健康成年男性身体成分对骨密度的影响

目的探讨健康成年男性身体成份对骨密度（BMD）的影响程度。方法对257名健康男性采用双能X线检测腰椎（L1-4）、髋部和全身BMD及身体成份一全身脂肪量（FM）和全身瘦组织量（I．M）,并测量身高和体重。结果FM是决定体重指数（BMI）的主要因素（R^2=0．675,LM：标准偏回归系数B=0．252,P=0．000;FM：标准偏回归系数p=0．692,P=0．000）;年龄、BMI、FM、LM和FM占体重百分比（FM％）均与股骨颈、全髋、L1-4和全身BMD呈显著正相关（P〈0．01）。躯干部脂肪组织量占体重百分比（TKFM％）只与L1-4BMD有相关性（P=0．011）。多元逐步回归分析显示,LM是决定股骨颈（R^2=0．264,p=0．211,P=0．001）和全身BMD（R^2=0．227,B=0．160,P=0．016）的独立影响因素。在控制年龄的基础上,分别控制FM和LM后,BMI与股骨颈、全髋、L1-4和全身BMD的偏相关分析结果一致,但在BMI的回归模型中FM是BMI的主要决定因子,因FM的B是LM的2倍多,LM与所测部位BMD的相关性要强于FM。结论LM是与全身和股骨颈BMD独立相关的主要因素。     

老年男性骨质疏松症患者骨密度和生化指标的变化

目的：了解老年男性骨质疏松症患者骨密度和骨代谢生化指标变化的特点。方法：对30例老年男性骨质疏松症患者进行腰椎（L2－4）骨密度（BMD）、骨矿含量（BMC）、血和尿骨代谢生化指标的测定,并与对照组进行比较。结果：骨质疏松（OP）组的BMD和BMC均显著小于对照组,分别比对照组下降21．6％和25％;OP组骨形成指标血清碱性磷酸酸（ALP）和C端骨钙素（BGP）明显高于对照组,分别上升25．4％和222％;骨吸收指标尿羟脯氨酸与肌酐的比值（HOP／Cr)和Ⅰ型胶原N－末端肽与肌酐的比值（INTX／Cr)明显高于对照组,分别上升22．6％和223％。OP组血清T水平明显低于对照组,两组血清25－羟维生素D3（25－OH－D3）均在正常低限或低于正常水平。结论：腰椎（L2－4）BMD和BMC是诊断男性骨质疏松症的主要依据;老年男性骨质疏松症患者一部分人属于骨代谢高转换型;雄激素对老年男性骨量的维持起重要作用;老年男性维生素D缺乏质疏松症发生的重要基础。     

50岁以上男性不同部位骨密度变化特征及骨质疏松检出率

目的探讨50岁以上男性骨密度(BMD)的变化特征及骨质疏松检出率。方法回顾性分析解放军总医院年度查体50岁以上男性的一般资料及用双能X线吸收法测定的BMD,根据年龄和WHO骨质疏松症诊断标准将受试者分组,比较组间BMD特点、不同测量部位骨质疏松及低骨量检出率。结果全髋及股骨颈BMD随增龄而逐渐降低,差异有统计学意义(P0.01);线性相关分析显示全髋及股骨颈BMD与年龄呈负相关(r=-0.36,r=-0.30;P0.05),腰椎BMD与年龄呈正相关(r=0.14,P0.05)。该人群骨质疏松总检出率为10.08%,低骨量检出率为43.21%;骨质疏松及低骨量检出率均随增龄而增加(P0.01);股骨颈部位骨质疏松及低骨量检出率与总检出率的差异无统计学意义(P0.05)。单侧股骨颈部位骨质疏松、低骨量检出率低于股骨颈部位总检出率。70岁以上者骨质疏松及低骨量检出率显著高于70岁以下者(14.88%比1.99%;47.75%比35.56%,P0.01)。结论 50岁以上男性全髋及股骨颈BMD随增龄而下降。骨质疏松及低骨量检出率随增龄而增加。股骨颈部位骨质疏松及低骨量检出率与总检出率接近,测量双侧股骨颈BMD有助于提高骨质疏松检出率。     

男性2型糖尿病患者骨密度和骨代谢指标的变化

男性骨质疏松与年龄有关,多发生在70岁以上人群。如果男性患有糖尿病(DM),则可能因代谢紊乱或DM慢性并发症等的影响而导致继发性骨质疏松。但目前有关2型DM对骨密度和骨代谢的研究尚存争议。本研究进一步评价男性2型DM骨密度和骨代谢指标的变化及其与病程和肾脏病变的关系。     

