伊班膦酸钠联合甲状旁腺素治疗卵巢切除后的骨质疏松症

背景：注射用重组人甲状旁腺素可以显著增加骨质形成、骨质密度,并显著减少骨折发生率,在治疗绝经后骨质疏松症方面具有良好的疗效。目的：观察伊班膦酸钠联合重组人甲状旁腺素（1-34）治疗卵巢切除大鼠骨质疏松症的效果。方法：32只健康大鼠随机数字表法均分成对照组、模型组、伊班膦酸钠组和伊班膦酸钠＋甲状旁腺素组,除对照组外其他3组均进行卵巢切除,4周后分别皮下注射生理盐水或伊班膦酸钠或伊班膦酸钠＋甲状旁腺素。结果与结论：模型组大鼠骨钙含量明显低于其他3组,伊班膦酸钠＋甲状旁腺素治疗可提高大鼠骨钙含量和骨密度,降低血钙和碱性磷酸酶水平,联合用药的作用优于单独用药。说明伊班膦酸钠对卵巢切除骨质疏松模型大鼠骨量的丢失有显著抑制作用,伊班膦酸钠联合甲状旁腺素可以增加骨含量,为治疗妇女绝经后骨质疏松提供了合理用药依据。     

伊班膦酸钠治疗乳腺癌骨转移的疗效分析

目的　探讨伊班膦酸钠 (艾本 )及其联合化疗对乳腺癌骨转移的疗效。方法　 2 3例单用伊班膦酸钠治疗 ,2 5例伊班膦酸钠联合化疗。比较两种方法的疗效。结果　单用伊班膦酸钠治疗 ,疼痛缓解率87% (2 0 / 2 3例 ) ,卡氏评分标准平均提高 10分 ;伊班膦酸钠加化疗组 ,疼痛缓解率 10 0 % (2 5 / 2 5例 ) ,卡氏评分标准平均提高 2 0分。结论　单用伊班膦酸钠或伊班膦酸钠加化疗对乳腺癌骨转移的疗效均好 ,可缓解疼痛 ,促进骨质修复。伊班膦酸钠加化疗效果更佳。     

伊班膦酸钠联合化疗对非小细胞肺癌骨转移患者炎性因子及骨代谢指标的影响

目的 探讨伊班膦酸钠联合化疗对非小细胞肺癌(NSCLC)骨转移患者炎性因子及骨代谢指标的影响。方法 选取120例NSCLC骨转移患者作为研究对象,其中肺腺癌患者采用培美曲塞、卡铂联合伊班膦酸钠治疗,肺鳞癌患者采用注射用紫杉醇脂质体或注射用白蛋白紫杉醇、卡铂联合伊班膦酸钠治疗,均化疗2个周期。比较化疗前和化疗2个周期后患者炎性因子[血清C反应蛋白(CRP)、降钙素原(PCT)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)]水平、骨代谢指标(血清骨钙素氨基中分子片段、Ⅰ型前胶原氨基端肽、Ⅰ型胶原羧基端肽β特殊序列、骨特异性碱性磷酸酶)水平、骨痛评分和不良反应发生情况。结果 化疗2个周期后,患者CRP、PCT、TNF-α、IL-6水平和Ⅰ型胶原羧基端肽β特殊序列水平均低于化疗前,血清骨代谢指标骨钙素氨基中分子片段、Ⅰ型前胶原氨基端肽、骨特异性碱性磷酸酶水平均高于化疗前,差异有统计学意义(P<0.05)。化疗2个周期后,患者骨痛评分为(2.47±1.79)分,低于化疗前的(15.56±3.89)分,差异有统计学意义(P<0.05)。化疗期间发生发热8例、恶心10例、呕...     

