重组人甲状旁腺激素（1-34）和依降钙素治疗原发性骨质疏松症的随机对照研究

目的评价重组人甲状旁腺激素(1-34)[rhPTH(1-34)]治疗原发性骨质疏松症(OP)的疗效和安全性,并与依降钙素进行对比。方法 60例原发性OP患者按3:1被随机分入rhPTH(1-34)组(PTH组)和依降钙素组(CT组)。PTH组予rhPTH(1-34)20μg每日1次皮下注射,连续用药18月。CT组予益钙宁20U每周1次肌肉注射,连续用药12月。受试前检测腰2-4椎体(L2-4)和股骨颈骨密度(BMD)、血钙、血磷、尿钙、血清骨特异性碱性磷酸酶(BSAP)、尿Ⅰ型胶原交基C端肽(CTX-I),治疗后6、12、18月复查上述指标。结果与基线时比较,PTH组L2-4BMD在治疗6、12、18月时显著升高,股骨颈BMD在18月时显著升高,BSAP在6、12月时均显著升高,CTX-I校正值在6、12、18月时均显著升高;CT组L2-4BMD在治疗12月前升高,股骨颈BMD在12、18月时升高,BSAP12、18月时均显著下降,CTX-I校正值治疗前后无统计学差异。两组比较,PTH组患者在6、12月和18月时L2-4的BMD增长值和增长率均高于CT组。但CT组在治疗12月时股骨颈BMD增长值高于PTH组,不良反应:两组差异无统计学意义;PTH组有一过性高钙血症。结论 rhPTH(1-34)治疗原发性OP安全有效,对改善椎体BMD起效时间、增长速度和增长幅度均优于依降钙素,但改善股骨颈BMD较依降钙素起效更慢,增长幅度更小。     

唑来膦酸在骨质疏松患者中的应用及疗效

目的观察唑来膦酸(5mg/100ml)在原发性骨质疏松症及糖尿病合并骨质疏松症患者中的疗效及安全性。方法收集我院住院的骨质疏松症患者46例,分为原发性骨质疏松症组25例及糖尿病合并骨质疏松症组21例,体格检查计算体质指数(BMI),葡萄糖氧化酶法检测血糖,双能X线骨密度仪测定腰椎(L2-L4)及左股骨颈BMD,所有患者均静脉给予唑来膦酸5mg治疗,观察不良反应。1年后再次复查骨密度,观察唑来膦酸治疗后骨密度变化。结果治疗前两组间年龄、体质指数、腰椎及股骨颈骨密度无明显差异(P0.05),给予唑来膦酸治疗后,两组均出现不同程度的发热、乏力、头痛、关节痛、恶心等反应,糖尿病组有7例出现血糖一过性升高,但3天后均症状消失、血糖回复正常。使用唑来膦酸1年后复查骨密度,原发性骨质疏松组腰椎骨密度升高4.27%,股骨颈升高4.11%,糖尿病合并骨质疏松组骨密度分别升高3.42%、3.26%。两组骨密度较用药前均有升高(P0.05),但两组间骨密度比较无差异(P0.05)。结论唑来膦酸可以提高骨质疏松症患者骨密度,在原发性骨质疏松症及糖尿病合并骨质疏松症患者中均有较好疗效。     

阿伦磷酸钠对绝经后2型糖尿病合并骨质疏松症患者骨代谢的影响

目的 探讨阿伦膦酸钠对绝经后2型糖尿病合并骨质疏松症患者骨代谢及骨密度的影响。方法 选择2012年1月至2013年1月在本院接受治疗的绝经后2型糖尿病合并骨质疏松症患者51例,给予阿伦膦酸钠治疗6个月。采用美国Norland双光能X线骨密度检测仪对所有患者进行腰椎L2-L4和左侧股骨近端（包括Neck、Troch、Ward三角区)骨密度测量,并测定身高、体重、空腹血糖(FBG)、HbAlc、PTH、OC、CTX、25（OH）VD、BALP等。对比治疗前后骨密度及骨代谢标志物变化。结果 用阿伦膦酸钠治疗6个月使绝经后2型糖尿病合并骨质疏松症患者的FBG、2hPG 、HbA1c降低,治疗前与治疗后相比较,差异有统计学意义（P〈0.05）。血Ca、P浓度治疗前与治疗后相比较,差异无统计学意义(P＞0.05)。骨代谢标志物CTX治疗前与治疗后相比,差异有统计学意义（P〈0.05）。OC 、PTH、BALP、25OHVD治疗前与治疗后相比较,差异无统计学意义(P>0.05)。治疗前腰椎和股骨颈骨密度与治疗后相比较,差异有统计学意义（P〈0.05）。Torch 、Ward部位骨密度治疗前与治疗后相比较,差异没有统计学意义(P＞0.05)。结论 阿伦膦酸钠治疗绝经后2型糖尿病合并骨质疏松症疗效明显,短时间内可改善骨代谢指标和提高腰椎骨密度。     

