重组人PTH(1-34)与依降钙素对绝经后女性骨质疏松患者骨代谢和血清SPARC的影响

目的 观察重组人甲状旁腺素(1-34)[ rhPTH(1-34)]和依降钙素对绝经后女性骨质疏松患者骨密度和骨代谢及血清富含半胱氨酸的酸性蛋白( SPARC)水平的影响.方法 124例绝经后女性骨质疏松症患者随机分为PTH组(n=89),给予rhPTH (1-34)200 U皮下注射每日一次和CT组(n=35),给予依降钙素20U肌肉注射每周一次,共12个月.于治疗前、治疗后6个月、12个月测定各组一般生化指标,腰椎L2-4、左股骨颈、大转子及Ward三角的骨密度、血清钙、磷水平.采用酶联免疫法(ELISA)测定血清骨碱性磷酸酶(BSAP)、富含半胱氨酸的酸性蛋白(SPARC)等骨代谢相关指标水平情况.结果 rhPTH治疗12个月后腰椎L2-4骨密度较基线增加了7.9％(P＜0.05);血清钙和BSAP水平12个月时较治疗前分别增加了8.3％和93.4％(均P＜0.05);血清SPARC水平12个月时较基线增加了12.6％(P＜0.05);与治疗前相比,依降钙素治疗12个月时腰椎L2-4骨密度增加了3.2％(P＜0.05);血清钙、BSAP和SPARC水平均无显著改变.结论 rhPTH (1-34)能显著促进骨合成代谢,其疗效优于依降钙素;血清SPARC水平的增加可能在rhPTH促进成骨过程中起重要作用.     

绝经后骨质疏松合并骨折患者外周血清瘦素表达水平

目的 观察绝经后骨质疏松(OP)合并骨折患者外周血瘦素表达水平.方法 连续选择21例绝经后OP合并骨折患者(OP合并骨折组)、26例绝经后OP组和30例绝经后正常骨密度女性(对照组),入选对象均在开始治疗前接受了腰椎骨质密度(BMD)、双侧股骨上端BMD、血清瘦素(LEP)、骨钙素(BGP)和碱性磷酸酶(AKP)等指标测定.结果 OP合并骨折组和OP组的血清LEP、BGP和AKP浓度均明显高于对照组,而OP合并骨折组上述3个骨代谢指标测定值也同时低于OP组(均P<0.01～0.05).OP合并骨折组和OP组的腰椎L1～L4和左、右股骨颈的BMD测定值均明显少于对照组,而OP合并骨折组上述3个部位BMD测定值也同时低于OP组(均P<0.01～0.05).结论 绝经后OP合并骨折患者存在明确外周血LEP高水平表达.     

云克联合低频脉冲电磁场强化治疗老年骨质疏松的疗效

目的 探讨云克联合低频脉冲电磁场(pulsed electromagnetic fields,PEMFs)强化治疗对老年骨质疏松(OP)疼痛症状及提高骨密度(BMD)的临床作用.方法 入选的124例原发性OP患者,采用前瞻对照配对分组,每组31例.云克治疗组,给予云克注射液静推;脉冲电磁场治疗组,给予PEMFs治疗;云克治疗+脉冲电磁场治疗组,给予云克+PEMFs治疗;阿仑膦酸钠对照组,给予阿仑膦酸钠(70 mg/片),晨起空腹每周1片口服.前三组均20d1个疗程,行3个疗程治疗.所有入选的病人均摄入适量的钙和维生素D.于治疗前、治疗后2个月及6个月观察患者疼痛症状的改变情况;测定第四腰椎(L4)及股骨颈BMD.结果 ①四组治疗2个月后疼痛改善效果的有效率分别为67.7%、74.2%、93.5%、35.5%;治疗6个月后疼痛症状缓解的有效率分别为80.6%、77.4%、96.8% 、61.3%.②云克治疗组治疗2个月后L4的BMD与治疗前差异显著,治疗6个月后L4及股骨颈的BMD与治疗前均有显著差异(P＜0.05);脉冲治疗组及联合治疗组治疗2个月、6个月后,L4和股骨颈的BMD增加明显,与治疗前差异显著(P＜0.05).对照组治疗6个月后,L4的BMD增加,与治疗前差异显著(P＜0.05).③联合治疗组治疗2个月、6个月后,L4及股骨颈的BMD增加明显,与云克治疗组、脉冲治疗组、对照组相比,有显著性差异(P＜0.05).结论 云克联合PEMFs强化治疗老年型骨质疏松能在短期内迅速有效地缓解患者的疼痛症状,提高患者的BMD.     