伊班磷酸钠静脉滴注治疗老年男性2型糖尿病并骨质疏松

目的 :探讨伊班磷酸钠 (艾本 )静脉滴注治疗老年男性 2型糖尿病并骨质疏松的疗效。方法 :老年男性 2型糖尿病并骨质疏松患者 60例。全部患者均每日予罗钙全 0 2 5 μg、钙尔奇 D 0 6g治疗。 3 0例同时予静脉滴注伊班磷酸钠 4mg ,每月静滴 1次 ,连续 3个月治疗。另 3 0例为对照组。两组患者年龄、体重指数、糖尿病病程及血糖相匹配。测定治疗前及治疗后 1个月、3个月、6个月、12个月患者的血清骨钙素 (BP)、脱氧吡啶啉 (DPD)、甲状旁腺素 (PTH)、降钙素 (CT)、血脂 ;治疗前、后骨密度。两组进行比较分析。结果 :治疗组较对照组治疗前后腰椎、Ward’s三角骨密度显著升高 ,CT、DPD治疗后第 1、3个月较治疗前显著降低 (P <0 0 0 1) ,第 6个月仍见显著差异 (P <0 0 5 )。余BMD变化不明显。血脂无显著降低。结论 :伊班磷酸钠静脉滴注治疗能够更有效的提高老年男性糖尿病并骨质疏松患者的腰椎、Ward’s三角骨密度。未见伊班磷酸钠静脉滴注治疗可显著降低老年男性糖尿病患者的血脂     

伊班膦酸钠联合放疗治疗乳腺癌骨转移疗效观察

目的 观察伊班膦酸钠联合放疗治疗乳腺癌骨转移疗效.方法 治疗组31例每21d应用伊班膦酸钠4 mg静脉滴注,同时联合放疗;对照组27例单纯应用放疗.结果 治疗组骨痛缓解有效率90.32％,3d疼痛缓解率45.16％,高钙血症患者9例治疗后血钙正常;对照组骨痛缓解有效率74.07％,3d疼痛缓率18.51％.结论 伊班膦酸钠联合放疗能够治疗乳腺癌骨转移引起骨痛,起效快,并且可以治疗高钙血症.     

伊班膦酸对卵巢切除大鼠骨质疏松的预防

目的观察伊班膦酸对卵巢切除大鼠骨质疏松的预防作用。方法取10～12月龄的SD大鼠54只,随机分为6组,5组大鼠作双侧卵巢切除,分别给予生理盐水,低、中、高(0.25、0.5、1.0mg/kg·d)3种剂量的伊班膦酸及尼尔雌醇(1mg/kg·周),另1组为假手术组,给予生理盐水,1次/d,共3个月。结果生理盐水对照组骨干重、灰重、钙含量和股骨骨密度低于其他各组均有显著意义(P<0.05或P<0.01),低、中、高3种剂量的伊班膦酸用药组全身骨密度分别较生理盐水对照组全身骨密度增加0.9%、9.9%和3.6%,伊班膦酸及尼尔雌醇组椎骨、胫骨骨小梁面积较生理盐水对照组明显增加。尿羟脯氨酸与肌酐(HOP/Cr)比值伊班膦酸及尼尔雌醇组低于生理盐水对照组均有显著意义(P<0.01)。结论伊班膦酸有明显预防卵巢切除大鼠发生骨质疏松的作用。     

降钙素联合唑来膦酸、维生素D3片治疗老年骨质疏松的疗效分析

目的分析降钙素联合唑来膦酸、维生素D3片治疗老年骨质疏松的临床效果。方法选取本院2017年5月～2018年10月收治的老年骨质疏松患者84例,根据入院先后将其均分为对照组和观察组各42例。对照组给予患者唑来膦酸+维生素D3片治疗,观察组给予患者降钙素+唑来膦酸+维生素D3片治疗。比较两组患者治疗前后骨代谢标记物N-端骨钙素(N-MID)、25-羟基维生素D[25-(OH)D]及骨密度情况,观察比较两组治疗疗效。结果治疗前,两组患者N-MID、25-(OH)D、骨密度比较,差异无统计学意义(P>0.05);治疗后,观察组N-MID低于对照组,25-(OH)D、骨密度高于对照组,差异有统计学意义(P<0.05);观察组治疗总有效率为92.85%,显著高于对照组的73.81%,差异有统计学意义(P<0.05)。结论对老年骨质疏松患者行降钙素联合唑来膦酸、维生素D3治疗,能够提升骨密度,恢复骨骼强度,治疗效果显著,具有推广应用价值。     