甲状旁腺激素(1-34)和阿仑膦酸钠治疗骨质疏松症合并类风湿关节炎疗效的对比研究

目的比较甲状旁腺激素(parathyroid hormone,PTH)(1-34)和阿仑膦酸钠(alendronate,ALN)治疗骨质疏松症合并类风湿关节炎(rheumatoid arthritis,RA)女性患者的疗效。方法选取98例于2017年2月至2017年11月在我院就诊诊断为骨质疏松症合并RA的绝经后女性患者。按照治疗方案将患者分为PTH组和ALN组,两组患者分别接受特立帕肽或阿仑膦酸钠治疗,观察治疗6个月后两组患者骨密度和骨代谢指标的改变。结果在两组治疗6个月后,腰椎的骨密度较治疗前均有显著增加(P0.05)。与ALN组相比,PTH组治疗6个月腰椎骨密度的平均变化百分比显然更高;而股骨颈骨密度仅在PTH组显著增加。结论甲状旁腺激素(1-34)在短期治疗骨质疏松症合并类风湿女性患者时,效果较阿仑膦酸钠更佳。     

强骨活力片治疗肾虚血瘀型骨质疏松症的临床研究

目的 评价强骨活力片治疗肾虚血瘀型骨质疏松症的临床疗效及安全性.方法 随机将60例患者分为治疗组35例(口服强骨活力片)和对照组25例(口服骨松宝颗粒),疗程6个月,观察治疗前后两组患者的症状总疗效,中医症候积分,骨密度[腰椎正位(L2-L4)、股骨颈、大粗隆及Ward's三角],生化指标[血清钙(Ca)、磷(P)、碱性磷酸酶(ALP)]的变化.结果 [1]与治疗前相比,两组中医症候积分、腰椎正位(L2-L4)和股骨颈骨密度,ALP均有显著差异(治疗组P＜0.01,对照组P＜0.05),治疗组大粗隆骨密度有显著差异(P＜0.05);[2]治疗后两组间比较,中医症候积分,疗效显效率,腰椎正位(L2-L4),股骨颈及大粗隆骨密度,ALP差异均有统计学意义(P＜0.05).结论 强骨活力片治疗原发性骨质疏松症(肾虚血瘀型)疗效确切、安全、不良反应少,值得临床大力推广使用.     

原发性肾病综合征患者应用糖皮质激素后对骨密度及骨钙素的影响

目的 观察原发性肾病综合征(PNS)患者应用糖皮质激素（GC)后骨密度(BMD)及骨钙素（OC)的变化。方法 20例正常对照为A组,将73例原发性肾病综合征患者根据应用糖皮质激素的时间分为四组,B组(2 -6个月）19例、C组(7 - 12 个月）21例、D组(13 - 18个月）17例、E组(超过18个月）16例,所有研究对象收集临床资料,测定骨密度,检测血骨钙素水平。结果①A-E组性别、年龄、体重指数无统计学差异,B-E组血红蛋白、血白蛋白、血碱性磷酸酶(ALP)、血钙、血磷的差异 无统计学意义;②B组腰椎L1骨密度较A组减少(P < 0. 05),C组腰椎L1-L4骨密度较A组减少（腰椎L1、L3,P <0.01;腰椎 L2、L4,P <0. 05),D组腰椎L1-L4、股骨颈、大粗隆骨密度较A组减少（腰椎L1-L4、大粗隆,P <0. 01;股骨颈,P <0.05),E组各部位骨密度均较A组减少(腰椎L1-L4,P <0. 01;股骨颈、Wards三角区、大粗隆,P<0. 05);③B组、C组骨钙素水平较A组降低(P <0. 05),D组、E组骨钙素水平较A组的差异无统计学意义;④单纯钙剂组及不规律或未应用抗骨质疏松药物组的各部位骨密度均较规律应用钙剂+活性维生素D组减少(P <0.05),不规律或未应用抗骨质疏松药物组与单纯钙剂组比较,仅大粗隆骨密度减少有统计学意义(P <0. 05)。结论 原发性肾病综合征患者应用糖皮质激素治疗的早期发生血骨钙素降低,长期应用可致骨密度减少,腰椎骨密度减少最为显著,钙剂联合活性维生素D治疗可防治糖皮质激素相关性骨量丢失。     

