%)大于股骨颈(1.05%)及大粗隆(1.57%)。5正常人双髋骨密度无显著性差异(P=0.32,P0.05)。672例随访患者Ward三角区的骨密度(BMD)变化先于股骨颈及正位腰椎出现。结论髋关节采用标准体位摆放,Ward三角区位置较为固定,可用于临床随访。     

强直性脊柱炎患者血清骨保护素、骨密度、骨代谢生化指标的研究

目的检测强直性脊柱炎(AS)患者血清骨保护素(OPG)、骨代谢指标及骨密度并观察AS患者临床症状、体征、病情活动指标,探讨OPG与AS的关系及与AS骨代谢指标、骨密度的相关性。方法应用酶联免疫法(ELISA)、放射免疫法检测100例AS患者及100例同期健康体检者血清OPG、骨钙素(BGP)、骨碱性磷酸酶(BALP)、Ⅰ型胶原羧基端延长肽(CICP)、Ⅰ型胶原交联C末端肽(CTX)及尿脱氧吡啶啉(DPD)水平。应用双能X线(DEXA)法检测健康对照组与AS患者腰椎、股骨颈、股骨粗隆骨密度,并评价AS患者的BATH功能指数(BASFI)、病情活动指数(BASDAI)、患者总体评价(PGA)、脊柱炎症、脊柱痛及枕墙距、指地距、颌柄距、胸廓活动度、脊柱活动度、Schober试验,对AS患者的血清OPG水平与其他骨代谢指标、骨密度、临床症状、体征指标进行相关性分析。结果AS患者中骨质疏松者35人(35%),骨量减少者42人(42%),AS患者血清OPG、CTX及尿DPD较健康对照组显著增高(P0.05、P0.001、P0.001),AS患者的腰椎、股骨颈、股骨粗隆骨密度较健康对照组显著降低(P0.01、P0.01、P0.01),OPG水平与AS患者各部位的骨密度呈负相关趋势,但无统计学差异。与其他临床指标及骨代谢指标无显著相关性。结论AS患者比健康对照组更易出现骨质疏松和骨量减少,AS患者的骨吸收增强,血清OPG水平增高,其增高原因可能是机体对抗过度骨吸收的保护性反应。     

抗阻力量训练对青年和老年女性骨密度的影响

目的探讨相同负荷强度的抗阻力量训练对青年和老年女性骨密度的影响。方法身高、体重相匹配的青年组(n=36)和老年组(n=34)进行16w躯干、上下肢的抗阻力量训练。测试受试者腰椎(L_2~L_4)、股骨近端(股骨颈、Ward三角区、大转子)骨密度,拉力和下肢肌力。结果 (1)(3)干预后青年组股骨颈、Ward三角区和腰椎(L_2~L_4)BMD和拉力显著增大(P0.05),大转子BMD无显著变化;老年组股骨颈、Ward三角区和腰椎(L_2~L_4)BMD、拉力和下肢肌力显著增大(P0.05),大转子BMD无显著变化。(2)拉力与腰椎(L_2~L_4)、股骨颈、Ward三角区和大转子BMD呈显著正相关(r=0.642、0.686、0.600、0.781)、下肢肌力与腰椎(L_2~L_4)和Ward三角区BMD呈显著正相关(r=0.526,r=0.619)。结论 16 w力量训练改善了青年和老年女性腰椎和股骨近端的骨密度且无年龄差异,但对大转子骨密度改善不显著。     