唑来膦酸治疗老年男性原发性骨质疏松的临床效果评估

【目的】评估唑来膦酸治疗老年男性原发性骨质疏松患者的临床效果。【方法】将76名年龄≥70岁的男性原发性骨质疏松患者随机分为两组。对照组（n＝39）每日补充钙剂和维生素D,治疗组（n＝37）在对照组的基础上给予一次静脉滴注唑来膦酸5 mg。随访12个月后观察所有研究对象骨密度和骨代谢标记物水平变化。【结果】治疗组的椎骨、全髋骨和股骨颈骨密度均显著高于对照组（P＜0．05）;血液骨代谢标记物β-CTx、PINP和BSAP水平则显著低于对照组（P ＜0．05）,两组严重不良反应发生率分别为24．32％和23．08％,差异无统计学意义（P＞0．05）。【结论】唑来膦酸治疗一年后可以显著提高患者骨密度和降低骨代谢标记物水平,降低老年男性原发性骨质疏松患者的骨折危险。     

唑来膦酸注射液治疗骨质疏松的疗效观察

目的观察唑来膦酸注射液抗骨质疏松的疗效。方法选取2018年6月至2020年6月郑州大学第五附属医院90例骨质疏松患者为研究对象,根据随机数字表法分为对照组(30例)与观察组(60例)。对照组给予基础治疗,观察组给予基础治疗联合唑来膦酸注射液治疗。比较两组骨密度和骨代谢标志物变化。结果治疗前,两组患者骨密度比较差异未见统计学意义(P>0.05)。治疗后,对照组骨密度值下降,其中腰椎骨密度值变化有统计学意义(P<0.05);颈部骨密度值变化差异未见统计学意义(P>0.05);观察组腰椎及颈部骨密度值增加,差异均有统计学意义(P<0.05)。治疗前,两组血清骨钙素、P1NP、β胶原特殊序列水平比较差异未见统计学意义(P>0.05)。治疗后两组骨钙素、P1NP水平比较差异未见统计学意义(P>0.05),β胶原特殊序列水平在对照组略有升高,差异未见统计学意义(P>0.05),观察组明显下降,差异有统计学意义(P<0.05),两组比较差异有统计学意义(P<0.05)。结论唑来膦酸注射液可改善骨密度、降低β胶原特殊序列水平。     

伊班膦酸对卵巢切除大鼠骨质疏松的预防

目的 观察伊班膦酸对卵巢切除大鼠骨质疏松的预防作用。方法 取10－12月龄的SD大鼠54只，随机分为6组，5组大鼠作双侧卵巢切除，分别给予生理盐水，低、中、高（0.25、0.5、1.0mg/kg&;#183;d）3种剂量的伊班膦酸及尼尔雌醇（1mg/kg&;#183;周），另1组为假手术组，给予生理盐水，1次／d，共3个月。结果 生理盐水对照组骨干重、灰重、钙含量和股骨骨密度低于其他各组均有显著意义（P＜0.05或P＜0.01)，低、中、高3种剂量的伊班膦酸用药组全身骨密度分别较生理盐水对照组全身骨密度增加0.9%、9.9%和3.6%，伊班膦酸及尼尔雌醇组椎骨、胫骨骨小梁面积较生理盐水对照组明显增加。尿羟脯氨酸与肌酐（HOP／Cr)比值伊班膦酸及尼尔雌醇组低于生理盐水对照组均有显著意义（P＜0.01)。结论 伊班膦酸有明显预防卵巢切除大鼠发生骨质疏松的作用。     

A circadian rhythm of serum osteocalcin levels in postmenopausal osteoporosis

The serum levels of osteocalcin, a 49 amino acid bone matrix protein, have been found to be a specific biochemical parameter of bone formation. The aim of our study was to assess the variability of serum osteocalcin and parathyroid hormone levels in postmenopausal osteoporosis. In 16 patients with postmenopausal osteoporosis, serum levels of osteocalcin and parathyroid hormone were determined in 4-hourly intervals by radioimmunoassay. Whereas the serum parathyroid hormone levels were similar throughout the day, the serum osteocalcin levels showed a circadian rhythm, with lowest levels in the morning and maximal levels during the night. These findings might suggest a circadian variation of bone formation in patients with postmenopausal osteoporosis.     