绝经后女性血清硒水平与骨质疏松骨密度和骨代谢指标相关性研究

目的探索血清硒水平与绝经后妇女骨代谢指标以及腰椎和髋部骨密度之间相关性。方法检测156例正常骨密度和162例骨质疏松症的血清硒、25-羟基维生素D、PTH、骨钙素、PINP、CTX和NTX/Cr等指标水平。腰椎和股骨颈的BMD通过双能X线吸收法测量。探索了血清硒水平与骨密度的关系。结果骨质疏松症女性的血清硒水平低于正常骨密度的女性(P0.05)。在骨质疏松症妇女中,血清硒水平与年龄、绝经年限、BMI、PTH、骨钙素、PINP、CTX和NTX/Cr水平呈负相关,与25-羟基维生素D水平呈正相关。在正常骨密度组,血清硒水平与这些参数均未发现明显的相关性。调整年龄和BMI后,腰椎和股骨颈骨密度与血清硒及25-羟基维生素D水平呈显著正相关,与绝经年限、PTH、骨钙素、PINP、CTX和NTX/Cr呈负相关。对年龄和BMI进行调整后,进行多元回归分析以确定BMD的预测因子,血清硒和PINP、CTX是腰椎和股骨颈骨密度的显著预测因子。结论绝经后女性患者血清硒水平降低与腰椎和股骨颈骨密度降低密切有关。     

IL-33与绝经后骨质疏松女性骨密度和骨代谢指标相关性研究

目的 探索血清白细胞介素-33(IL-33)与绝经后骨质疏松女性骨密度和骨代谢指标相关性。方法 采用酶联免疫吸附法测定50例绝经后骨质疏松患者和50例正常绝经后妇女血清IL-33水平。采用双能X线骨密度仪(DXA)测量患者和对照组的骨密度(BMD)。检测维生素D、钙、碱性磷酸酶(ALP)、甲状旁腺激素(PTH)水平,以及1型胶原C末端肽(CTX)和1型前胶原N端前肽(P1NP)等骨转换指标。结果 在绝经后骨质疏松症女性中,IL-33水平显著低于健康对照组[(3.53±2.45) pg/mL vs (13.72±5.39) pg/mL,P=0.007];Spearman相关分析表明血清IL-33水平与年龄、BMI、PTH、CTX和P1NP水平呈负相关,与腰椎BMD和股骨颈BMD呈正相关。多元回归分析表明,年龄、BMI、腰椎BMD、PTH、股骨颈BMD和血清CTX和P1NP水平是骨质疏松症患者血清IL-33水平降低的独立预测因子。结论 血清IL-33降低是绝经后骨质疏松患者股骨颈和腰椎骨密度降低和骨转换增速的危险因素。     

特立帕肽治疗原发性骨质疏松症的短期疗效观察

目的：观察特立帕肽（ Teriparatide ）治疗原发性骨质疏松症的短期疗效和安全性。方法采用自身前后对照临床研究,纳入2011年12月-2012年12月在解放军第309医院骨内科住院的原发性骨质疏松症患者共10名,所有患者在每天口服补充元素钙600 mg和活性维生素D 0.25μg的同时,分别接受特立帕肽治疗,疗程6个月,具体用法为每日皮下注射特立帕肽20μg。所有患者均于用药前、用药后3、6个月采用双能X线吸收法（DEXA）测定腰椎（L2-4）、股骨颈、Ward’s区和大粗隆骨密度（BMD）,用酶联免疫吸附法（ELISA）测定血清骨钙素（sOC）、骨碱性磷酸酶（sBAP）和Ⅰ型胶原交联C端肽（sCTX）水平。观察患者治疗前后骨密度和骨标志物的变化并进行对比分析,记录患者的不良事件。结果10名患者均完成全疗程治疗。治疗3个月时,腰椎（L2-4）、股骨颈、Ward’s区和大粗隆骨密度改善不明显（P＞0.05）,血清骨钙素（sOC）和骨碱性磷酸酶（sBAP）较治疗前明显升高（P＜0.05）。治疗6个月时,腰椎（L2-4）骨密度较治疗前明显增高（P＜0.05）,而股骨颈、Ward’s区和大粗隆骨密度改善不明显（P＞0.05）。血清骨钙素（sOC）和骨碱性磷酸酶（sBAP）呈持续升高趋势（P＜0.05）,Ⅰ型胶原交联C端肽（sCTX）较治疗前略升高,但差异无统计学意义（P＞0.05）。治疗期间不良事件的发生情况：头晕发生2例,恶心发生1例,上述情况均较轻微,没有给予特殊处理即自行缓解。结论特立帕肽能在3个月内改善患者的骨代谢状况（促进骨形成）,6个月内有效增加原发性骨质疏松症患者的腰椎骨密度,适用于绝经后及老年性骨质疏松症患者的治疗。     