DEXA在诊断糖尿病骨质疏松中的价值

本文测定１４９例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者腰椎（Ｌ１～Ｌ４）及股骨上端（股骨颈、Ｗａｒｄ三角、股骨粗隆）骨密度，结果显示，不论男女患者＞４０岁以上各年龄组骨密度均低于正常对照组，提示糖尿病患者有骨量减少。腰椎及股骨上端相关分析表明腰椎（Ｌ１～Ｌ４）各椎体之间相关非常显著（Ｐ＜０．００１），提示腰椎各椎体骨密度丢失速度一致；腰椎与股骨颈、Ｗａｒｄ三角、股骨粗隆相关显著（Ｐ＜０．０１），但相对较小，股骨上端Ｗａｒｄ三角区骨密度减低最为显著。因此，股骨上端骨密度检测优于腰椎，一旦Ｗａｒｄ三角区骨密度降低至２．０ＳＤ以下时，即应做出骨质疏松的诊断。     

脊柱结核与骨量减低相关研究

背景：脊柱结核是骨结核中最常见的类型。近年来,老年性脊柱结核的发病率逐渐升高,甚至伴发骨质疏松。而结核病是否会引起患者骨量减低的研究相对较少。目的：通过对脊柱结核患者和健康正常人群的骨密度及骨生化指标的分析比较,探讨脊柱结核与骨量减低的相关性。方法：本研究纳入110例脊柱结核患者和98例健康正常人。双光能X线骨密度仪测定正位腰椎（L3-L4）及左股骨颈、股骨大转子、Ward角、整体髋的骨密度;电化学发光免疫分析法检测骨碱性磷酸酶（BAP）、骨钙素（BGP）、I型胶原羧基端前肽（CTX）。结果：两组间性别、年龄差异无统计学意义（P〉0．05）。脊柱结核组腰椎及左侧股骨颈、股骨大转子、Ward三角、整体髋骨密度低于对照组（P〈0．05）,且脊柱结核组骨量减少、骨质疏松发生率较对照组显著增高（P〈0．05）;在骨生化指标方面,脊柱结核组CTX水平高于对照组（P〈0．05）。脊柱结核患者腰椎及左侧股骨颈、股骨大转子、Ward三角、整体髋骨密度与CTX水平呈负相关（P〈O．05）。结论：脊柱结核可能会导致骨量减少,其发生与破骨细胞活性增强,促进骨吸收有关;骨质疏松预防性治疗可减少脊柱结核术后并发症的发生。     

探讨体重指数对绝经后老年妇女不同部位骨密度的影响

目的分析不同体重指数患者的腰椎和股骨近端、股骨颈、Ward’s三角区的骨密度及T值评分,探讨体重指数对绝经老年妇女不同部位骨密度的影响。方法以我院225例年龄均为60以上的绝经老年妇女为研究对象,计算体重指数将患者分为体瘦组、正常组和肥胖组,检测患者腰椎和股骨近端、股骨颈、Ward’s三角区的骨密度,分析各部位骨密度变化与体重指数的关系。结果体瘦组的患者各部位骨密度明显低于正常和肥胖组的患者,体瘦组与正常组或肥胖组比较,腰椎(L1～L4)、股骨颈、股骨近端、Ward’s三角区的骨密度均有显著的差异(P<0.01);正常组与肥胖组比较,仅L3和L4的骨密度有显著的差异(P<0.05),其余部位的骨密度无显著的差异(P>0.05)。结论体重和体重指数是影响骨密度的一个重要因素,体重和体重指数与绝经老年妇女不同部位的骨密度存在一定的相关性,低体重指数的绝经老年妇女,骨丢失而引起的骨量减少明显,易发生骨质疏松。     

老年股骨颈骨折骨密度、Singh指数的研究

目的研究骨密度和Singh指数在衡量股骨近端骨强度和预测股骨颈骨折中的意义.方法对21名60岁以上、因轻度创伤所致新鲜股骨颈骨折老年人进行股骨近端骨密度、Singh指数及Ward三角矿化骨体积进行测量.结果本组患者股骨近端骨密度减少规律,Ward三角>股骨颈>股骨粗隆,骨密度减少的下限(±s)是股骨颈1.14SD、粗隆部0.35SD、Ward三角2.04SD;Singh指数4级以下(含4级)20名(95.2%);Singh指数与MBV呈正相关(r=0.517P<0.05),与粗隆部骨密度及减少的标准差呈正相关(r=0.457,0.474P<0.05).结论骨密度较峰值骨量减少的标准差数在股骨颈大于1.14、粗隆部大于0.35、Ward三角大于2.04,加上Singh指数低于4级(含4级)提示股骨颈骨折的危险性明显增高.     

