驱铜联合活性维生素D3治疗对Wilson’s病患者骨骼及代谢的影响

目的 观察Wilson＇s病患者骨骼X线摄片表现，及驱铜治疗联合活性维生素D3补充治疗对骨代谢的影响。方法 对35例入选Wilson＇s病患者入院时进行骨骼X线摄片，并分别于治疗前及二巯基丙磺酸钠驱铜辅以活性维生素D3治疗8疗程后，放射免疫法测定骨代谢相关激素：PTH、CT、及血清BGP水平；用生化法测定血钙、血磷，尿钙、尿磷等。并用单光子吸收法（SPA）测定尺桡骨中远端1/3处平均骨密度值。结果 Wilson＇s病患者手腕部X线检测异常率达60%。治疗后，血PTH、血钙均降低，骨密度（BMD）值升高，较治疗前差异有统计学意义（P〈0.05）；血磷、尿钙、磷及血清CT、BGP水平较治疗前差异无显著性。结论 Wilson＇s病患者常并发骨质疏松或骨质软化等代谢性骨病，驱铜治疗联合活性维生素D3补充治疗可更好改善骨骼代谢，更快改善其骨密度。     

未绝经女性甲亢患者血25羟维生素D水平与骨密度的关系

目的 观察未绝经女性甲亢患者骨密度及血钙、血磷、血碱性磷酸酶（ALP）、血浆25羟维生素D[25(OH)D]、血浆甲状旁腺激素（PTH）水平变化,分析未绝经女性甲亢患者血浆25(OH)D与骨密度的关系。方法 选取50例初发或复发的未绝经女性甲亢患者,51例正常对照人群,应用双能X线吸收仪（DXA）测定腰椎1-4、股骨颈、股骨大转子、Ward三角和全股骨的骨密度,电化学发光法测定血浆25(OH)D和PTH,生化法测定血钙、磷、ALP。结果 甲亢组L1、Ward三角骨密度均低于对照组,差异有统计学意义。与对照组相比,甲亢组血钙、血ALP、血浆25(OH)D水平升高,血浆PTH降低,差异均有统计学意义。甲亢组维生素D缺乏17例(34%) , 不足19例(38%) , 充足14例(28%)。对照组维生素D缺乏30例(59%) , 不足18例(35%), 充足3例(6%)。相关分析示,两组血浆25（OH）D与L1、L2、L3、L4、L1-4、股骨颈、股骨大转子、Ward三角、全股骨骨密度均无相关性。Pearson相关分析示,甲亢组血浆25(OH)D与PTH呈负相关（r=-0.378,P<0.01）。结论 未绝经女性甲亢患者L1、Ward三角骨密度降低。未绝经女性甲亢患者血浆25(OH)D升高,可能与高血钙、PTH分泌抑制、高血磷导致1-α-羟化酶活性降低有关。未绝经女性甲亢患者血浆25(OH)D水平与骨密度无直接关系。     

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.1,25(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.     

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。     

血清骨碱性磷酸酶水平与老年骨质疏松症患者骨容积的相关性

目的 探讨血清骨碱性磷酸酶(bone alkaline phosphatase, BALP)水平与老年骨质疏松症(osteoporosis, OP)患者骨容积的相关性。方法 选择2019年6月至2020年6月新疆维吾尔自治区人民医院73例老年OP患者，调查并记录患者基线资料，其中男22例，女51例；年龄63～82岁，平均年龄(71.25±4.31)岁。检测患者血清骨代谢标志物[血钙、血磷、BALP、骨钙素(bone gla protein, BGP)],影像学检查测量骨容积、骨密度，均接受钙剂和/或维生素D等药物治疗24周，比较治疗前、治疗24周血清骨代谢标志物、骨容积、骨密度变化，分析骨代谢与骨容积、骨密度的相关性，对比不同资料患者骨容积，重点分析BALP与骨容积的相关性。结果 治疗前、治疗24周，血钙、血磷水平比较差异无统计学意义(P>0.05);治疗24周，血清BALP水平较治疗前降低，血清BGP水平、骨容积、骨密度升高，差异有统计学意义(P<0.05);经Pearson相关性分析显示，血钙、血清BALP水平与骨容积、骨密度呈负相关(r=-0.294、-0.776,P...     