帕米膦酸二钠治疗绝经后妇女骨质疏松症3年临床观察

目的观察帕米膦酸二钠治疗绝经后妇女骨质疏松症3年疗效。方法选取2007年8月至2008年6月PMOP患者97例.每月三次静脉输注帕米膦酸钠30mg.同时每天补充钙剂800 mg～1200mg和活性维生素D 0.25ug.疗程3年。定期测定治疗前后的腰椎、股骨颈与全髋骨密度值(BMD)及骨转换标记物(血清CTX、尿CTX、NTX、血清TRACP5b)。结果①治疗3年后.腰椎、股骨颈和全髋部位BMD均较治疗前显著提高(P<0.001);②治疗6个月,血清I型胶原交联羧基端肽(CTX)、I型胶原交联氨基端肽(NTX)、尿CTX/Cr、尿NTX/Cr、尿吡啶啉/肌酐(PYD/Cr)、尿脱氧吡啶啉/肌酐(DPYD/Cr)和血浆抗酒石酸酸性磷酸酶均较治疗前显著下降(P<0.01),其后各骨转换标记物仍维持较低水平,但无进一步下降。Pearson相关分析显示治疗6个月时尿吡啶啉和脱氧吡啶啉、血浆抗酒石酸酸性磷酸酶的变化与3年后腰椎、股骨颈和全髋部位BMD的变化值均呈负相关(P<0.01)。③治疗后疼痛明显缓解生活能力明显改善,治疗期间新发骨折2例。结论帕米膦酸二钠是治疗PMOP安全有效,早期骨转换标记物的下降与3年后骨密度的改善呈负相关。     

甲状旁腺激素(1-34)联合伊班膦酸钠治疗严重骨质疏松症的临床研究

目的甲状旁腺激素(parathyroid hormone,PTH)(1-34)联合伊班膦酸钠治疗严重骨质疏松症效果临床观察。方法98例严重绝经后骨质疏松症合并骨骼疼痛患者随机分为治疗组和对照组,治疗组使用PTH联合伊班膦酸钠治疗,对照组单纯予以伊班膦酸钠治疗,为期12个月。分别检测两组受试者腰椎及髋部骨密度、血清骨代谢指标治疗前后的改变。结果药物治疗6个月后两组患者腰椎L1~4及股骨粗隆、左侧股骨颈、Ward三角区的骨密度明显增加,且12个月后骨密度进一步增加,显著高于对照组(P0.05);药物治疗12个月后两组血清及碱性磷酸酶(ALP)、血清Ⅰ型胶原C末端肽(s-CTX)、血清抗酒石酸酸性磷酸酶-5b(TRACP-5b)、血清骨源性碱性磷酸酶(BAP)及血清骨钙素(OC)水平均显著改变,且治疗组对ALP及s-CTX、BAP、OC及TRACP-5b影响更明显(P0.05),而两组血钙(Ca)及血磷(P)治疗前后无明显差异(P0.05)。结论PTH联合伊班膦酸钠使用能有效提高严重骨质疏松症患者髋部及腰椎骨密度,改善骨代谢。     

Bone mass continues to increase at the hip after parathyroid hormone treatment is discontinued in glucocorticoid-induced osteoporosis: results of a randomized controlled clinical trial.