105例Ⅱ型糖尿病患者骨密度变化的分析

目的 研究Ⅱ型糖尿病患骨密度的变化规律和临床特点，更深入了解糖尿病对骨代谢的影响。方法 使用双能X线骨密度测定仪测定105例Ⅱ型糖尿病患腰椎L1～L4、Ward’s三角区、股骨颈、股骨大转子区的骨密度(BMD)，并以同年龄、同性别的健康的骨密度比较，研究其骨密度的变化规律和临床特点。结果 ①女性Ⅱ型糖尿病患BMD测定值与同年龄对照组比较差异无显性。②男性Ⅱ型糖尿病患BMD测定值除了51～60岁年龄组差异有显性外，61岁以上年龄组差异无显性。③男性Ⅱ型糖尿病患BMD测定值明显高于同年龄的女性。各年龄组Ward’s三角区BMD测定值明显低于腰椎和股骨颈及股骨大转子区。结论 ①雌激素水平下降是绝经后妇女骨质疏松的主要原因。②Ⅱ型糖尿病能使部分老年患易患有骨质疏松症。③骨质疏松患最早出现骨密度改变在Ward’s三角区。     

福州地区绝经后妇女骨钙素基因Hind Ⅲ多态性与骨密度的关系

目的 探讨绝经后妇女骨钙素基因(OC)Hind Ⅲ多态性与骨密度的关系.方法 用双能X线骨密度仪检测247例绝经后妇女的腰椎、股骨颈、大转子和Wards三角骨密度,应用PCR-RFLP技术检测OC基因Hind Ⅲ多态性.结果 ①OC基因型分布频率为HH型4.9%,hh型49%,Hh型46.1%.等位基因频率为H 27.94%,h 72.06%,基因型分布符合Hardy-Weinberg定律.②HH基因型与hh型在股骨颈、大转子、Wards三角区骨密度有显著性差异(P<0.05);HH基因型与Hh型在大转子、Wards三角区骨密度也有显著性差异(P<0.05).③有h等位基因的股骨颈、大转子、Wards三角区骨密度显著低于无h等位基因(P<0.05).结论 福州地区绝经后妇女OC基因多态性与骨密度存在相关性,有h等位基因绝经后妇女在股骨颈、大转子、Wards三角区有低骨密度风险.     

强直性脊柱炎患者血清TNF-a、BGP和CTX水平与骨密度的关系

目的探讨强直性脊柱炎(AS)患者骨质疏松(OP)的发病机制。方法分别测定36例男性AS患者血清肿瘤坏死因子-a(TNF-a)、骨钙素(BGP)I、-型胶原C末端肽(CTX)水平及腰椎和股骨颈的骨密度(BMD)值,并与20例健康者对照。结果AS早期腰椎和股骨颈BMD均低于对照组,晚期股骨颈BMD更低于对照组。AS血清TNF-a、CTX水平较对照组显著增高(P<0.01;P<0.05),而血清BGP水平较对照组无显著差差异(P>0.05)。AS患者中OP组TNF-a、CTX水平较NOP组显著增高(P<0.01;P<0.05),OP组中血清TNF-a与CTX呈正相关,与股骨颈密度呈负相关;与BGP无明显相关性。结论AS患者主要是由于骨吸收增加而导致骨质疏松的发生。血清TNF-α水平的增高可促进骨吸收加强,是AS骨质疏松的重要原因之一。降低血清TNF-a水平,对AS患者骨质疏松的防治可能有积极的意义。     

