载阿仑膦酸钠骨水泥抑制钛磨屑诱导的假体周围骨溶解

目的 比较载阿仑膦酸钠丙烯酸骨水泥与皮下注射阿仑膦酸钠抑制钛磨眉诱导的骨溶解的效果.方法 48只成年雄性新西兰兔随机均分为无钛磨屑且无阿仑膦酸钠组(A组),有钛磨屑注射且无阿仑膦酸钠组(B组),钛磨屑分别注射0.1%、0.5%、1.0%载阿仑膦酸钠丙烯酸骨水泥组(C、I)、E组),钛磨屑注射且皮下手射阿仑膦酸钠组(F组),每组8只.将载阿仑膦酸钠骨水泥植入兔股骨远端.制备磨屑诱导骨溶解动物模型.术后8周对股骨行组织形态学分析、骨密度(bone mineral density,BMD)测定及界面力学测试结果 B组假体周围可见明显的骨溶解,而C、D、E、F组骨溶解明显少于B组.B组假体周围BMD和骨-骨水泥界面抗剪强度分别较A组下降17%和56%;D组假体周围BMD和界面抗剪强度较B组分别增加29%和62%;E组假体周围BMD和界画抗剪强度较B组分别增加37%和29%;F组假体周围BMD和界面抗剪强度较B组分别增加51%和69%;C组、D组、E组分别与F组比较,假体周围BMD和界面抗剪强度的差异均无统计学意义.结论 载阿仑瞵酸钠丙烯酸骨水泥与皮下注射阿仑瞵酸钠均可在一定程度上抑制磨屑诱导的骨吸收,增强界画抗剪强度.     

唑来膦酸与阿仑膦酸钠治疗骨质疏松患者的疗效比较及对血清25-(OH)D、BALP、BGP的影响分析

目的比较唑来膦酸与阿仑膦酸钠治疗骨质疏松(OP)患者的疗效及对血清25羟维生素D[25-(OH)D]、骨钙素(BGP)、骨特异性碱性磷酸酶(BALP)的影响。方法将我院收治的82例OP患者随机分为观察组41例和对照组41例。在钙尔奇D和骨化三醇胶丸常规治疗的基础上,观察组患者行唑来膦酸治疗,对照组患者行阿仑膦酸钠治疗。评价两组患者的临床治疗效果,于两组患者治疗前后检测骨密度(BMD)及血清相关骨代谢标志物,包括25-(OH)D、BGP、BALP。结果观察组患者临床治疗的总有效率为90.25%,对照组为80.48%,两组比较差异具有统计学意义(P0.05)。治疗6个月后,两组患者的平均腰椎正位(L2-4)及右股骨颈BMD较治疗前均增大(P0.05),但治疗12个月后观察组患者腰椎正位(L2-4)及右股骨颈BMD的增大幅度均高于对照组(P0.05)。治疗12个月后,两组患者的平均25-(OH)D较治疗前均升高(P0.05),BGP、BALP较治疗前均下降(P0.05),但观察组患者BGP、BALP两指标的下降幅度要高于对照组(P0.05)。结论唑来膦酸治疗OP的临床疗效较阿仑膦酸钠显著,能有效下调BALP、BGP水平,提高患者骨密度,值得临床推广应用。     

补肾壮骨冲剂对老年男性骨量减少及骨质疏松患者骨代谢指标影响的临床观察

目的 通过比较补肾壮骨冲剂组服药前、服药半年后骨密度及骨代谢指标的变化情况,并将补肾壮骨冲剂组与阿仑膦酸钠及钙尔奇D组分别做对比,观察补肾壮骨冲剂治疗老年男性骨量减少及骨质疏松、改善其骨代谢的临床疗效。方法 采用电化学发光免疫分析法分析血清中PINP、β-Crosslaps及N-MID的含量;采用美国GE公司生产的Lunar Prodigy双能X线（DXA）骨密度仪,检测各部位BMD;将研究对象按就诊时间分为3组,补肾壮骨冲剂组服用补肾壮骨冲剂+钙尔奇D,阿仑膦酸钠组服用阿仑膦酸钠+钙尔奇D,钙尔奇D组只服用钙尔奇D。 结果 补肾壮骨冲剂组治疗半年后血清中的PINP、β-Crosslaps及 N-MID下降显著;与治疗前相比,左侧股骨颈、Ward’s三角和左侧股骨近端处的BMD提高明显;补肾壮骨冲剂组改善老年男性骨代谢及提高骨密度的效果优于钙尔奇D组;与临床疗效公认的阿仑膦酸钠组比较,补肾壮骨冲剂显示出与其相近的改善骨代谢和提高骨密度疗效。结论 补肾壮骨冲剂是治疗老年性骨量减少及骨质疏松、提高骨量、改善老年男性骨代谢情况的安全有效药物。     