女性Graves患者骨密度、骨代谢特点及131I治疗后的转归分析

目的研究女性Graves患者的骨密度、骨代谢指标及131I治疗后的变化情况,为Graves患者骨代谢异常的诊治提供科学的临床依据。方法回顾性分析2013年5月至2015年5月期间,经我院131I治疗的90例女性Graves患者的资料,根据患者绝经情况,分为绝经组和未绝经组,各45例。两组患者治疗前、后均采用双能X线骨密度仪对腰椎、髋部行骨密度(BMD)测量并检测血钙(Ca)、磷(P)、甲状旁腺激素(PTH)、碱性磷酸酶(ALP)、血骨钙素(BGP)等骨代谢指标,记录并行统计学分析。结果治疗前,绝经组所测部位的BMD略低于未绝经组,骨代谢指标略高于未绝经组,差异无统计学意义(P0.05);治疗后,未绝经组骨密度的改善效果强于绝经组与治疗前,髋部及腰部BMD明显上升,ALP、BGP水平明显降低,统计学差异显著(P0.05),但两组血Ca、P、PTH的差异无统计学意义(P0.05)。结论131I治疗可以改善女性Graves患者的骨密度及骨代谢情况,对指导防治骨质疏松起着积极的作用。     

老年骨质疏松症股骨颈骨折术后抗骨质疏松治疗的初步观察

目的探讨老年人骨质疏松症股骨颈骨折术后应用（密盖息＋钙＋维生素D3）方案抗骨质疏松治疗的效果。方法随机选择诊断为“原发性骨质疏松症＋股骨颈病理性骨折”的老年患者56例,人工关节置换术后除髋关节康复锻炼外,应用（密盖息＋钙＋维生素D3）方案治疗3个月,比较治疗前后临床症状和空腹血钙、磷、甲状旁腺激素、碱性磷酸酶、24h尿钙、磷以及定量CT腰椎骨密度值变化。结果周身疼痛症状改善有效率为50％;治疗3个月前、后空腹血钙、磷、甲状旁腺激素、碱性磷酸酶、24h尿钙、磷变化间的差异无统计学意义（P〉0．05）;腰椎骨密度值间的差异有统计学意义（P〈0．01）。结论老年人股骨颈骨折术后应用（密盖息＋钙＋维生素D3）方案抗骨质疏松治疗能有效增加骨密度,改善疼痛,从而预防再次骨折。     

老年男性2型糖尿病患者各种钙调激素与骨密度改变的关系

目的测定老年男性2型糖尿病患者各种钙调激素及骨密度,探讨老年男性2型糖尿病患者骨质疏松的发病机理,为其防治提供理论依据。方法用双能X线吸收法测定70例老年男性2型糖尿病患者及60例年龄、体重指数相匹配的对照者的腰椎及髋部骨密度,并采用放免法测定血清骨钙索(BGP)、抗酒石酸酸性磷酸酶(TRAP)、甲状旁腺素(PTH)、降钙素(CT)、1,25(OH)2D3、25(OH)D3、尿羟脯氨酸(HOP)等,两组进行比较。结果 老年男性2型糖尿病患者较对照组骨密度显著降低。血BGP、CT、1,25(OH)2D3浓度低于对照组(P<0.05).TRAP、PTH、尿HOP显著高于对照组(P<0.05)。结论老年男性2型糖尿病患者PTH、CT、1,25(OH)2D3等钙调激素分泌及代谢失常,影响骨代谢,出现糖尿病性骨质疏松,表现为骨吸收增加,骨形成减少与缓慢,骨吸收过程大于骨形成。     

维生素D对甲亢患者骨密度及钙代谢的影响

维生素Ｄ对甲亢患者骨密度及钙代谢的影响张富华甲状腺激素影响骨和矿物盐代谢，引起骨量减少，骨密度降低。我们观察了６３例甲状腺机能亢进症的骨密度和血尿钙磷碱性磷酸酶，观察其骨密度及血钙磷，ＡＫＰ恢复情况，以摸索甲亢性骨病的有效防治措施。ｌ材料和方法１．１...     