Glucocorticoid-induced osteoporosis is the most common secondary cause of osteoporosis. In this 24-month study, we report changes in bone turnover and bone mass after 12 months of daily injections of human parathyroid hormone 1-34 [hPTH(1-34)] and 12 months off treatment in postmenopausal women (mean age, 63 years) with osteoporosis treated with glucocorticoid and hormone replacement therapy. Response to the treatment was assessed with bone mineral density (BMD) measurements of the lumbar spine by quantitative computed tomography (QCT); BMD measurements of the lumbar spine, hip, and forearm by dual-energy X-ray absorptiometry (DXA); and biochemical markers of bone turnover. The mean (+/-SEM) change in BMD of the lumbar spine by QCT and DXA in the PTH group at 24 months was 45.9+/-6.4% and 12.6+/-2.2% (p < 0.001). The change in total hip and femoral neck BMD was not significant at 12 months but increased to 4.7+/-0.9% (p < 0.01) and 5.2+/-1.3% at 24 months, respectively, as compared with a relatively small change of 1.3+/-0.9% and 2.6+/-1.7% in the estrogen-only group. The mean percent differences in BMD of the lumbar spine by QCT and DXA between the groups at 24 months were 43.1% and 11.9%, respectively (p < 0.001). The mean percent differences over the estrogen-only group in hip BMD were 3.4% for total hip (p < 0.01) and 2.6% for femoral neck at 24 months. Biochemical markers of bone turnover increased to more than 150% during the first 6 months of therapy, remained elevated throughout the 12-month treatment period, and returned to baseline values within 6 months of discontinuing the PTH treatment. These results suggest that PTH dramatically increases bone mass in the lumbar spine and hip in postmenopausal women with glucocorticoid-induced osteoporosis who are taking hormone replacement therapy. However, the maximum effect of this anabolic agent on bone mass at the hip after 12 months of treatment requires at least 6-12 months after the PTH treatment is discontinued.     

甲状旁腺激素联合低频脉冲电磁场治疗老年骨质疏松性股骨粗隆骨折的临床疗效观察

目的探索抗骨质疏松药物PTH联合低频脉冲电磁场(LFPEF)辅助治疗老年骨质疏松股骨粗隆骨折效果。方法2013年7月~2015年4月间收治的老年骨质疏松性股骨粗隆骨折98例,采用随机数字表法将其分为治疗组和对照组,每组49例,两组患者均接受PFNA治疗。对照组术后给予PTH治疗,治疗患者术后给予PTH联合LFPEF治疗,比较两组患者治疗后患者视觉模拟痛疼评分(VAS)、髋关节Harris功能评分、骨折愈合时间、股骨颈及腰椎的骨密度和骨代谢指标的改变。结果术后1个月、3个月、6个月两组患者VAS评分均明显降低,且治疗组患者评分明显低于对照组(P0.05);术后3个月、6个月两组患者的Harris评分均明显上升,且治疗组患者评分明显高于对照组(P0.05);治疗组骨折愈合的时间明显少于对照组(P0.05);术后6个月两组患者股骨颈及腰椎的骨密度,治疗组患者骨密度较术前显著改善(P0.05)。术后6个月,治疗组的BALP和BGP水平显著上升,而TRACP-5b和CTX水平显著下降,与治疗前和对照组比较均有显著性差异(P0.05);而对照组治疗后BALP、BGP、TRACP-5b、CTX水平较治疗前显著增高(P0.05)。结论抗骨质疏松药物联合LFPEF是一种安全有效的辅助治疗老年骨质疏松粗隆骨折方法,值得临床推广。     

Effects of cinacalcet on bone mineral density and bone markers in hemodialysis patients with secondary hyperparathyroidism

Background

Cinacalcet markedly reduces the serum intact parathyroid hormone (PTH) level of hemodialysis (HD) patients with secondary hyperparathyroidism. Parathyroidectomy also reduces the serum intact PTH level of HD patients and it increases their bone mineral density (BMD). However, there is little information about the effect of cinacalcet on BMD or on the associations between bone markers and BMD in HD patients.

Methods

We performed a 1-year cohort study of 25 HD patients who had a serum intact PTH level above 300 pg/ml during treatment by conventional therapies, such as with active vitamin D, and cinacalcet was prescribed for 14 of them. BMD of the femoral neck and the serum levels of two circulating bone markers, alkaline phosphatase (ALP) and bone-specific alkaline phosphatase (BSAP), were measured before and after treatment. The other 11 HD patients without cinacalcet treatment were defined as control group.