唑来膦酸钠治疗老年骨质疏松症的临床观察

目的观察唑来膦酸钠治疗老年骨质疏松症的治疗效果。方法临床收集老年骨质疏松症患者60例,随机分为治疗组30例,给予钙尔奇+阿法D3+唑来膦酸钠;对照组30例给予钙尔奇+阿法D3。观察治疗前和治疗6个月后两组患者疼痛评分、腰椎及髋部骨密度,同时观察药物不良反应情况。结果治疗后6月对照组及治疗组VAS评分均较治疗前下降,有统计学差异(P0.05);对照组患者治疗6月后腰椎及髋部BMD与治疗前比较,无统计学差异(P0.05);治疗组患者治疗6月后腰椎及髋部BMD与治疗前比较均增加,有统计学差异(P0.05)。治疗组VAS评分、腰椎及髋部BMD治疗6月前后差值均明显低于对照组,有统计学差异(P0.05)。结论唑来膦酸钠能缓解骨质疏松症患者骨痛并提高骨密度。     

阿仑膦酸钠对类风湿关节炎合并骨质疏松患者骨强度的影响

目的 分析阿仑膦酸钠对类风湿关节炎（rheumatoid arthritis,RA）合并骨质疏松（osteoporosis,OP）患者骨强度的影响。方法 选取华北理工大学附属医院骨质疏松门诊2012年6月至2020年6月诊治的OP患者120例,分为RA+OP组（60例）和OP组（60例）,且均口服阿仑膦酸钠联合骨化三醇、钙尔奇D持续12个月。比较治疗前后表征髋部力学结构强度的参数值CSA、CSMI、Z、CT和BR值（分别代表股骨颈抗轴向压缩力、骨骼刚度、抗屈曲负荷系数、皮质骨厚薄及屈曲比）、骨密度（BMD）、骨折发生率、炎性指标及临床体征。结果 经治疗6月、12月后,除RA+OP组全髋部位BMD外,OP组全髋、两组患者腰椎、股骨颈BMD、CSA、CSMI、Z、CT值均高于治疗前（P＜0.05）,BR值均低于治疗前（P＜0.05）;治疗12月后,RA+OP组股骨颈、全髋BMD、CSA、CSMI、Z值均低于OP组（P＜0.05）,腰椎BMD、CT、BR值无差异;治疗6至12月期间,RA+OP组股骨颈、全髋BMD增长率低于OP组（P＜0.05）;RA+OP组治疗前骨折发生率显著高于OP组,所有RA患者疾病活动性控制良好。结论 阿仑膦酸钠联合骨化三醇和钙剂可明显提升RA患者骨密度及髋部骨强度,提高骨骼稳定性,这种提升随疗程延长比正常骨质疏松患者缓慢。     

联用鲑鱼降钙素、阿仑膦酸钠、钙尔奇D治疗老年 骨质疏松症疗效观察

目的评价联合应用鲑鱼降钙素、阿仑膦酸钠、钙尔奇D对老年骨质疏松症患者骨痛症状、骨代谢标记物、骨密度的影 响。方法2011年6月~ 2012年6月间选取原发性骨质疏松症患者45例.随机分为对照组和治疗组.连续治疗24周。所有 患者均每日口服1片钙尔奇D(600 mg);治疗组患者同时每周口服1片阿仑膦酸钠(70 mg).每日经鼻吸人1喷鲑鱼降钙素 (120IU)。各组分别于治疗前、治疗4周后、24周后进行疼痛分级评分。于治疗前、治疗24周后应用双能X线吸收法测定腰 椎L14、左侧股骨颈骨密度,测定血清骨钙素、抗酒石酸酸性磷酸酶浓度。结果治疗组接受治疗24周后骨痛症状明显缓 解,治疗组总有效率优于对照组(P <0. 05)。治疗组24周时骨钙素、抗酒石酸酸性磷酸酶浓度与治疗前相比差异有统计学意 义(P <0.05)。治疗组治疗前后腰椎L14骨密度均值差异有统计学意义(P <0. 05);两组治疗前后左侧股骨颈骨密度差异无 统计学意义(P >0. 05)。结论联用鲑鱼降钙素、阿仑膦酸钠、钙尔奇D治疗老年骨质疏松症临床疗效确切。     