鲑鱼降钙素联合碳酸钙治疗原发性Ⅱ型骨质疏松症的临床观察

目的:探讨鲑鱼降钙素联合碳酸钙对老年人骨质疏松症(OP)的治疗效果。方法:回顾性分析78例老年OP患者的临床资料,随机分为2组,使用鲑鱼降钙素联合碳酸钙剂为治疗组42例;使用单纯口服碳酸钙为对照组36例,以定量CT(QCT)测定2~4腰椎的骨密度(BMD),比较治疗前及治疗6个月后BMD和临床症状的改善情况。结果:治疗组总有效率90.5%;腰2~4椎BMD升高,同时骨痛症状明显改善。对照组总有效率41.7%,治疗前、后BMD无明显改变。结论:鲑鱼降钙素能改善OP患者腰椎的BMD,其机制与增加骨合成和降低骨吸收有关。     

阿仑膦酸钠与唑来膦酸治疗绝经后骨质疏松症疗效比较

目的回顾性分析口服阿仑膦酸钠以及静脉注射唑来膦酸治疗绝经后骨质疏松症的临床疗效。方法从2014年12月-2016年1月就诊的绝经后骨质疏松妇女中筛选出接受阿仑膦酸钠治疗至少1年和接受唑来膦酸治疗至少1年的妇女各80例作为研究对象,分别为口服阿仑膦酸钠组(70 mg/周)以及静脉注射唑来膦酸组(5 mg/年),所有患者均口服碳酸钙600 mg/d和维生素D 125 IU/d。采集所有患者基线及治疗12个月后腰椎L1-4、股骨颈和全髋部位的骨密度(bone mineral density,BMD),血清I型胶原羧基端肽交联(carboxy-telopeptide of type Ⅰ collagen,β-CTX)等资料,进行组间及药物治疗前后对照。结果阿仑膦酸钠组患者平均年龄(66.48±8.39)岁,唑来膦酸组患者平均年龄(65.11±7.69)岁。治疗12个月后,阿仑膦酸钠组腰椎BMD上升(5.46±4.42)%、股骨颈BMD上升(2.81±3.83)%,全髋BMD上升(2.72±2.76)%(均P0.001)。唑来膦酸组腰椎BMD上升(6.66±6.37)%、股骨颈BMD上升(1.97±3.13)%,全髋BMD上升(2.20±3.63)%(均P0.001)。分别比较两药物组腰椎、股骨颈、全髋BMD以及β-CTX变化率差异均无统计学意义(P值分别为0.216、0.132、0.312、0.066)。结论阿仑膦酸钠70 mg/周和唑来膦酸5 mg/年治疗1年均能够显著提高绝经后骨质疏松妇女的腰椎以及髋部BMD,两者疗效比较,差异无统计学意义(P0.05)。     

重组人甲状旁腺激素(1-34)对骨质疏松患者血清Cbfa-1和MMP-13水平的影响

探讨重组人甲状旁腺素[rhPTH(1-34)]对绝经后骨质疏松患者血清核心结合因子a-1(Cbfa-1)和基质金属蛋白酶13(MMP-13)水平的影响.rhPTH(1-34)治疗6个月后,血清Cbfa~(-1)[(54.0±2.4)对(62.2±2.8)μg/L,P<0.05]、MMP-13[(2.51±0.15)对(3.96±0.24)μg/L,P<0.01]显著降低;相关性分析显示治疗前血清Cbfa-1与MMP-13呈正相关(r=0.74,P<0.01).提示小剂量rhPTH(1-34)皮下注射能促进骨的合成,并使血清Cbfa-1和MMP-13水平下降.     