活性维生素D对骨量减少的强直性脊柱炎患者骨代谢指标及病情的影响

目的探讨补充活性维生素D对于骨量减少的强直性脊柱炎(AS)患者骨代谢标志物、骨密度及炎性指标的影响。方法选取骨量减少的AS患者60例为研究对象,同期健康体检者20例作为健康组,比较两组受试者血清骨特异性碱性磷酸酶(BALP)、抗酒石酸酸性磷酸酶异构体-5b(TRACP-5b)、25-(OH)D3的水平。将上述AS患者随机分为治疗组和对照组,每组30例,对照组口服美洛昔康、柳氮磺吡啶、碳酸钙,治疗组在此基础上加用骨化三醇口服。比较2组治疗前后BALP、TRACP-5b、25-(OH)D3,骨密度(BMD)以及红细胞沉降率(ESR)、C反应蛋白(CRP)等指标的变化水平。结果 AS组BALP、TRACP-5b高于健康组,25-(OH)D3低于健康组(P0.05)。治疗组和对照组治疗后血清BALP、25-(OH)D3水平均有升高(P0.05),TRACP-5b水平均有下降(P0.05);治疗组BALP及25-(OH)D3治疗前后差值高于对照组(P0.05)。6个月后治疗组复查腰椎、大转子、转子间BMD较对照组均有不同程度的提升(P0.05),5例骨量恢复正常;对照组6个月后BMD变化不明显;治疗组治疗前后腰椎、大转子、转子间BMD变化差值均高于对照组(P0.05);治疗组与对照组ESR、CRP及BASDAI评分较前均有所降低(P0.05),其中治疗组ESR下降水平较对照组差异具有统计学意义(P0.05)。结论活性维生素D可以改善骨量减少的强直性脊柱炎患者的骨代谢指标并降低疾病活动度。     

强直性脊柱炎患者腰椎定量CT骨密度测定及分析

目的 测定强直性脊柱炎患者腰椎骨密度(BMD),分析骨量变化相关因素,指导治疗。方法 选取强直性脊柱炎患者66例为实验组,26例健康查体者为对照组,登记一般资料及病程、ESR、CRP、BASFI及HLA-B27等指标,应用定量CT测定腰1-5椎体BMD,进行两组间BMD比较及危险因素相关分析。结果 实验组腰椎皮质骨及松质骨BMD均显著低于对照组（269.1±39.8 vs 308.2±49.3 mg/mL,140.8±18.6 vs 190.1±15.7 mg/mL,P<0.01）,实验组腰椎松质骨BMD丢失百分率显著高于皮质骨（25.9±10.3% vs 12.7±13.2%,P<0.01）,实验组骨量减少和骨质疏松发生率分别为45.5%和39.4%。病程及骶髂关节破坏程度与骨密度负相关,身高、体重、BMI、BASFI、ESR和/或CRP是否升高及HLA-B27阳性与否均与骨密度无相关性。结论 强直性脊柱炎患者腰椎BMD显著降低,骨质疏松发生率高,应早期评估BMD,及时应用生物制剂等防治骨量丢失。     

慢性阻塞性肺疾病合并骨质疏松时肿瘤坏死因子α、白细胞介素6的表达及意义

目的观察慢性阻塞性肺疾病（chronic obstructive pulmonary diseases,COPD）患者骨密度（BMD）的变化与血清炎性细胞因子肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）的关系。方法选取稳定期COPD患者72例（COPD组）,另选匹配正常对照组60例,所有对象均测定腰椎（L2-4）的BMD、肺功能,并测定所有入选对象的血钙、血磷、血清碱性磷酸酶（ALP）、TNF-α、IL-6、骨钙素及尿吡啶啉/肌酐。结果 COPD组与对照组比较血钙、血磷、ALP差异均无统计学意义（P〉0.05）;COPD组BMD及骨钙素较对照组低,差异有统计学意义（P〈0.05或P〈0.01）,且COPD组血清TNF-α、IL-6及尿吡啶啉/肌酐较对照组高,差异有统计学意义（P〈0.05或P〈0.01）。COPD患者的血清TNF-α、IL-6水平分别与BMD及骨钙素均呈负相关（均P〈0.05）,与尿吡啶啉/肌酐呈正相关（r=0.457,P〈0.05）,而与血钙、血磷、ALP无相关性（P〉0.05）。结论 COPD患者骨吸收增加、BMD减低与炎症因子TNF-α、IL-6的增高相关,COPD的全身炎症反应可能促进骨质疏松的发生。     