阿仑膦酸钠治疗绝经后妇女骨质疏松症临床分析

目的评价阿仑膦酸钠片治疗绝经后妇女骨质疏松症的临床疗效、安全性、依从性。方法对50例患骨质疏松症的绝经后妇女随机分为治疗组30例,服用阿仑膦酸钠,1次/周;对照组20例,服用钙尔奇D片,1次/天,两组疗程均为6个月。结果阿仑膦酸钠治疗组骨密度定量测定较治疗前有明显提高（P〈0.01）,疼痛症状改善;总有效率93.5%,与钙尔奇D组比较有统计学意义（P〈0.05）。结论阿仑膦酸钠治疗绝经后妇女骨质疏松症疗效好。     

胰岛素、阿仑膦酸钠治疗新诊断老年糖尿病骨质疏松症患者骨密度及骨转换指标的研究

目的通过观察胰岛素、阿仑膦酸钠干预,观察在糖尿病骨质疏松症治疗12个月后股骨颈(Femur Neck)骨密度(BMD)及骨特异性碱性磷酸酶(BAP)、骨钙素(BGP)、抗酒石酸酸性磷酸酶-5b(TRAP-5b)等血清骨转换指标的变化。方法选取在我院治疗的糖尿病骨质疏松症患者128例,随机分成4组,即对照组(METF)、胰岛素组(INSU)、二甲双胍+阿仑膦酸钠组(METF+ALEN)、胰岛素+阿仑膦酸钠组(INSU+ALEN),每组同时服用钙尔奇D片作为基础用药,分别于服药前及服药12月后,测定4组患者股骨颈BMD及血BAP、BGP、TRAP-5b,分析治疗前后以及治疗组与对照组间的差异。结果 INSU+ALEN组治疗12月可见患者骨密度较前增加,治疗前后有统计学意义(P0.05),METF、INSU组较前无明显改变,治疗前后无统计学意义(P0.05),METF+ALEN组治疗12月可见患者BMD较前略有增加,治疗前后无统计学意义(P0.05),INSU+ALEN组治疗后BMD的增加明显高于其它组(P均0.05)。INSU+ALEN治疗组患者治疗12月后血清BAP、BGP显著升高(P0.05),TRAP-5b显著降低(P0.05);将上述指标与对照组、其它治疗组比较,BAP、BGP、TRAP-5b差异显著(P均0.01);METF、INSU、METF+ALEN组治疗12月可见患者血清BAP、BGP较前略有增加,TRAP-5b略有降低,治疗前后无统计学意义(P0.05)。结论胰岛素是糖尿病骨质疏松症首选治疗,可增加骨量,预防骨丢失。阿仑膦酸钠能抑制骨吸收,促进骨形成,减缓骨量丢失,提高骨密度,二者联用可有效防治糖尿病骨质疏松症。     

利塞膦酸钠和阿仑膦酸钠治疗对股骨粗隆下侧皮质骨密度变化的影响对比研究

目的回顾性评估利塞膦酸钠和阿仑膦酸钠治疗对股骨粗隆下侧皮质(subtrochanteric lateral cortex,STLC)骨密度(bone mineral density,BMD)变化的影响。方法共有168例受试者,使用双能X线骨密度仪(dual energy X-ray absorptiometry,DXA)对其BMD进行2～4年间隔随访,纳入本次回顾性研究,分为3组:46例未服用任何抗骨质疏松药物(对照组),69例使用阿仑膦酸钠(阿仑膦酸钠组),53例使用利塞膦酸盐(利塞膦酸盐组)。通过在骨皮质上绘制矩形感兴趣区,在每位患者的STLC和转子下内侧皮质(subtrochanteric medial cortex,STMC)中测量BMD。通过使用协方差模型控制来分析STLC中BMD的百分比变化,以控制年龄、体质量指数、STMC百分比变化、髋轴长度、DXA检查之间的时间间隔的5个独立变量。结果对照组、阿仑膦酸盐组和利塞膦酸盐组BMD的最小均数±标准差分别为1.47±1.51、2.24±1.27和6.98±1.23。与对照组(调整后的P=0.010)或阿仑膦酸盐组(调整后的P=0.011)相比,利塞膦酸盐组的STLC显示出更高的BMD百分比变化。结论利塞膦酸盐组中STLC的BMD变化百分比大于阿仑膦酸盐组和对照组。     