女性围绝经期骨密度和E2、PTH、CT相关性分析

目的 本文分析了女性在围绝经期血清雌二醇(E2)、甲状旁腺素(PTH)、降钙素(CT)水平的变化对骨密度(BMD)的影响. 方法 测定绝经前期正常体检(A)组、绝经期(B)组和绝经时间＞1年(C)组的腰椎L2～L4、股骨颈、大转子、华氏三角区正侧位的BMD及血清中E2、PTH、CT的浓度,对BMD与多个变量之间的关系进行相关性分析. 结果 与A组比较,B组及C组BMD、E2及CT 水平显著降低,而 PTH水平显著升高.C组BMD、E2水平显著低于B组,而CT及PTH在2组间差异无统计学意义.相关性分析显示在绝经期妇女中E2、CT与BMD呈正相关;PTH与BMD呈负相关. 结论 女性E2、PTH、CT水平影响骨形成、骨吸收和BMD,使骨代谢趋向于负平衡,是女性易发骨质疏松的重要原因.     

鲑鱼降钙素治疗老年骨质疏松患者的疗效观察

目的 探讨鲑鱼降钙素注射液治疗老年骨质疏松(0P)患者的疗效.方法 将120例OP患者随机分成实验组和对照组,每组各60人,实验组用鲑鱼降钙素联合钙剂治疗,对照组单纯使用钙剂治疗.两组治疗前后均测定24腰椎、骨股颈及wards三角骨密度,记录患者临床症状.结果 治疗2个月后,实验组骨痛改善率明显高于对照组(P＜0.05),治疗6个月后实验组血清钙均值及尿羟脯氨酸(HOP)均值均有明显变化(P＜0.05),实验组患者L2-L3、腰椎均值骨密度(BMD)较前明显升高(P＜0.05).对照组BMD治疗前后无明显变化(P＞0.05).结论 鲑鱼降钙素与钙剂联合应用治疗老年OP,能明显减轻患者疼痛,改善症状,增加BMD,是一种疗效良好的安全方法.     

绝经后女性骨髓脂肪含量与骨密度的相关性

目的探讨基于磁共振波谱成像(magnetic resonance spectroscopy,MRS)评估绝经后女性腰椎骨髓脂肪含量的变化规律及其与骨密度(bone mineral density,BMD)的关联性。方法 42例绝经后女性分别行MRS扫描计测L3椎体骨髓脂肪分数(fat fraction,FF)及双能X线吸收检测(dual-energy X-ray absorptiometry,DXA)扫描获取腰椎(L1-4)T值及BMD值,按T值分为正常骨量组、低骨量组及骨质疏松(osteoporosis,OP)组。采用协方差分析及偏相关分析组间FF变化规律及FF值与BMD的相关性。结果正常骨量组、低骨量组及OP组FF分别为51.28±11.03、59.73±10.09、69.96±11.42。协方差分析,校正年龄、绝经年龄、BMI混杂因素后,不同骨量组间FF值差异仍存在统计学意义(F=4.14,P=0.005)。FF与BMD存在中度负相关性(r=-0.557,P=0.000),校正上述混杂因素,其相关性依然存在(r=-0.510,P=0.001)。结论绝经后妇女骨受损伴随着骨髓脂肪增多,FF对OP的诊疗有一定评估价值     

2型糖尿病对绝经后妇女骨密度的影响

目的探讨2型糖尿病(T2DM)和绝经后妇女骨密度(BMD)的相关性。方法选择四川绵阳地区绝经后妇女208例,用双能X线骨密度仪(DEXA)检测正位第2～4腰椎、左侧股骨颈、股骨大转子和Ward’s三角区BMD;T2DM诊断根据美国糖尿病协会2010年诊断标准。结果T2DM患者骨质疏松(OP)患病率53.13%、非T2DM患者OP患病率45.10%,T2DM绝经后女性OP患病率显著高于非T2DM患者(P<0.01)。T2DM患者股骨颈(0.647±0.138)、Ward’s三角区(0.608±0.149)BMD明显低于非T2DM患者股骨颈(0.836±0.186)、Ward’s三角区(0.731±0.097)BMD(P<0.05),T2DM患者第2～4腰椎、大转子BMD与非T2DM组比较无明显差异(P>0.05)。结论 T2DM与绝经后妇女的BMD存在相关性,T2DM是导致绝经后妇女低BMD的一个危险因素。     

Increased urinary N-telopeptide cross-linked type 1 collagen predicts bone loss in patients with inflammatory bowel disease