老年人骨质疏松与动脉硬化的关系

目的通过对骨密度与冠状动脉钙化积分、颈动脉内中膜厚度及斑块关系的分析, 探讨骨质疏松与动脉硬化的关系.方法对66例老年冠心病、高血压或脑动脉硬化患者行双能X线骨密度仪测定腰椎、髋部、前臂的骨密度, 螺旋CT检测冠状动脉钙化积分及冠状动脉总钙化积分, 颈动脉超声检测颈动脉内中膜厚度及斑块,测定血甲状旁腺激素全段、骨钙素、血钙.据骨密度分骨质疏松组(A组),非骨质疏松组(B组).结果 A组患者的冠状动脉各分支钙化积分及冠状动脉总钙化积分、颈动脉内中膜厚度、颈动脉多发性硬斑发生率高于B组(P<0.01).冠状动脉钙化积分、颈动脉内中膜厚度与甲状旁腺激素呈正相关,与骨钙素、血钙呈负相关, 与各部位的骨密度呈负相关.结论骨质疏松症与动脉硬化有密切的关系, 骨质疏松时钙从骨中溶出增加,体循环中的钙可异常沉积在血管内膜中,造成血管壁动脉粥样硬化、钙化.     

脱氢表雄酮硫酸酯治疗老年男性骨质疏松症120例

目的：虽然已经有较多的证据提示脱氢表雄酮在骨质代谢中具有良性作用，但还需要更加合理和深入的实验来剔除其衍生激素的生物学效应，以更好地明确脱氢表雄酮对骨质代谢的作用。实验拟进一步验证脱氢表雄酮硫酸酯治疗老年男性骨质疏松症的疗效及安全性。 方法：①试验对象：选择2005—10／2006-10本院老年男性门诊及住院原发性骨质疏松症患者120例。诊断标准参照WHO新标准：所测骨密度值低于同性别骨峰值2．5个标准差以上诊断为骨质疏松，从未用过性激素。所有患者随机分为治疗组和对照组，每组60名。②试验方法：治疗组口服脱氢表雄酮硫酸酯100mg、钙尔奇D600mg；对照组口服钙尔奇D600mg。③试验评估：6个月后测定骨密度、血生化指标、骨吸收指标和骨形成指标以及副作用等方面的变化。 结果：纳入骨质疏松患者120例，均进入结果分析。①腰椎1、腰椎2-4、股骨颈、股骨上端部位骨密度与治疗前及对照组比较，差异显著（P〈0.01）。②治疗后治疗组脱氢表雄酮硫酸酯、胰岛素样生长因子Ⅰ、血清钙、碱性磷酸酶、尿吡啶啉、骨钙素较治疗前及对照组明显提高（P〈0．01，P〈0、05）。对游离睾丸酮、雌二醇、前列腺特异抗原、谷丙转氨酶、尿素氮、肌酐则无明显影响（P〉0．05）。 结论：脱氢表雄酮硫酸酯治疗老年男性骨质疏松症有较好疗效且安全可靠，无明显不良反应。     

An evaluation of several biochemical markers for bone formation and resorption in a protocol utilizing cyclical parathyroid hormone and calcitonin therapy for osteoporosis.

Female patients (n = 20) with osteoporosis, aged 66 +/- 5 yr were studied during a 24-h infusion of parathyroid hormone (PTH [1-34]) at a rate of 0.5 IU equivalents/kg.h, and then during a 28-d period of subcutaneous injections, at a dose of 800 IU equivalents per day. Thereafter half the patients received subcutaneous injections of calcitonin, 75 U/d for 42 d, and all patients were followed to the end of a 90-d cycle. Biochemical markers of bone formation (serum alkaline phosphatase, osteocalcin, and the carboxy-terminal extension peptide of pro-collagen 1) and bone resorption (fasting urine calcium, hydroxyproline, and deoxypyridinoline) were compared during treatment by the intravenous and subcutaneous route of PTH administration, and subsequently during calcitonin therapy. During intravenous PTH infusion there were significant reductions in all three bone formation markers, despite expected rises in urinary calcium and hydroxyproline. By contrast, the circulating markers of bone formation increased rapidly by > 100% of baseline values during daily PTH injections (P < 0.001). Significant increases in bone resorption markers were only seen at the end of the 28 d of injections, but were < 100% over baseline values, (P < 0.05). Quantitative bone histomorphometry from biopsies obtained after 28 d of PTH treatment confirmed that bone formation at both the cellular and tissue levels were two to five times higher than similar indices measured in a control group of biopsies from untreated osteoporotic women. Subsequent treatment of these patients with calcitonin showed no significant changes in the biochemical markers of bone formation and only a modest attenuation of bone resorption. Thus, PTH infusion may inhibit bone formation, as judged by circulating biochemical markers, whereas daily injections confirm the potent anabolic actions of the hormone. Sequential calcitonin therapy does not appear to act synergistically with PTH in cyclical therapeutic protocols.     