不同剂量骨化三醇治疗绝经后骨质疏松疗效对比

目的对比不同剂量骨化三醇治疗绝经后骨质疏松的临床疗效。方法将我院门诊治疗的786例绝经后骨质疏松患者随机分为两组,每组393例。一组给予骨化三醇0.25μg(骨化三醇0.25μg治疗组),每日一次;另一组给予骨化三醇0.50μg(骨化三醇0.50μg治疗组),每日一次。两组患者都给予钙尔奇D 2粒(每粒含离子钙600 mg和活性维生素D 3.125μg),阿仑膦酸钠70 mg每周一次,连续治疗一年。测量、评价并统计两组患者治疗前后和两组患者治疗后腰椎正位(L_(2-4))和左右股骨颈骨密度(Bone Mineral Density,BMD)和腰背疼痛程度。结果治疗一年后两组患者腰椎和股骨颈BMD均显著增加(P0.05);治疗后,骨化三醇0.50μg治疗组腰椎和股骨颈BMD显著高于骨化三醇0.25μg治疗组;疼痛程度显著低于骨化三醇0.25μg治疗组(P0.05)。结论绝经后骨质疏松的三联疗法(钙、活性维生素D、双膦酸盐),骨化三醇0.25μg剂量不足,0.5μg能显著提高临床疗效。     

Response to Alendronate in Osteoporosis after Previous Treatment with Etidronate

Bisphosphonates such as etidronate and alendronate are widely accepted as effective agents for the treatment of osteoporosis. However, some physicians find the choice of which one to use in different patients, and the comparative magnitude of response, unclear. Fifty postmenopausal women with osteoporosis [group 1: 27 women who had received 3 years of previous cyclical etidronate treatment, mean age 70.5 years, bone mineral density (BMD) mean T-score lumbar spine (LS) −3.58 and femoral neck (FN) −2.51; group 2: 23 women who had not previously received cyclical etidronate treatment, mean age 73.7 years, BMD mean T-score LS −3.65 and FN −2.96] were treated with 10 mg alendronate daily, to determine whether pretreatment with etidronate affected the response to alendronate, and whether patients who did not respond to etidronate, responded to alendronate. There was a significant increase in LS BMD after 2 years of treatment with alendronate compared with baseline (group 1: 7.84%, p<0.001; group 2: 6.69%, p<0.001), but there was no statistical difference between the groups. In the group 1 patients there was a significant difference between the initial response (at the LS BMD) to 2 years of cyclical etidronate (1.86%) and later response to 2 years of alendronate (7.84%) (p<0.0001). The 10 patients who did not respond at the LS to etidronate alone, showed a significantly better response (mean BMD change +6.3%) when subsequently treated with alendronate (a net difference of 9.3%, p = 0.002). In 15 patients who did not respond at the FN to etidronate alone, the mean response to alendronate was +0.96% (a difference of 7%, p = 0.004). This study shows that pretreatment with 3 years of cyclical etidronate is not detrimental to the subsequent LS BMD response to alendronate. There is evidence that alendronate produced a greater bone density response than etidronate, and patients who did not respond to etidronate with an increase in LS bone density, subsequently did so following alendronate. Received: 22 June 1999 / Accepted: 18 January 2000     

T-Score as an Indicator of Fracture Risk During Treatment With Romosozumab or Alendronate in the ARCH Trial