118例甲亢患者骨密度及骨代谢指标的研究

目的：为探讨甲亢患者骨密度与骨代谢指标的改变。方法：本文测定了１１８例甲亢患者腰椎（Ｌ２～４）及股骨上端（Ｎｅｃｋ、Ｗａｒｄ三角、Ｔｒｏｃｈ）骨密度、血清骨钙素（ＢＧＰ）、甲状旁腺素中间片段（ＰＴＨ－ｍ）及尿脱氧吡啶啉（Ｄｐｄ）。结果：甲亢患者骨密度低于正常对照组，ｔ检验具显著差异（ｐ＜０．０１）、血清ＢＧＰ及Ｄｐｄ高于正常对照组，ｔ检验具显著差异（ｐ＜０．０１），与骨密度呈负相关ｒ＝－０．２１３５、－０．２０５０（ｐ＜０．０５）；而ＰＴＨ－ｍ低于正常对照组，与骨密度无相关性ｒ＝０．０８３０（ｐ＞０．０５）。结论：甲亢为高转换型骨质疏松，ＢＧＰ、Ｄｐｄ可作为骨形成及骨吸收的敏感指标     

慢性肝病患者血清VitD3水平与骨代谢的关系

检测了部分慢性乙型肝炎（下简称慢乙肝）及肝硬化患者的血清1，25（OH）2D3，骨钙素（BGP），甲状旁腺素（PTH），钙，磷及尺桡平均密度（BMD），并与对照组比较，结果两组患者血清1，25（OH）2D3，BGP及BMD值均明显下降，肝硬化组下降尤为显著，肝硬化组血清PTH显著升高，两组患者血钙明显降低，而血磷三组间无差异，1，5（OH）2D3水平与BGP，BMD呈显著正相关；PTH与血钙，BMD无相关性。提示慢性肝病患者存在以骨形成减少为主的骨代谢紊乱，其中血清1，25（OH）2D3减少为关键因素，PTH虽升高，但与肝病患者骨密度变化无相关。     

Vitamin D receptor initiation codon polymorphism, bone density and inflammatory activity of patients with ankylosing spondylitis

Objectives Osteoporosis is a common finding in ankylosing spondylitis (AS) and may contribute to spinal deformity and bone pain. Bone metabolism as well as inflammatory processes are influenced by the vitamin D receptor gene (VDR). We investigated initiation codon (FokI) and 3UTR (BsmI) polymorphisms of the VDR for whether there could be an association with bone mineral density (BMD) in relation to bone metabolism or inflammatory activity in patients with AS.Methods In this study, 104 patients with AS (m/w 71/33, mean age 41±12 years) were investigated for their lumbar and femoral BMD by DEXA and in part by QCT measurements and compared to 54 healthy controls. Disease activity indices, serum markers of bone metabolism and inflammation were recorded. FokI and BsmI polymorphisms of the VDR were genotyped using genomic DNA from peripheral leukocytes with present or absent restriction sites defined as alleles f and b or F and B, respectively.Results In male AS patients, FokI genotypes were significantly associated with spinal but not with femoral BMD values (P=0.01) as independent predictors of low BMD, which was also influenced by BMI, and inflammatory and pain indices. CRP and ESR values were also significantly associated with FokI genotypes. BMD in female patients showed no significant association with either FokI or BsmI genotypes of the VDR.Conclusion This is the first evidence that the VDR gene may be involved in BMD differences, bone metabolism and inflammatory processes in ankylosing spondylitis. A possible interaction of the vitamin D system, cytokines and bone could define new diagnostic and therapeutic implications in ankylosing spondylitis.     