OBJECTIVE: Reduced bone mineral density (BMD) is common in patients with inflammatory bowel disease (IBD), but the factors associated with its longitudinal rate of change have not been established. We prospectively assessed the rate of change in BMD, and its association with biochemical markers of bone turnover. METHODS: Twenty-two patients with Crohn's disease and 14 ulcerative colitis patients age 37.1 +/- 11.6 yr were followed for 2 yr. Lumbar spine (L2-L4) and femoral neck BMD were measured by dual x-ray absorptiometry at baseline and 24 months. Bone-specific alkaline phosphatase, osteocalcin, urinary N-telopeptide crosslinked type 1 collagen (NTx), parathyroid hormone, and 25-hydroxyvitamin-D were determined at baseline. RESULTS: At baseline, 59% of Crohn's patients and 43% of ulcerative colitis patients were osteoporotic, with spine or femoral neck BMD T-score < -2.5. Spine BMD, and spine and femoral neck T-scores were lower and disease duration was longer in nine patients with ileal resection compared with nonoperated patients (0.84 +/- 0.15 g/cm2 vs 0.96 +/- 0.11 g/cm2, -3.0 +/- 1.5 vs -1.7 +/- 1.3, -3.2 +/- 1.5 vs -2.2 +/- 1.0, respectively; all p < 0.05). At 24 months, 13/36 (36%) and 14/36 (39%) patients experienced spinal and femoral neck bone loss, respectively, with mean annual percent BMD changes of -2.0% and -1.5%, respectively. NTx, a bone resorption marker, inversely correlated with spinal BMD rate of change (r = -0.4, p < 0.05). Using quartiles analysis, patients with the highest NTx (Q4) experienced the greatest decrease in spine BMD compared with patients with the lowest NTx (Q1). CONCLUSIONS: Spine and femoral neck bone loss continues over time in more than one-third of IBD patients. Increased NTx level predicts spinal bone loss in IBD patients.     

Opposite bone remodeling effects of teriparatide and alendronate in increasing bone mass

BACKGROUND: Antiresorptive agents for the treatment of osteoporosis suppress bone remodeling and reestablish bone turnover at a lower rate to reduce bone loss. Recombinant teriparatide (human parathyroid hormone 1-34) stimulates bone formation, increases bone mass, and improves bone microarchitecture. We contrasted the effects of once-daily doses of 20 mug of teriparatide and 10 mg of alendronate sodium on bone mineral density (BMD) and markers of bone turnover. METHODS: Markers of bone turnover and areal BMD were assessed in 203 postmenopausal women with osteoporosis in an 18-month randomized parallel double-blind study; volumetric BMD was measured in a subset of women. RESULTS: Teriparatide significantly increased markers of bone turnover that peaked at 6 months (serum procollagen type I N-terminal propeptide, 218%, and urinary N-telopeptide corrected for creatinine, 58%; P<.001); alendronate significantly decreased the markers at 6 months (-67% and -72%, respectively; P<.001). At 18 months, areal and volumetric spine BMDs were significantly higher with teriparatide than with alendronate (10.3% vs 5.5% [P<.001] and 19.0% vs 3.8% [P<.01], respectively). Areal femoral neck BMD was significantly higher than baseline in the teriparatide and alendronate groups (3.9% and 3.5%, respectively). There were no significant differences in trabecular femoral neck BMD between the teriparatide and alendronate groups (4.9% and 2.2%, respectively). Cortical volumetric femoral neck BMD was significantly different between the teriparatide and alendronate groups (-1.2% and 7.7%, respectively; P = .05). CONCLUSION: Two distinct options for the management of osteoporosis lead to increases in BMD by opposite mechanisms of action on bone remodeling.     

Effect of alendronate and MK-677 (a growth hormone secretagogue), individually and in combination, on markers of bone turnover and bone mineral density in postmenopausal osteoporotic women