In the Active-Controlled Fracture Study in Postmenopausal Women With Osteoporosis at High Risk (ARCH) clinical trial (NCT01631214), 1 year of romosozumab followed by alendronate reduced the risk of vertebral and nonvertebral fractures compared to alendronate alone in women with prevalent fracture. We performed post hoc analyses of data from patients in ARCH (romosozumab, n = 1739; alendronate, n = 1726) who had a baseline BMD measurement and received at least one open-label alendronate dose. We evaluated 1-year mean BMD and corresponding T-score changes; proportions of patients achieving T-scores > −2.5 at the total hip (TH), femoral neck (FN), and lumbar spine (LS); and group differences in fracture rates after 12 months, while all participants were on alendronate. Subsequently, we investigated the relationship between T-scores achieved at the TH, FN, and LS at 12 months and subsequent fracture incidence. At 1 year, mean change from baseline in TH BMD was 6.3% (T-score change 0.31) with romosozumab versus 2.9% (T-score change 0.15) with alendronate (p < .001). The proportion of patients with TH T-score > −2.5 increased from 34% at baseline to 55% after 1 year of romosozumab and from 32% at baseline to 44% after 1 year of alendronate. Compared with patients receiving alendronate in year 1, those receiving romosozumab had a 75% reduction in new or worsening vertebral fracture (p < .001) in year 2, and a 19% reduction in nonvertebral fracture (p = .120) and 40% reduction in hip fracture (p = .041) during the open-label period. TH and FN T-scores achieved at month 12 were associated with subsequent nonvertebral and vertebral fracture rates and the relationships were independent of treatment received. LS T-score at 12 months was associated with vertebral but not nonvertebral fracture risk. We conclude that 1 year of romosozumab leads to larger BMD gains versus alendronate, and that the T-score achieved with either therapy is related to subsequent fracture risk. These data support the use of T-score as a therapeutic target for patients with osteoporosis. © 2020 The Authors. Journal of Bone and Mineral Research published by American Society for Bone and Mineral Research.     

Better late than never? Experience with intravenous pamidronate treatment in patients with low bone mass or fractures following cardiac or liver transplantation

 Organ transplantation is associated with a high turnover of bone metabolism, and an increased loss of bone mass and incidence of osteoporotic fractures. Established therapies for osteoporosis after organ transplantation are still lacking, however. We report on an intravenous bisphosphonate therapy initiated in transplant patients because of a high rate of bone loss or incident osteoporotic fractures. Twenty-one patients after liver transplantation and 13 patients after heart transplantation received 30 mg pamidronate intravenously every 3 months, combined with 1000 mg calcium and 1000 IU vitamin D per day. The median time interval between transplantation and start of pamidronate treatment was 1.9 years in cardiac patients and 2.3 years in liver patients. Lumbar spine bone mineral density (LS BMD) and femoral neck BMD (FN BMD) were measured before and every 6 months after pamidronate therapy was initiated. Spinal radiographs were performed annually. Biochemical markers of bone metabolism were determined every 3 months, immediately before pamidronate administration. From a previous observational study, 58 patients treated only with calcium and vitamin D were matched for age, sex, pretransplantation LS BMD and time interval between transplantation and the first pamidronate treatment. In the pamidronate-treated patients, the mean increase in LS BMD adjusted for baseline values amounted to 0.080 ± 0.038 g/cm² (8.6 ± 4.0 %) after 1 year and 0.091 ± 0.058 g/cm² (10.4 ± 6.1%) after 2 years compared with 0.001 ± 0.037 g/cm² (0.26 ± 4.0%) after 1 year and 0.015 ± 0.057 g/cm² (1.8 ± 6.0%) after 2 years in the historical control group (absolute LS BMD changes pamidronate group vs historical group p < 0.0001 after 1 and 2 years). The changes of FN BMD were 0.024 ± 0.043 g/cm² (3.2 ± 6.1%) after 1 year and 0.046 ± 0.052 g/cm² (7.0 ± 6.1%) after 2 years in the pamidronate group compared with −0.012 ± 0.043 g/cm² (−1.6 ± 6.1%) after 1 year and −0.013 ± 0.052 g/cm² (−1.1 ± 6.1%) after 2 years in the historical control group (absolute FN BMD changes pamidronate group vs historical group p=0.003 after 1 year and p=0.001 after 2 years). From a total of 287 application cycles of pamidronate treatment, no severe side effects were observed and non-severe side effects were seen in only 39 cycles (13.6%). We conclude that cyclic intravenous pamidronate treatment is beneficial to patients with low bone mass or osteoporotic fractures following transplant, even when not immediately initiated. Received: 5 March 2002 / Accepted: 27 August 2002     

Calcitriol does not prevent bone loss in patients with asthma receiving corticosteroid therapy: a double-blind placebo-controlled trial