Hyperthyroidism Influences Ultrasound Bone Measurement on the Os Calcis

The objective of our study was to compare bone mineral density (BMD) measured by dual-energy X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) parameters in women with hyperthyroidism and controls. In this cross-sectional study, QUS parameters and BMD values observed in untreated hyperthyroid patients were compared with data obtained from age-matched controls. Twenty-four women with Graves' disease were studied. Eight patients were postmenopausal. All patients had evidence of thyrotoxicosis as indicated by a raised total serum thyroxine and a suppressed serum thyroid stimulating hormone. BMD of the hip, lumbar spine and whole body, and body composition, were measured by DXA. Ultrasound evaluation on the os calcis was performed with an Achilles device. All measurements were performed before antithyroid therapy. The QUS parameters of BUA, SOS and Stiffness were significantly lower in hyperthyroid patients than in controls. Similar results were observed for the BMD of lumbar spine, femoral neck and total skeleton. Lean tissue and fat mass were also significantly decreased in hyperthyroid patients. In conclusion, these findings suggest that hyperthyroidism affects cortical and trabecular bone equally, as well as bone quality. QUS measurements may be helpful for assessing, using a simple and non-irradiating method, the bone effects of thyrotoxicosis. Received: 9 June 1997 / Accepted: 27 October 1997     

Osteoprotegerin and Bone Mass in Squamous Cell Head and Neck Cancer Patients

Osteoprotegerin (OPG) is considered one of the main regulators of bone remodeling. Various patterns of serum OPG levels have been described in different types of tumors. We undertook this study to determine serum OPG levels in patients with squamous cell head and neck cancer (SCHNC), analyzing their relationship with other metabolic bone parameters and bone mineral density (BMD), as well as the possible influence of chemotherapy. Forty male patients with localized SCHNC were studied, and their results were compared with those of 40 healthy male controls. The type of treatment followed by each patient was noted. Age, weight, height, and lifestyle habits were recorded; and OPG, Ca²⁺, intact parathyroid hormone (iPTH), 25-Hydroxyvitamin D (25OHD) and 1,25-Dihydroxyvitamin D (1,25(OH)₂D), bone alkaline phosphatase, osteocalcin, and serum C-terminal cross-links telopeptide of type I collagen (ICTP) were determined. Dual-energy X-ray absorptiometry BMD at the lumbar spine, femoral neck, and hip was also measured. Serum OPG was higher in patients than in controls (91.7 ± 25.8 vs. 77.2 ± 26.3, P = 0.02). ICTP (a bone resorption marker) was 37% higher in patients (P = 0.007). Bone mass was lower in patients at the lumbar spine, femoral neck, and total hip. Lumbar spine Z-score showed a significant progressive decrease in controls, stage I-III patients, and stage IV patients. Logistic regression analysis showed a significant association between the disease and serum OPG levels, the odds ratio per standard deviation increase of this being 1.9 (95% confidence interval 1.1–3.8, P = 0.04) after adjusting for bone mass and ICTP serum levels, as well as for alcohol and smoking history. Adjustment for alcohol intake and tobacco use did not cancel out BMD differences between patients and controls. Patients with SCHNC show increased OPG serum levels, increased bone resorption, and decreased bone mass. The OPG rise appears to be unrelated to the BMD decrease, and the BMD decrease seems to be, at least in part, independent of smoking and drinking habits. No differences in either OPG or BMD were seen between patients with and without chemotherapy. Further studies are needed to clarify the mechanisms responsible for OPG and BMD changes in SCHNC.