GH increases bone turnover and stimulates osteoblast activity. We hypothesized that administration of MK-677, an orally active GH secretagogue, together with alendronate, a potent inhibitor of bone resorption, would maintain a higher bone formation rate relative to that seen with alendronate alone, thereby generating greater enhancement of bone mineral density (BMD) in women with postmenopausal osteoporosis. We determined the individual and combined effects of MK-677 and alendronate administration on insulin-like growth factor I levels and biochemical markers of bone formation (osteocalcin and bone-specific alkaline phosphatase) and resorption [urinary N-telopeptide cross-links (NTx)] for 12 months and BMD for 18 months. In a multicenter, randomized, double blind, placebo-controlled, 18-month study, 292 women (64-85 yr old) with low femoral neck BMD were randomly assigned in a 3:3:1:1 ratio to 1 of 4 daily treatment groups for 12 months: MK-677 (25 mg) plus alendronate (10 mg); alendronate (10 mg); MK-677 (25 mg); or a double dummy placebo. Patients who received MK-677 alone or placebo through month 12 received MK-677 (25 mg) plus alendronate (10 mg) from months 12-18. All other patients remained on their assigned therapy. All patients received 500 mg/day calcium. The primary results, except for BMD, are provided for month 12. MK-677, with or without alendronate, increased insulin-like growth factor I levels from baseline (39% and 45%; P < 0.05 vs. placebo). MK-677 increased osteocalcin and urinary NTx by 22% and 41%, on the average, respectively (P < 0.05 vs. placebo). MK-677 and alendronate mitigated the reduction in bone formation compared with alendronate alone based on mean relative changes in serum osteocalcin (-40% vs. -54%; P < 0.05, combination vs. alendronate) and reduced the effect of alendronate on resorption (NTx) as well (-52% vs. -61%; P < 0.05, combination vs. alendronate). MK-677 plus alendronate increased BMD at the femoral neck (4.2% vs. 2.5% for alendronate; P < 0.05). However, similar enhancement was not seen with MK-677 plus alendronate in BMD of the lumbar spine, total hip, or total body compared with alendronate alone. GH-mediated side effects were noted in the groups receiving MK-677, although adverse events resulting in discontinuation from the study were relatively infrequent. In conclusion, the anabolic effect of GH, as produced through the GH secretagogue MK-677, attenuated the indirect suppressive effect of alendronate on bone formation, but did not translate into significant increases in BMD at sites other than the femoral neck. Although the femoral neck is an important site for fracture prevention, the lack of enhancement in bone mass at other sites compared with that seen with alendronate alone is a concern when weighed against the potential side effects of enhanced GH secretion.     

Risedronate reverses bone loss in postmenopausal women with low bone mass: results from a multinational, double-blind, placebo-controlled trial. BMD-MN Study Group

Our objective was to investigate the efficacy and tolerability of risedronate in postmenopausal women with low bone mass. Women with a mean lumbar spine T-score of -2 or less (n = 543) received 24 months of placebo or risedronate (2.5 or 5 mg/day). All received calcium (1 g/day). The principal outcome measures were bone mineral density (BMD) at the lumbar spine, femoral neck, and femoral trochanter. At 24 months, lumbar spine BMD increased from baseline by 4% with 5 mg risedronate and 1.4% in the 2.5-mg group, compared with no change with placebo. Efficacy was similar in women who were less than 5 yr and more than 5 yr postmenopausal. At 24 months, risedronate (5 mg) had also increased BMD at the femoral neck and trochanter, whereas BMD decreased in the placebo group. BMD increases were seen at all three sites with risedronate (5 mg) after only 6 months of therapy. Risedronate was well tolerated; upper gastrointestinal adverse events were similar to placebo. We conclude that risedronate (5 mg) increases BMD rapidly and effectively and is well tolerated in postmenopausal women with low bone mass, regardless of time since menopause.     

Reduced bone mineral density in male rheumatoid arthritis patients: frequencies and associations with demographic and disease variables in ninety-four patients in the Oslo County Rheumatoid Arthritis Register

OBJECTIVE: To examine reductions in bone mineral density (BMD) and factors associated with reduced BMD in 94 male rheumatoid arthritis (RA) registry patients ages 20-70 years. METHODS: Dual-energy x-ray absorptiometry was used to measure BMD in the anteroposterior lumbar spine at L2-LA, the femoral neck, and the total hip, and clinical data were collected. The patients were recruited from a validated county RA registry (completeness 85%) comprising 192 men ages 20-70 years. Age-specific BMD values were compared with a pooled healthy European/United States population. Bivariate and multivariate analyses were performed to determine demographic and disease-related associations with BMD and reduced bone mass (Z score of < or =1 SD below the mean value in controls). RESULTS: A statistically significant BMD reduction was found only for the oldest age group (60-70 years): 5.2% reduction in the femoral neck and 6.9% in the total hip. No BMD reduction was found at L2-L4. The proportions (95% confidence intervals) of RA patients with Z scores of < or =1 SD below control (16% expected) were 30.9% (21.6-40.2) for L2-L4, 30.8% (95% CI 21.3-40.3) for the femoral neck, and 33.0% (95% CI 23.3-42.7) for the total hip. Disease activity and severity measures were, in general, not associated with BMD or reduced bone mass. CONCLUSION: A 2-fold statistically significant increased frequency of patients with reduced bone mass (Z score of < or =1 SD below control; 16% expected) was found for both the spine and the hip. The only significant reduction in BMD by age group was for the hip in patients who were ages 60-70 years, with no reduction in L2-LA BMD. Multivariate analyses did not reveal consistent associations between reduced BMD and demographic or disease variables.     