老年男性骨密度的影响因素

目的 研究老年男性饮食、运动、吸烟、嗜酒、体重指数(BMI)、高血压、冠心病、胃及十二指肠球部溃疡、慢性支气管炎等因素对骨密度(BMD)的影响.方法 双能X线BMD仪检测前臂远端BMD,测量身高、体重.用自制的问卷调查表记录受试者生活习惯、慢性病史等,并进行统计学分析.结果 老年男性年龄、BMI、饮食结构、运动、吸烟、嗜酒、高血压、胃及十二指肠球部溃疡与BMD相关,具有统计学意义.冠心、慢性支气管炎与BMD无关.结论 吸烟、嗜酒、低BMI、高血压、胃及十二指肠球部溃疡是骨质疏松(OP)的危险因素.饮食、运动是OP的可控因素.     

老年男性骨密度与钙调节激素测定

目的　探讨钙调节激素在老年男性骨质疏松症发病机制中的作用。　 方法 　 6 3例老年男性分为骨质疏松组与非骨质疏松组 ,测定骨密度 (BMD)、血清钙 (Ca)、磷 (P)、碱性磷酸酶 (AKP)、甲状旁腺激素 (PTH)、降钙素 (CT)、2 5羟维生素D[2 5 (OH) VitD] ,并与 37例青年男性对照。　 结果　老年男性BMD、CT、2 5 (OH) VitD均较对照组降低、PTH增高 (P <0 0 0 1)。骨质疏松组CT、2 5 (OH) VitD较非骨质疏松组降低、PTH增高 (P <0 0 1～ 0 0 0 1)。Ca、P、AKP无明显差异。　 结论 　增龄、钙调节激素异常是引致老年男性骨质疏松症的重要原因之一。     

老年男性慢性阻塞性肺疾病患者骨代谢与骨密度的关系

目的　探讨老年男性慢性阻塞性肺疾病 (COPD)患者继发性骨代谢与骨密度 (BMD)变化的原因、临床特点及相互关系。方法　根据COPD肺功能诊断标准将 5 0例老年男性稳定期单纯COPD患者分为中度组和重度组 ,另设老年男性健康对照组 3 0例。检测并分析血气分析 ,BMD ,骨矿含量 (BMC) ,与骨吸收和骨形成有关的血、尿骨代谢生化指标的变化。结果　中、重度组患者的BMD和BMC较健康对照组明显降低 (P <0 .0 5或 0 .0 1) ,其中 ,重度组BMD、BMC的降低与氧分压降低明显相关 (r =0 .48～ 0 .5 3 ,P <0 .0 1)。骨吸收指标中尿钙 /肌酐比值明显升高 (P <0 .0 1) ;骨形成指标血清Ⅰ型前胶原羧基端前肽 ,碱性磷酸酶 ,骨钙素 ,2 5 (OH)D3 和雌二醇均明显升高 (P <0 .0 1或 0 .0 5 )。结论　根据WHO有关骨质疏松 (OP)诊断标准 ,多数老年男性COPD患者主要表现为骨量减低 ,很少发生OP ,这可能与机体代偿性对抗OP发生有关。其骨代谢特点与高转换Ⅰ型OP相似 ,与原发性老年男性Ⅱ型OP不同。治疗原发病 ,改善COPD患者缺氧状态可能是一种重要的防治方法。     

中青年男性健康体检者骨密度测定分析

骨质疏松症(osteoporosis,OP)正日益危害着人类的健康,已成为严重的公共卫生问题之一[1]。因男性骨质疏松症发病率较女性低,故目前普遍将骨质疏松与绝经后女性相联系,对男性尤     

绝经妇女桡骨骨密度变化的多因素分析

目的探讨绝经后骨量丢失的主要危险因素。方法对１５７例绝经后妇女的桡骨骨矿含量与年龄、绝经年龄、身高、体重分别进行简单相关分析和多元线性回归分析。结果桡骨骨矿含量与年龄呈非常显著的负相关（Ｐ＜０．００１），与绝经年龄呈非常显著的正相关（Ｐ＜０．００１），与身高呈显著的正相关（Ｐ＜０．０１），与体重呈显著的正相关（Ｐ＜０．０５）；多元回归中偏回归系数的偏相关系数绝对值的大小依次为：绝经年龄、年龄、身高、体重。结论早绝经是绝经后骨量丢失的主要危险因素     