继发性甲状旁腺功能亢进症的治疗进展

CKD早期就会出现钙、磷、维生素D和PTH代谢失衡,并引起继发性甲状旁腺功能亢进症(SHPT),随着肾功能下降,SHPT也愈加明显。SHPT的治疗相当棘手,标准的治疗方法包括补钙、限制磷摄入、磷结合剂及维生素D制剂的应用。但这些治疗通常会影响血钙、磷浓度,从而加重疾病并增加骨骼外并发症的发病率和死亡率。本文就SHPT的治疗方面作一综述。     

The effect of adding PTH(1–84) to conventional treatment of hypoparathyroidism: A randomized,placebo‐controlled study

In hypoparathyroidism, plasma parathyroid hormone (PTH) levels are inadequate to maintain plasma calcium concentration within the reference range. On conventional treatment with calcium supplements and active vitamin D analogues, bone turnover is abnormally low, and BMD is markedly increased. We aimed to study the effects of PTH‐replacement therapy (PTH‐RT) on calcium‐phosphate homeostasis and BMD. In a double‐blind design, we randomized 62 patients with hypoparathyroidism to daily treatment with PTH(1–84) 100 µg or similar placebo for 24 weeks as add‐on therapy to conventional treatment. Compared with placebo, patients on PTH(1–84) reduced their daily dose of calcium and active vitamin D significantly by 75% and 73%, respectively, without developing hypocalcemia. However, hypercalcemia occurred frequently during the downtitration of calcium and active vitamin D. Plasma phosphate and renal calcium and phosphate excretion did not change. Compared with placebo, PTH(1–84) treatment significantly increased plasma levels of bone‐specific alkaline phosphatase (+226% ± 36%), osteocalcin (+807% ± 186%), N‐terminal propeptide of procollagen 1 (P1NP; +1315% ± 330%), cross‐linked C‐telopeptide of type 1 collagen (CTX; +1209% ± 459%), and urinary cross‐linked N‐telopeptide of type 1 collagen (NTX; (+830% ± 165%), whereas BMD decreased at the hip (?1.59% ± 0.57%), lumbar spine (?1.76% ± 1.03%), and whole body (?1.26% ± 0.49%) but not at the forearm. In conclusion, the need for calcium and active vitamin D is reduced significantly during PTH‐RT, whereas plasma calcium and phosphate levels are maintained within the physiologic range. In contrast to the effect of PTH(1–84) treatment in patients with osteoporosis, PTH‐RT in hypoparathyroidism causes a decrease in BMD. This is most likely due to the marked increased bone turnover. Accordingly, PTH‐RT counteracts the state of overmineralized bone and, during long‐term treatment, may cause a more physiologic bone metabolism. © 2011 American Society for Bone and Mineral Research     

长春市35?79岁人群骨代谢指标与骨密度相关性研究

目的研究抗酒石酸酸性磷酸酶(TRACP)、Ⅰ型胶原C端肽(CTX-1)、骨特异性碱性磷酸酶(BALP)、降钙素(CT)、骨钙素(BGP)、甲状旁腺激素(PTH)、25-羟基维生素D3(25(OH)D3)与前臂远端骨密度相关关系。方法采用美国Osteometer Medi Tech公司生产的DTX-200型骨密度仪检测受试者非受力侧前臂桡、尺骨远端三分之一处骨密度(BMD);采用美国贝克曼公司全自动化学发光免疫分析仪、美国Thermo公司酶标免疫分析仪检测骨代谢指标;将791例受试者检测结果按不同性别,每5岁为一个年龄段分组;应用SPSS13.0分析软件进行统计分析。结果35～49岁人群TRACP、CTX-1、BALP、BGP等指标性别间不存在差异;50～79岁人群性别间差异显著,女性高于男性。TRACP、CTX-1与BMD负相关;女性BALP、BGP在50～64年龄段明显升高,与BMD负相关,65岁以后开始下降。25(OH)D3与BMD正相关;CT降低出现在65～79岁年龄段,与BMD显著正相关。结论骨代谢指标测定是监测骨量变化及骨质疏松早期诊断的重要技术手段。     