Introduction Oral glucocorticoid therapy reduces bone mineral density (BMD) and increases fracture risk. It is uncertain whether inhaled glucocorticoids, the most commonly used long-term therapy for asthma, have a similar effect. If bone loss does occur, it is unclear whether this is preventable by calcitriol. Patients with asthma receiving inhalational plus intermittent oral glucocorticoids lose bone, and treatment with 0.5 μg/day of calcitriol will prevent bone loss.Methods A 2-year randomized double-blind placebo-controlled trial. One hundred eight patients with asthma were stratified by gender, age, and inhaled glucocorticoid dose and treated with calcitriol (n=55) or placebo (n=53). There were 41 men (mean age 53.2±1.7 years) and 67 women (mean age 49.1±1 years) with moderate to severe asthma (requiring ≥800 μg/day of beclomethasone dipropionate or equivalent maintenance therapy). BMD values at the lumbar spine (LS) and femoral neck (FN) were measured at baseline and at 6, 12, and 24 months using dual x-ray absorptiometry.Results Changes in LS and FN BMD. Bone loss occurred in both groups at the FN (both p<0.03) and at the LS in the calcitriol (p<0.001), but not the control, group. Bone loss was not less in the calcitriol group at either site.Conclusion Patients with asthma receiving inhalational plus intermittent short courses of oral glucocorticoids lose bone. Calcitriol is unlikely to be appropriate therapy against this bone loss.     

Peripheral quantitative computed tomography is useful to monitor response to alendronate therapy in postmenopausal women

A forearm fracture (Colles’ fracture) is often the first sign of osteoporosis and may suggest underlying skeletal fragility. Therefore, establishment of a more accurate and reliable method for the measurement of bone mineral density (BMD) at the distal radius would be beneficial for patients who suffer from osteoporosis. The objective of this study was to evaluate the usefulness of peripheral quantitative computed tomography (pQCT) to monitor the response to alendronate therapy at the distal radius in early postmenopausal Japanese women. Thirty-two early postmenopausal women who were diagnosed with osteoporosis or osteopenia were randomized to either alendronate or control treatment. We analyzed the BMD of the distal radius by pQCT, lumbar spine by dual-energy X-ray absorptiometry (DXA) and the biochemical markers of bone turnover (deoxypyridinoline) at baseline, 3, 6 and 12 months. The control group showed a significant decrease from baseline in the trabecular BMD of the radius at 12 months (3.5 ± 3.7%; p < 0.01), whereas the alendronate group showed a significant increase (4.3 ± 8.1%). The changes in the trabecular BMD of the radius between the alendronate and control groups were statistically different at 6 and 12 months (p < 0.01). However, in the total BMD at the diaphysis of the radius, no significant differences were seen in the changes in bone densities between the alendronate and control groups after 1 year of treatment. pQCT detected significant differences in BMD of the radius in early postmenopausal women after 1 year of treatment with alendronate. Collectively, our preliminary clinical trial showed that pQCT might be useful to monitor response to alendronate therapy, especially at the radius, and it might explain why alendronate prevents Colles’ fracture.     

Bone mineral density and osteoporosis among a predominantly Caucasian elderly population in the city of São Paulo, Brazil

This cross-sectional study covered 301 individuals over 70 years of age—207 women (W) and 94 men (M)—living in the city of São Paulo, Brazil. Our aims were to evaluate the prevalence of low bone mineral density (BMD) in this population and the possible factors that influence BMD. The subjects were submitted to a bone densitometry scan (DXA) to evaluate the BMD at lumbar spine (LS), femoral neck (FN), trochanter (T), total femur (TF) and total body composition. At the time, the participants filled in a questionnaire about lifestyle habits, diet and medical history, as well as having blood samples taken to check hormone and biochemical levels. Anthropometric parameters were measured. Osteopenia and osteoporosis were defined in accordance with the criteria suggested by the World Health Organization. In the different sites studied, the prevalence of osteopenia and osteoporosis varied, in men ranging 33.3–57.4% and 6.4–16.1%, respectively, and in women ranging 36.6–56.5% and 22.2–33.2%, respectively. Weight was the variable that most strongly correlated with BMD at the proximal femur in both sexes (men, r =0.44–0.52; women, r =0.48–0.52) and with BMD at LS in women ( r =0.44). Height was the parameter that best correlated with BMD at LS in men ( r =0.34). In men follicle-stimulating hormone, growth hormone and glycemia correlated with BMD at T and TF, while plasma albumin only correlated with BMD at T. In women glycemia correlated with BMD at LS, and follicle-stimulating hormone correlated with BMD at FN, T and TF. In conclusion, we found a high prevalence of osteopenia and osteoporosis in this population, with weight being the best predictor of BMD. The prevalence of osteoporosis and osteopenia at FN was as high in men as that observed in women.     