Bone health in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED): findings in 25 adults

OBJECTIVE: Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is characterized by chronic mucocutaneous candidiasis and autoimmune destruction of endocrine organs. The resulting endocrinopathies and their treatment may impact bone health. The purpose of our study was to assess bone health and its correlates in adult patients with APECED. PATIENTS AND METHODS: Twenty-five adults (12 males) with APECED were prospectively assessed. Data on their previous medical history were collected from hospital records. Areal bone mineral density (aBMD) for the lumbar spine (L1-L4), femoral neck and whole body as well as volumetric BMD (vBMD) for the lumbar spine (L2-L4) were measured with dual-energy X-ray absorptiometry (DXA). RESULTS: Mean age was 34 years (range 21-59 years). All patients had 1-4 autoimmune endocrinopathies, the most common being adrenocortical failure (20 patients) and hypoparathyroidism (18 patients). Osteopaenia or osteoporosis was present in 28%. The median (range) aBMD Z-scores were for the lumbar spine -0.3 (-2.3 to +3.3) and for the femoral neck, -0.1 (-2.2 to +2.0). The BMD Z-scores tended to be higher in patients with hypoparathyroidism than in patients with normal parathyroid function (at the lumbar spine +0.4 vs.-1.2, P = 0.016, and at the femoral neck +0.3 vs.-0.4, P = 0.090). Adrenocortical failure had a negative impact on BMD. Six patients had had low-impact fractures and three were diagnosed with compression fractures. CONCLUSIONS: Despite the complex endocrine problems, the overall prevalence of symptomatic osteoporosis is low in adults treated for APECED. Osteopaenia is frequently observed and warrants follow-up. Treated hypoparathyroidism may have a positive, and adrenocortical failure a negative, impact on bone health.     

Bone loss in patients treated with pulses of methylprednisolone is not negligible: a short term prospective observational study

OBJECTIVE: To examine the influence of intravenous pulsed methylprednisolone (MP) on bone mass. METHODS: 38 patients (30 women) with various rheumatic disorders requiring intravenous MP pulse treatment were examined at baseline and after 6 months with dual energy x ray absorptiometry (DXA), measuring hip and lumbar spine bone mineral density (BMD). Demographic and clinical data were collected. RESULTS: Demographics showed: mean (SD) age 48.4 (16.3) years, body mass index 24.9 (5.1) kg/m(2), and median (range) disease duration 3.2 (0.1-40.0) years. During follow up patients received a mean cumulative MP dose of 3.0 (1.6) g given as 5.7 (2.0) pulses over a median period of 5.7 (2.3-33.7) months. 34/38 (89%) patients were also pulsed with cyclophosphamide, 20 (53%) were taking oral corticosteroids, and 8 (21%) were using either bisphosphonates or oestrogen. At the end of the study mean BMD was reduced by -2.2% at the femoral neck, -1.1% at the total hip, and -1.0% at the spine L2-4. In subgroups BMD increased in patients treated with bisphosphonates or oestrogen (femoral neck +1.6%, total hip +3.2%, spine L2-4 +4.5%), whereas BMD decreased at all sites in patients not treated with antirersorptive treatment, both for users (femoral neck -4.4%, total hip -2.4%, spine L2-4 -2.1%) and non-users of concomitant oral prednisolone (femoral neck -1.7%, total hip -1.9%, spine L2-4 -2.6%). CONCLUSION: Treatment with intravenous pulses of MP leads to a high rate of bone loss. Prevention of bone loss in these patients with bisphosphonates and oestrogens should be considered.     