Role of parathyroid hormone and therapy with active vitamin D sterols in renal osteodystrophy

Renal osteodystrophy (ROD) represents a spectrum of bone lesions ranging from a high-turnover to a low-turnover state. The expression of the histologic bone lesions is modulated by parathyroid hormone (PTH), vitamin D, calcium, phosphorus, and aluminum that act as major regulators of osteoblastic activity and bone formation rate. The availability of immunometric PTH assays has allowed reasonable prediction of the subtypes of bone lesions in patients with chronic kidney disease (CKD). PTH levels as measured by these assays, however, may not reflect the true bone turnover state during treatment with intermittent active vitamin D. Early diagnosis and appropriate treatment of renal bone disease are essential in preventing the debilitating consequences of ROD on the growing skeleton. Calcitriol and calcium-containing phosphate binders have been the mainstay of treatment for secondary hyperparathyroidism. Complications such as hypercalcemia, vascular calcifications, and the development of adynamic bone may arise from aggressive treatment. New vitamin D analogs and calcium-free phosphate binders are promising in terms of limiting these complications. The management of ROD should be tailored to maintain normal rates of bone formation and turnover with age-appropriate serum calcium and phosphorus levels and with serum PTH levels that correspond to normal rates of skeletal remodeling. These treatment goals would maintain bone health, maximize growth potential, and prevent the development of soft tissue and vascular calcifications.     

原发性肾病综合征患者血清胰岛素样生长因子1的变化及其与骨代谢的关系

目的 探讨原发性肾病综合征（PNS）患者血清胰岛素样生长因子1（IGF-1）的变化及其与骨代谢指标之间的关系。评价IGF-1在PNS患者骨代谢异常机制中的临床价值。方法 随机选取2008年1月至2009年5月临床资料完整的慢性肾脏病（CKD）1、2期PNS患者30例为对象;健康体检者61例为健康对照组。测定血清IGF-1、钙、磷、PTH、25羟基维生素D3[25-（OH）D3]、骨钙素（BGP）、I型胶原吡啶交联C终端肽（CTx）及尿钙/尿肌酐（UCa/Cr）。双能X线骨密度仪检测患者骨密度（BMD）。 结果 与健康对照组比较,PNS组血Ca、25-（OH）D3及BGP水平显著降低;血CTx水平及UCa/Cr比值显著增高（均P < 0.05）;BMD水平降低[（1.078±0.090） g/cm2 比（1.090±0.062） g/cm2,P > 0.05],但差异无统计学意义。PNS组血清IGF-1水平显著低于健康对照组,差异有统计学意义[（155.75±17.48） μg/L比（223.17± 16.44） μg/L,P < 0.05],且与24 h尿蛋白量及CTx呈负相关（r = -0.757和r = -0.786,均 P < 0.05）;与血BGP和BMD呈正相关（r = 0.861和r = 0.584,均P < 0.05）。 结论 PNS患者（CKD 1、2期）存在骨代谢异常,表现为骨形成减少、骨吸收增加。血清IGF-1与血BGP、CTx及BMD相关,可作为反映PNS患者骨代谢改变的临床指标之一。     