Overlapping and Continued Alendronate or Raloxifene Administration in Patients on Teriparatide: Effects on Areal and Volumetric Bone Mineral Density—The CONFORS Study

Nine month teriparatide (TPTD) monotherapy followed by co‐administration of raloxifene (RAL) or alendronate (ALN) for another nine 9 months resulted in incremental bone mineral density (BMD) increase. The aim of this study was to investigate the effects of continued antiresorptive treatments for 12 months in the extension phase. Postmenopausal women (n = 125) with severe osteoporosis on ongoing TPTD treatment for 9 months were randomized into three open‐label groups for another 9 months: ALN (70 mg/week, n = 41), RAL (60 mg/d, n = 37) in addition to TPTD or no additional medication (n = 47) except Ca and vitamin D. After discontinuation of TPTD the respective antiresorptives were continued for a further 12 months, while patients in the TPTD monotherapy group received Ca and vitamin D. Amino‐terminal propeptide of type I procollagen (P1NP) and cross‐linked C‐telopeptide (CTX), areal and volumetric BMD at the lumbar spine (LS) and hip were assessed. ALN resulted in continued BMD increase in LS (4.3 ± 1.5%; mean ± SD), femoral neck (4.2 ± 1.6%) and total hip (4 ± 1.6%; p < 0.001 for all), while RAL was only effective at the LS (2.4 ± 1.7%, p < 0.001) but no changes at the femoral neck (0.4 ± 1.4%) or total hip (?0.8 ± 1.5%) were observed. Cortical bone only increased in the ALN group (femoral neck 6.7 ± 2.7% and ?1.3 ± 2.5%; total hip 13.8 ± 2.9% and ?2.3 ± 2.5% for ALN and RAL, p < 0.001 for all; respectively). Analyzing the entire 30 months of therapy, the ALN group revealed the largest BMD increase in all regions. Our results suggest that the addition of ALN to ongoing TPTD and continuing ALN after TPTD was stopped may be beneficial for patients in terms of areal and volumetric BMD increase. Further research is warranted to determine the optimal timing of the initiation of the combination treatment, the respective antiresorptive medication and the potential benefit of this BMD increase regarding fracture prevention. © 2014 American Society for Bone and Mineral Research     

Contribution of Lumbar Spine BMD to Fracture Risk in Individuals With T‐Score Discordance

Fracture risk estimates are usually based on femoral neck (FN) BMD. It is unclear how to address T‐score discordance, where lumbar spine (LS) T‐score is lower than FN T‐score. The objective of this work was to examine the impact of LS BMD on fracture risk, in individuals with lower LS T‐score than FN T‐score. Participants aged 60+ years from the Dubbo Osteoporosis Epidemiology Study with LS and FN BMD measured at first visit, and were followed from 1989 to 2014. Five‐hundred and seventy‐three (573) of 2270 women and 131 of 1373 men had lower LS than FN T‐score by ≥0.6 standard deviation (SD) (low‐LS group based on least significant change). In low‐LS women, each 1 SD lower LS T‐score than FN was associated with a 30% increase in fracture risk (hazard ratio [HR] 1.30; 95% CI, 1.11 to 1.45). For low‐LS men there was a 20% nonsignificant increase in fracture risk for each 1 SD lower LS than FN T‐score (HR 1.20; 95% CI, 0.10 to 1.67). Low‐LS women had greater absolute fracture risks than the rest of the women. This increased risk was more apparent for lower levels of FN T‐score and in older age groups. At an FN T‐score of –2, low‐LS women had a 3%, 10%, and 23% higher 5‐year absolute fracture risk than non‐low LS women in the 60 to 69 year, 70 to 79 year, and 80+ years age‐groups, respectively. Furthermore, an osteoporotic LS T‐score increased 5‐year absolute fracture risk for women with normal or osteopenic FN T‐score by 10% to 13%. Men in the low‐LS group had very few fractures; therefore, a meaningful analyses of fracture risk could not be conducted. This study shows the significant contribution of lower LS BMD to fracture risk over and above FN BMD in women. A LS BMD lower than FN BMD should be incorporated into fracture risk calculators at least for women in older age‐groups. © 2015 American Society for Bone and Mineral Research.     