178例老年男性骨密度及25羟维生素D水平分析

目的评估178名老年男性骨密度与25羟维生素D(25OHD)水平,分析两者之间的关系。方法记录178名受试者的年龄、身高、体重、体重指数(BMI),测量受试者腰椎1-4(L1-4)、左侧股骨颈(femeralneck,FN)、Wards三角(Wards)、大粗隆(troch)、左侧股骨上端(femur)的骨密度,并用电化学免疫发光法测定血清25OHD水平,根据骨密度水平将受试者分为3组:骨量正常组、骨量减少组和骨质疏松组,对每组受试者身高、体重、体重指数(BMI)、25OHD进行统计学描述,并进行方差分析。分别对3组受试者血清25OHD水平进行充足(75～375nmol/L)、相对缺乏(50～75nmol/L)、绝对缺乏(<50nmol/L)的描述。结果骨量正常组、骨量减少组、骨质疏松组的人数分别为70例(39.33%)、66例(37.08%)和42例(23.59%)人。各组年龄差异无统计学意义(P>0.05),身高、体重、体重指数之间的差异有统计学意义(P<0.05);各组25OHD充足的比例分别为22.86%、18.18%、19.05%,血清25OHD在骨量正常组、骨量减少组、骨质疏松组的平均值分别为60.00、59.88和52.88nmol/L,3组之间血清25OHD水平差异无统计学意义(P>0.05)。结论老年男性人群中广泛存在骨质疏松及维生素D缺乏,应注意加强宣教及防治。骨密度与身高、体重、体重指数呈负相关,尚未发现25OHD与骨密度之间存在着直接相关关系,需扩大样本进一步探讨。     

Pattern of bone mineral density in idiopathic male osteoporosis

The mechanisms of male idiopathic osteoporosis are little known. We evaluated bone mineral loss by dual-energy X-ray absorptiometry and determined its cortical or trabecular nature in a cohort of men with idiopathic osteoporosis with fractures. Thirty-nine men (mean age 60?±?13?years), with negative investigations for the cause of osteoporosis, were studied. All had fragility fractures: vertebral 51%, peripheral 25%, and both types 24%. Bone density was measured at the lumbar spine (L2-L4), total hip and whole body. The limb/axial skeleton (spine?+?hips) and hip/L2-L4 BMD ratios were calculated. Serum 25-hydroxy-vitamin D, PTH, bone alkaline phosphatase and CTX were measured. Bone mineral loss predominated at the lumbar spine (mean L2-L4 T-score -3?±?0.93, mean total hip T-score -1.87?±?0.75). Limb/axial skeleton and total hip/L2-L4 BMD were strongly correlated, but not hip and spine BMD. The ratio values were widely scattered, indicating markedly heterogeneous bone loss. Vitamin D, PTH, bone alkaline phosphatase and CTX levels did not differ between predominantly trabecular and cortical osteoporosis. Bone mineral density measurement in male idiopathic osteoporosis with fractures demonstrated that bone loss predominated in the spine and that it was very heterogeneous, principally affecting cortical or trabecular bone depending on the patient.     

女性2型糖尿病患者骨密度调查与评估

目的观察女性2型糖尿病（T2DM）患者的骨密度（BMD）变化，探讨BMD数据比较的方法。方法选取女性T2DM患者484例，健康女性志愿者868例，测量正侧位腰椎2至4的椎体、左侧股骨颈、大转子和Ward三角区BMD。确立健康女性各骨骼部位BMD随年龄的变化关系，以三次回归模型建立数据库。结果（1）糖尿病组BMD值与正常人比较无统计学差异。（2）与峰值BMD比较，糖尿病组随年龄增加BMD值下降，且受累骨骼部位增加。（3）同年龄组糖尿病和正常人与峰值骨量差值比较，差异无统计学意义。结论T2DM患者BMD变化与正常人群无统计学差异；比较与峰值骨量的差值是判断骨质疏松程度的标准。     