Bone Development in the Fetus and Neonate: Role of the Calciotropic Hormones

During embryonic and fetal development much of the skeleton initiates as a cartilaginous scaffold, which is progressively resorbed and replaced by bone. Endochondral bone formation continues until the growth plates fuse during puberty. At all life stages adequate delivery of mineral is required for the skeleton to achieve and maintain appropriate mineral content and strength. During fetal development the placenta actively transports calcium, phosphorus, and magnesium. Postnatally passive and then active absorption from the intestines becomes the main supply of minerals to the skeleton. Animal and human data indicate that fetal bone development requires parathyroid hormone (PTH) and PTH-related protein but not vitamin D/calcitriol, calcitonin, or (possibly) sex steroids. During the postnatal period, when intestinal calcium absorption becomes an active process, skeletal development begins to depend upon vitamin D/calcitriol but this requirement can be bypassed by increasing the calcium content of the diet or by administering intermittent calcium infusions.     

绝经后妇女血清调钙激素水平与骨代谢关系探讨

目的 探讨绝经后妇女血清调钙激素水平对骨形成、骨吸收及骨密度的影响。方法 142名健康绝经后妇女测定血雌二醇（E2）、睾酮（T）、总三碘甲状腺原氨酸（TT3）、总甲状腺素（TT4)、甲状旁腺激素全段（PTH－SP）、降钙素（CT）、骨钙素（BGP）、尿脱氧吡啶啉（DPD）、尿肌酐（Cr）。双能X线骨密度仪测定腰椎、髋部、前臂骨密度（BMD）,对检测结果进行分析。结果 本组骨质疏松患病率为60．48％,低骨量32．39％,正常骨量7．13％。血清6种调钙激素中T、E2、TT3、TT4、CT与BMD、BGP呈正相关,与年龄负相关;PTH－SP与BMD呈负相关,与年龄、DPD／Cr呈正相关。结论 绝经后妇女血调钙激素水平影响骨形成、骨吸收和骨密度,使骨代谢趋向于负平衡,是绝经后妇女易发生骨质疏松症的重要原因。     

糖皮质激素诱导胰岛素样生长因子1降低对原发性肾病综合征患者骨代谢的影响

目的 观察糖皮质激素（GC）治疗的原发性肾病综合征（PNS）患者胰岛素样生长因子1（IGF-1）变化,探讨其水平改变对PNS患者骨代谢的影响及意义。 方法 以本院2008年1月至2009年8月临床资料完整的PNS患者39例为对象。口服泼尼松0.8~1.0 mg&#8226;kg-1&#8226;d-1,完全缓解2周后,以每2周减去原剂量的5％～10％的方式减量。最终每日或隔日5～10 mg维持（总疗程>24周）。测定应用激素前、治疗第4、8、12、24周末血白蛋白、24 h尿蛋白量、血清钙、磷、甲状旁腺激素（PTH）、25羟基维生素D3（25-（OH）D3）、骨钙素（BGP）、I型胶原吡啶交联C终端肽（CTx）及尿钙/肌酐;双能X线骨密度仪检测患者骨密度（BMD）;酶联免疫法测定血清IGF-1水平。使用Pearson 相关分析探讨IGF-1与骨代谢改变的关系。 结果 36例完成随访,并具备完整临床数据。治疗第4、8、12和24周与治疗前比较,患者血钙、25-（OH）D3水平均呈时间依赖性升高（P < 0.05）,相关分析提示,与尿蛋白量呈负相关 （r=-0.749,r=-0.831,P < 0.05）。骨形成指标血BGP、IGF-1水平呈时间依赖性降低（P < 0.05）,骨吸收指标CTx逐渐升高,至第12周起差异有统计学意义（P < 0.05）。第4周各部位BMD与治疗前差异均无统计学意义;第8周起腰椎（L1~L4）BMD值较治疗前显著下降（P < 0.05）;第 24 周,股骨颈和股骨干的BMD与治疗前差异有统计学意义（P < 0.05）。PNS患者经糖皮质激素治疗后,IGF-1与BMD和BGP呈正相关（r=0.495和r=0.896,均P < 0.05）,与血CTx呈负相关（r=-0.697,P < 0.05）。 结论 糖皮质激素呈时间依赖性导致PNS患者血清IGF-1水平降低。IGF-1下降与患者早期骨形成指标降低、骨吸收指标增高及后期骨密度下降相关。IGF-1途径可能参与GC 引起的PNS患者骨代谢改变。IGF-1有望成为反映或预测糖皮质激素诱导的骨质疏松的新型生化指标。     