Soluble cathepsin-L: a marker of bone resorption and bone density?

We sought to evaluate cathepsin L serum levels in the peripheral blood of patients with low bone density. Blood samples from 60 patients (32 osteoporotic, 28 osteopenic) and 16 healthy controls were taken and quantitative measurements of cathepsin L were performed with the use of a commercially available enzyme-linked immunosorbent assay. Dual x-ray absorptionometry measurements and serum levels of alkaline phosphatase, bone-specific alkaline phosphatase, osteocalcin, parathyroid hormone, sexual hormones, and N -terminal crosslinks of type I collagen were examined. Group comparisons between patients with osteoporosis and controls showed significant differences with respect to cathepsin L ( t = -2.839; df = 29; P =.008). Osteoporosis treatment decreased the serum level of cathespsin L in a statistically significant fashion ( P =.002). These results suggest that the serum level of cathepsin L can serve as a marker of bone resorption and bone density.     

唑来磷酸治疗老年骨质疏松症18例的骨痛缓解及安全性观察

【目的】观察唑来磷酸治疗老年骨质疏松症的缓解疼痛的效果及安全性。【方法】应用唑来磷酸注射液治疗18例65-85岁老年骨质疏松症患者,观察治疗前后患者骨痛的缓解情况,血钙、磷、碱性磷酸酶变化及不良反应情况,采用双能x线骨密度仪测定患者治疗前后骨密度变化。【结果】治疗后患者骨痛症状明显改善,血钙、磷无显著变化（P〉0．05）,血碱性磷酸酶明显下降（P〈0．05）,骨密度较治疗前显著增加（P〈0．01,P〈0．05）,18例患者不良反应发生率为56．0％,但患者能耐受。【结论】唑来磷酸是治疗老年性骨质疏松症的安全有效性药物。     

静脉注射与口服骨化三醇冲击治疗腹膜透析患者继发性甲状旁腺功能亢进的疗效比较

目的:观察骨化三醇注射液和口服药冲击治疗慢性肾衰竭腹膜透析患者继发甲状旁腺功能亢进(SHPT)的疗效。方法:慢性肾衰竭腹膜透析患者58例,血清全段甲状旁腺激素(iPTH)水平>300 ng/L,随机分为注射骨化三醇冲击组(A组)和口服冲击组(B组)各29例,根据血iPTH水平确定骨化三醇的剂量,测定两组治疗前、后的iPTH、碱性磷酸酶(AKP)、血钙、磷水平,监测不良反应。结果:治疗4、8、12周两组iPTH水平明显下降,A、B组iPTH达标率分别为41%、83%、97%和28%、66%、90%,与治疗前比较有统计学意义(P均<0.05);治疗4、8、12周时A、B组血清iPTH比较差异具统计学意义(P均<0.05);两组血钙、磷水平变化不大,不良反应轻微。结论:静脉与口服骨化三醇冲击治疗腹膜透析SHPT安全有效,但静脉冲击疗效更显著。     

CALCITONINS AND OSTEOPOROSIS

SUMMARY Calcitonin, a polypeptide hormone secreted by the parafollicular C cells of the thyroid gland, lowers serum calcium by decreasing bone resorption and tubular calcium reabsorption. An analgesic action, possibly mediated via β-endorphins, is also evident. Parenteral calcitonin has been shown to stabilise and increase indices of cortical and trabecular bone mass and total body calcium when administered to patients with established osteoporosis. The routine use of this route of administration has been limited by poor patient compliance and tolerability. An intranasal preparation of calcitonin provided a more convenient means of administration. Several clinical trials have shown that intranasal calcitonin is effective and well tolerated both in prevention of postmenopausal bone loss and in established osteoporosis. Calcitonin therapy is particularly indicated for patients with high-turnover osteoporosis where results show a net gain of bone mineral in the axial skeleton and a slowing of bone loss in the appendicular bones. Due to receptor downregulation a resistance to the hormone may occur after 12-18 months of continuous treatment. This resistance can be avoided and delayed by the cyclical or discontinued administration of the hormone. Further research is needed to confirm longer-term efficacy and effects on fracture rate.