Effect of alendronate on bone mineral density in male idiopathic osteoporosis

Idiopathic osteoporosis in men is an increasingly recognized disorder accounting for up to 200,000 hip fractures worldwide each year. Although there is no widely accepted or proven efficacious treatment for men with idiopathic osteoporosis, we attempted to examine the effectiveness of alendronate in this disorder. We retrospectively compared the clinical records of male patients with osteopenia (hip or spine T scores less than -1.0, with or without low-trauma fractures) treated either with alendronate 10 mg orally/day and calcium and vitamin D replacement versus conservative treatment with calcium and vitamin D alone. Review included analysis of laboratory studies and bone turnover markers in a subset of patients. We documented bone mineral density (BMD) by dual-energy x-ray absorptiometry (DXA) and repeated BMD after an average follow-up of 1.9 and 2.7 years in the alendronate-treated and conservative treatment groups, respectively. At baseline, conservatively-treated and alendronate-treated patients had similar BMD at the lumbar spine and hip. Over the period of observation, the conservatively-treated patients exhibited insignificant changes in BMD at all measured sites. In contrast, alendronate treatment resulted in a significant increase in BMD of the spine (+4.6%, P =.002), trochanter (+6.4%, P =.002), and total hip (+4.7%, P =.002). Indeed, compared with conservative treatment, alendronate-treated patients sustained a significant annualized percent increment of the BMD in the spine (2.7 +/- 0.6 v 1.1 +/- 0.3, P =.025), trochanter (4.7 +/- 1.7 v 0.7 +/- 0.6, P =.025), and total hip BMD (3.3 +/- 0.9 v 0.1 +/- 0.4, P =.0009). These data are among the first that illustrate the potential efficacy of alendronate in the management of idiopathic osteoporosis in men.     

Growth hormone and the maintenance of adult bone mineral density

Growth hormone serves many important functions in man. It influences carbohydrate, lipid and protein metabolism, regulates the secretion and action of a variety of other hormones, and interacts with the immune system. Its most studied role, however, as its name implies, is the orchestration of longitudinal growth, which occurs predominantly at the epiphyseal plate. Here, GH acts both directly and indirectly, through the systemic and local production of IGF-I (Isaksson et al. , 1987). A separate role for the GH/IGF-I axis in the maintenance of normal bone mineral density (BMD) after epiphyseal closure is also apparent and is an area of active clinical investigation. In this review, we examine the effects of GH on mature bone, summarize the findings of studies on the skeletal effects of GH in adults, and consider the potential use of GH as an anabolic agent in the treatment of osteoporosis.     

中青年甲状腺功能亢进患者骨密度特点

目的分析中青年甲状腺功能亢进(甲亢)患者骨密度特点及其与病程、病情严重程度的关系。方法使用双能X线骨密度仪分别测定340例中青年甲亢患者及160名年龄匹配的正常对照者的前臂、腰椎及股骨颈骨密度,用化学发光法测定甲亢患者游离三碘甲腺原氨酸(FT3)、游离甲状腺激素(FT4)及促甲状腺激素(TSH),用自动生化仪检测血清钙(Ca)、血清磷(P)、碱性磷酸酶(ALP),比较2组间骨密度及Ca、P、ALP的差异。根据国际临床骨密度学会(ISCD)和国际骨质疏松基金会(IOF)对中青年骨质疏松诊断的不同定义分别将甲亢患者分为骨量正常组(ON1)和骨质疏松组(OP1)、骨量正常组(ON2)、骨量减少组(OD2)、骨质疏松组(OP2),比较使用2种诊断方法得出的骨质疏松检出率,比较各组甲状腺激素(TH)及TSH的差异。结果与正常对照组相比,甲亢患者桡骨全部、腰椎L2-4及股骨颈骨密度均明显降低(均P0.05)。根据ISCD定义得出的骨质疏松检出率为46.8%,根据IOF定义得出的骨质疏松检出率为27.1%,前臂较腰椎、股骨颈骨密度降低更明显。甲亢患者骨质疏松组较骨量正常组的FT3、FT4明显升高(P0.05),TSH明显降低(P0.05)。多元线性回归分析显示桡骨骨密度与FT4、Ca呈负相关,与TSH呈正相关。结论中青年甲亢患者骨质疏松患病率高,骨量丢失较明显的部位为桡骨,过量甲状腺激素及低TSH均可导致骨代谢紊乱。     

血清炎性细胞因子与急性冠脉综合征的临床相关性

目的探讨血清炎性细胞因子在急性冠脉综合征（ACS）发生发展中的作用。方法 152例入选对象经临床及冠脉造影检查明确诊断后分为：ACS组（急性心肌梗死组和不稳定型心绞痛组）75例,稳定型心绞痛（SAP）组41例和对照组36例。应用ELISA法检测各组血清基质金属蛋白酶-9（MMP-9）、高敏C反应蛋白（hs-CRP）、肿瘤坏死因子-α（TNF-α）及巨噬细胞集落刺激因子（M-CSF）的浓度并进行统计学分析。结果与SAP组及对照组比较,ACS组血清MMP-9,TNF-α,hs-CRP及M-CSF水平均明显升高（P〈0.01）。Logistic回归显示,MMP-9及M-CSF与冠心病相关。Spearman相关分析显示4种因子之间存在正相关关系。结论血清MMP-9,hs-CRP,TNF-α及M-CSF等炎性细胞因子水平的升高是动脉硬化斑块不稳定的标志,各种炎性细胞因子之间相互诱导、相互协同或拮抗,贯穿于ACS发生发展的各个环节。     

Coeliac disease and bone mineral density in adult female patients.