Serial changes in bone mineral density and bone turnover after correction of secondary hyperparathyroidism in a patient with pseudohypoparathyroidism type Ib.

Pseudohypoparathyroidism (PHP) is a disorder characterized by hypocalcemia and secondary hyperparathyroidism caused by primarily renal resistance to the effects of parathyroid hormone (PTH). However, as an indication of normal PTH responsiveness in bone, some patients with PHP develop skeletal disease because of longstanding secondary hyperparathyroidism. A patient is described with hypocalcemia, hyperphosphatemia, marked secondary hyperparathyroidism, and an increased alkaline phosphatase level. Subsequent evaluation revealed a diagnosis of PHP type Ib. The patient had radiographic evidence of skeletal disease caused by secondary hyperparathyroidism. A urinary level of N-telopeptide cross-links of type I collagen (NTX) was elevated markedly. Bone mineral density (BMD) was in the normal range at all measured sites, with BMD at the spine being higher than at the femur and distal radius. Treatment was initiated with calcium and calcitriol. Seven months later, calcium and PTH levels had normalized. The level of urinary NTX fell by 83%. Spinal BMD improved by 15%, and BMD at the femoral neck improved by 11%. Radial BMD was unchanged. This case emphasizes the importance of evaluating patients with PHP for hyperparathyroid bone disease and shows that correction of secondary hyperparathyroidism in patients with PHP can result in a significant suppression of previously accelerated bone turnover and to substantial gains in BMD at sites containing a major percentage of cancellous bone. The case also implies that assessment of bone turnover with urinary NTX and measurement of BMD with dual-energy X-ray absorptiometry (DEXA) may be useful in following the response of the skeleton to therapy in these patients and suggests the need for more studies of both NTX and BMD in patients with PHP.     

Calcification Inhibitors and Wnt Signaling Proteins Are Implicated in Bovine Artery Smooth Muscle Cell Calcification in the Presence of Phosphate and Vitamin D Sterols

Administration of active vitamin D sterols to treat secondary hyperparathyroidism in patients with chronic kidney disease receiving dialysis has been associated with elevated serum calcium and phosphorus levels, which may lead to increased risk of vascular calcification. However, calcimimetics, by binding to the parathyroid gland calcium-sensing receptors, reduce serum parathyroid hormone, calcium, phosphorus, and the calcium-phosphorus product. Using cultured bovine aorta vascular smooth muscle cells (BASMCs), an in vitro model of vascular calcification, we compared calcification levels and gene expression profiles after exposure to the phosphate source ss-glycerolphosphate (BGP), the active vitamin D sterols calcitriol and paricalcitol, the calcimimetic R-568, or BGP with the active vitamin D sterols or R-568. Cells exposed to BGP (10 mM) alone or with calcitriol or paricalcitol showed dose-dependent BASMC calcification. No change in calcification was observed in cultures exposed to BGP with R-568, consistent with the observed lack of calcium-sensing receptor expression. Microarray analysis using total cellular RNA from cultures exposed to vehicle or BGP in the absence and presence of 10(-8) M calcitriol or paricalcitol for 7 days showed that cells exposed to BGP with calcitriol or BGP with paricalcitol had virtually identical gene expression profiles, which differed from those of cells treated with BGP or vehicle alone. Several osteoblast- and chondrocyte-associated genes were modulated by BGP and vitamin D exposure. In this study, exposure of BASMCs to phosphate and active vitamin D sterols induced calcification and changes in expression of genes associated with mineralized tissue.