Effect of L-000845704, an alphaVbeta3 integrin antagonist, on markers of bone turnover and bone mineral density in postmenopausal osteoporotic women

The alphaVbeta3 integrin (vitronectin receptor) plays a pivotal role in bone resorption. We hypothesized that L-000845704, an alphaVbeta3 integrin antagonist, would potently inhibit bone resorption, thereby increasing bone mass as assessed by bone mineral density (BMD) in women with postmenopausal osteoporosis. In a multicenter, randomized, double-blind, placebo-controlled, 12-month study, 227 women (average 63 yr) with low lumbar spine or femoral neck BMD were randomly assigned to receive 100 or 400 mg L-000845704 once daily (qd), 200 mg L-000845704 twice daily (bid), or placebo. L-000845704 increased lumbar spine BMD (2.1, 3.1, and 3.5% for the 100-mg-qd, 400-mg-qd, and 200-mg-bid treatment groups, respectively, vs. -0.1% for placebo; P < 0.01 all treatments vs. placebo). Only 200 mg L-000845704 bid significantly increased BMD at the hip (1.7 vs. 0.3% for placebo; P < 0.03) and femoral neck (2.4 vs. 0.7% for placebo; P < 0.05). No L-000845704 group increased total body BMD. All doses of L-000845704 resulted in a similar approximately 42% decrease from baseline of N-telopeptide cross-links (P < 0.001 vs. placebo). L-000845704 was generally well tolerated; adverse events resulting in discontinuation from the study were relatively infrequent. In conclusion, the antiresorptive effect of the alphaVbeta3 integrin antagonist L-000845704 translated into significant increases in lumbar spine BMD. Furthermore, 200 mg L-000845704 bid provided efficacy at the hip sites. These data suggest that the alphaVbeta3 integrin antagonist L-000845704 could be developed as an effective therapeutic agent for osteoporosis.     

重组人甲状旁腺素（1-34）治疗原发性骨质疏松症疗效观察

目的 观察对比重组人甲状旁腺素（1-34）[PTH（1-34）]和降钙素对原发性骨质疏松症的疗效.方法 将20例原发性骨质疏松症患者随机分为试验组和对照组.试验组皮下注射PTH（1-34）20μg,每天1次;对照组肌肉注射降钙素20 IU,每周1次,两组均每日口服钙尔奇D 600mg,连续治疗6个月.所有患者于治疗前后枪测腰椎（L2～L4）、股骨颈骨密度、血钙及血清骨特异性碱性磷酸酶（BSAP）、血清I型胶原交基C端肽（CTX）、PTH等指标及观察有无不良反应.结果 治疗后PTH组和降钙素组腰椎（L2～L4）骨密度变化较治疗前均有明显增加,且有统计学意义.治疗后两组股骨颈骨密度变化较治疗前无明显改善（P〉0.05）,两组间比较无明显差异（P〉0.05）.PTH组BSAP变化值明显高于对照组,两组间比较差异有统计学意义（P〈0.01）;两组治疗后血、尿常规、肝、肾功能均未见明显异常.结论 PTH（1-34）与降钙素都能显著提高腰椎（L2～L4）骨密度,对于原发性骨质疏松症治疗安全有效.     

Comparison of alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women

This study compared the effects of oral alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women. Women at least 5 yr postmenopause (n = 299) were randomized to either 10 mg alendronate, matching alendronate placebo, or open-label intranasal calcitonin 200 IU daily for 12 months. Hip and spine bone mineral density (BMD) and markers of bone turnover were measured, and safety and tolerability were assessed. Alendronate produced greater increases in BMD than calcitonin at 12 months at the lumbar spine (5.16% vs. 1.18%; P < 0.001), trochanter (4.73% vs. 0.47%; P < 0.001), and femoral neck (2.78% vs. 0.58%; P < 0.001). Changes in BMD with calcitonin were greater than with placebo at the femoral neck, but were not different from placebo at either the trochanter or lumbar spine. Greater decreases in bone turnover were seen with alendronate than with calcitonin (serum bone-specific alkaline phosphatase, 43% vs. 9%, P < 0.001; urinary N-telopeptide, 62% vs. 11%, P < 0.001). Similar percentages of patients in each group reported an adverse experience during the study. We conclude that, in postmenopausal women with osteoporosis, 12 months of therapy with alendronate produced significantly greater increases in BMD of the hip and spine and greater decreases in bone turnover than intranasal calcitonin.