Use of Phalangeal Bone Mineral Density and Multi-site Speed of Sound Conduction to Monitor Therapy with Alendronate in Postmenopausal Women

In women with postmenopausal osteoporosis (PMO), response to therapy with bisphosphonates is conventionally monitored using central-site (hip and spine) bone mineral density (BMD), but more convenient alternatives are desirable. During a randomized parallel-group study of the efficacy of once-weekly (80 mg vs 160 mg) oral alendronate in the treatment of PMO, 81 women (mean age 70.2 years ± 4.6 SD) had BMD measurements of total hip (TH) and lumbar spine (LS) (L1–L4, Hologic); and of the middle phalanx of the middle digit of the non-dominant hand (accuDXA) at baseline and after 6 and 12 months of therapy with alendronate. At the same timepoints, subjects also had measurements of speed of sound (SOS) through bone at four sites (distal 1/3 radius, proximal phalanx of the third finger, midshaft of the tibia and fifth metatarsal) using the Sunlight Omnisense Ultrasound Bone Sonometer. Data from both patient groups were pooled for this analysis. Mean TH BMD at baseline was 0.705 g/cm²± 0.093 (SD) and increased by 1.7%± 2.3% and 2.5%± 2.3% at 6 and 12 months respectively (p= 0.09 and p<0.0001). Mean LS BMD at baseline was 0.718 ± 0.076 g/cm² and increased by 3.9%± 3.6% and 6.1%± 3.5 % at 6 and 12 months respectively (both p<0.0001). There was no statistically significant change from baseline in mean BMD by accuDXA at either 6 or 12 months. The only statistically significant changes in SOS were at the radius (decrease in SOS at 12 months, p = 0.04) and tibia (increase at 6 months, p<0.01, but no change between baseline and 12 months). Baseline correlation coefficients between accuDXA and LS and TH DXA were 0.22 (p= 0.05) and 0.27 (p= 0.02) respectively. Correlation coefficients between SOS and LS DXA ranged from 0.05 to 0.22; and between SOS and TH DXA ranged from –0.08 to 0.10 (all p= NS). These data suggest that the response to alendronate therapy over this time period cannot be measured by accuDXA or Sunlight SOS at the sites studied. Received: 26 June 2001 / Accepted: 27 September 2001     

Effect of Teriparatide or Risedronate in Elderly Patients With a Recent Pertrochanteric Hip Fracture: Final Results of a 78‐Week Randomized Clinical Trial

We present final results of a study comparing teriparatide 20 μg every day (QD) with risedronate 35 mg once per week (QW) started within 2 weeks after surgery for a pertrochanteric hip fracture. Patients with BMD T‐score ≤ –2.0 and 25OHD ≥9.2 ng/mL were randomized to receive 26‐week double‐dummy treatment plus calcium and vitamin D, followed by 52‐week open‐label treatment with the same assigned active drug. Primary endpoint was change from baseline in lumbar spine (LS) BMD at 78 weeks. Secondary and exploratory endpoints were change in BMD at the proximal femur, function, hip pain (Charnley score and 100 mm Visual Analog Scale [VAS]), quality of life (Short Form‐36), radiology outcomes, and safety. Data were analyzed with mixed models for repeated measures (MMRM) and logistic regression. Totally, 224 patients were randomized; 171 (teriparatide: 86) contributed to the efficacy analyses (mean ± SD age: 77 ± 7.7 years, 77% females). Mean baseline LS, femoral neck (FN), and total hip (TH) T‐scores were –2.16, –2.63, and –2.51, respectively. At 78 weeks, BMD increased significantly more with teriparatide compared to risedronate at the LS (+11.08% versus +6.45%; p < 0.001) and FN (+1.96% versus –1.19%; p = 0.003), with no significant between‐group difference in TH BMD. Timed up‐and‐go (TUG) test was significantly faster with teriparatide at 6, 12, 18, and 26 weeks (differences: –3.2 to –5.9 s; p = 0.045 for overall difference). Hip pain during TUG test by 100 mm VAS was significantly lower with teriparatide at 18 weeks (adjusted difference: –11.3 mm, p = 0.033; –10.0 and –9.3 mm at 12 and 26 weeks, respectively; p = 0.079 for overall difference). Other secondary and exploratory outcomes were not different. Teriparatide group showed two new hip fractures versus seven with risedronate (p = 0.171) and more frequent hypercalcemia and hyperuricemia. In conclusion, 78‐week treatment with teriparatide showed significantly greater increases in LS and FN BMD, less pain, and a faster TUG test versus risedronate. © 2016 American Society for Bone and Mineral Research.