A cross sectional study was undertaken to examine the relationship between coeliac disease and bone mineral density. The 135 female coeliac patients registered on the database of the Department of Gastroenterology at Hull Royal Infirmary were approached by letter, advising them of a potential risk of osteoporosis and inviting them to undergo bone densitometry. A total of 81 registered women (60%) attended the Osteoporosis Laboratory, Princess Royal Hospital and underwent dual energy x ray absorptiometry at the lumbar spine (L2-L4) and femoral neck. Historical data relating to the time of diagnosis and adherence to a gluten free diet were obtained. A control group was selected from the local normal population and was first matched for height, weight, and menopausal status. Postmenopausal patients were then further matched to controls of equivalent menopausal age. In coeliac patients, bone mineral density expressed in g/cm2 as mean (SD) was significantly lower at the lumbar spine (1.076 (0.186)) than in the control group (1.155 (0.143), p < 0.001). This was also the case at the femoral neck (0.887 (0.142) versus 0.965 (0.127), p < 0.001). When the coeliac patients were stratified by menopausal status, it was found that femoral neck bone mineral density was significantly below control values in both premenopausal and postmenopausal women. Spinal bone mineral density exhibited a significant decrement only in the postmenopausal group. The age at diagnosis of coeliac disease and adherence to a gluten free diet did not influence bone mineral density at either hip or spine. These results confirm coeliac patients' higher risk of osteopenia. Coeliac disease should be added to the list of medical conditions which constitute an indication for bone densitometry in order that the individual risk of osteoporosis related fracture may be determined.     

Bone mineral density and abstention-induced changes in bone and mineral metabolism in noncirrhotic male alcoholics.

BACKGROUND AND PURPOSE: Abuse of alcohol may derange bone metabolism and cause osteoporosis. Due to confounding factors associated with alcohol abuse, however, the effect of alcohol itself on bone loss remains obscure. The influence of alcohol intake on bone and mineral metabolism is rather well known, but how the metabolism normalizes during withdrawal has rarely been investigated. The aims of the present study were to evaluate the alcohol-induced changes of bone and mineral metabolism and their recovery during abstention, and to reassess any possible link between alcohol abuse and osteoporosis. PATIENTS AND METHODS: We studied 27 non-cirrhotic male alcoholics hospitalized for 2 weeks for withdrawal. For comparison, three groups of control subjects were examined. Serum and urinary parameters of bone and mineral metabolism as well as intestinal absorption of calcium were determined at the beginning and end of the treatment period. Bone mineral density (BMD) was measured by dual-energy x-ray absorptiometry at four axial sites (lumbar spine, femoral neck, Ward's triangle, trochanter). RESULTS: On admission, bone formation in the alcoholics was reduced as reflected by decreased serum levels of osteocalcin (-28%; p < 0.05) and procollagen I carboxyterminal propeptide (-17%; p < 0.05). Both parameters normalized within 2 weeks of abstention (p < 0.0001 and p < 0.01, respectively). Urinary hydroxyproline, a parameter of bone resorption, was at the control level on admission and increased slightly during abstention (p < 0.05). Serum ionized calcium increased by 3% (p < 0.0001) during withdrawal. Concomitantly, serum free fatty acids (FFA) decreased by 38% (p < 0.001), and there existed an inverse correlation (r = -0.50, p < 0.05) between changes in ionized calcium and FFA. Serum levels of intact parathyroid hormone and vitamin D metabolites were similar in patients and controls throughout the whole observation period. Intestinal absorption of calcium measured by stable strontium was 37% higher in alcoholics than in controls (p < 0.001); it decreased to nearly normal toward the end of the treatment period. Mean axial BMD did not differ between patients and controls at any of the four measurement sites. However, BMD decreased parallel with duration of drinking history in the alcoholics at all axial sites (p < 0.05 to < 0.01, analysis of covariance with age and weight as covariates). CONCLUSIONS: Decreased bone formation, which is uncoupled from ongoing bone resorption, recovers completely during 2 weeks of abstention. In the absence of confounding factors, the central BMD is normal in noncirrhotic male alcoholics, although the negative effect of alcohol on BMD is evident when duration of excessive drinking is taken into account.