Results

BMD significantly increased by 7.3 % during the 1 year of treatment in the cinacalcet group and decreased by 6.2 % during the same period in the control group, and cinacalcet therapy was independently associated with the changes in BMD after multiple regression analysis that included intact PTH (β = 7.57, P < 0.01). In the cinacalcet group, the serum ALP levels (R ² = 0.315, P < 0.05) and BSAP levels (R ² = 0.682, P < 0.01) levels were significantly negatively correlated with the changes in BMD, but the serum intact PTH levels were not significantly associated with the changes in BMD (R ² = 0.011, P = 0.72).

Conclusions

One year of treatment with cinacalcet increased the BMD of the femoral neck in the HD cohort, especially in the patients who had higher serum ALP and BSAP levels at baseline.     

Effects of cyclic versus daily hPTH(1-34) regimens on bone strength in association with BMD, biochemical markers, and bone structure in mice.

We developed a cyclic PTH regimen with repeated cycles of 1-week on and off daily PTH injection and explored its effects on bone strength, BMD, bone markers, and bone structure in mice. Cyclic protocols produced 60-85% of the effects achieved by daily protocols with 57% of the total PTH given, indicating more economic use of PTH. The study supports further exploration of cyclic PTH regimens for the treatment of osteoporosis. INTRODUCTION: To minimize the cost and the catabolic action of hPTH(1-34), a cyclic PTH regimen with repeated 3-month cycles of on-and-off daily injection of hPTH(1-34) was developed in humans and shown to be as effective as a daily regimen in increasing vertebral BMD. However, changes in BMD may not adequately predict changes in bone strength. A murine model was developed to explore the efficacy of a cyclic PTH regimen on bone strength in association with other bone variables. MATERIALS AND METHODS: Twenty-week-old, intact, female C57BL/J6 mice (n = 7/group) were treated with (1) daily injection with vehicle for 7 weeks (control); (2) daily injection with hPTH(1-34) (40 microg/kg/day) for 7 weeks (daily PTH); and (3) daily injection with hPTH(1-34) and vehicle alternating weekly for 7 weeks (cyclic PTH). BMD was measured weekly by DXA, and serum bone markers, bone structure, and strength were measured at 7 weeks. RESULTS: Daily and cyclic PTH regimens increased BMD at all sites by 16-17% and 9-12%, respectively (all p < 0.01). The most dramatic effect of cyclic PTH occurred during the second week of treatment when PTH was off, with femoral and tibial BMD continuing to increase to the same extent as that produced by daily PTH. Both daily and cyclic PTH regimens significantly increased osteocalcin (daily, 330%; cyclic, 260%), mTRACP (daily, 145%; cyclic, 70%), femoral cortical width (daily, 23%; cyclic, 13%), periosteal circumference (daily, 5%; cyclic, 3.5%), and bone strength (max load: daily, 48%; cyclic, 28%; energy absorbed: daily, 103%; cyclic, 61%), respectively. Femoral bone strength was positively correlated with BMD, bone markers, and cortical structure. Neither regimen had an effect on vertebral bone strength. Although actual effects of cyclic PTH were 60-85% of those produced by daily PTH, the effects of cyclic PTH per unit amount administered were slightly greater than those of daily PTH for most measures. CONCLUSIONS: PTH-enhanced femoral bone strength is positively correlated with its effects on femoral BMD, bone markers, and bone structure. Cyclic PTH regimens represent a potential economic use of PTH and warrant further study.     

维生素K2联合咪达普利对合并高血压的老年女性骨质疏松患者的疗效观察

目的研究合并高血压病的老年女性骨质疏松患者口服维生素K2联合咪达普利对骨密度(bone mineral density,BMD)、骨代谢、新发骨折率及不良反应的影响。方法选择2018年7月至2019年8月石家庄市第一医院收治的合并高血压的老年女性骨质疏松患者40例为研究对象,随机分为观察组、对照组,各20例,对照组服用咪达普利,观察组在此基础上加服四烯甲萘醌软胶囊。6个月后,观察两组患者新发骨折率、不良反应率,测定血清骨代谢指标和腰及髋部BMD的水平。结果治疗6个月后,与治疗前相比两组25(OH)D3增加、PTH下降(P<0.05),两组OC、BAP及各处BMD升高,TRACP-5b、s-CTX降低(P<0.001);与对照组相比,观察组BAP、OC更高,TRACP-5b、s-CTX更低,经校正P<0.001;与对照组相比,观察组腰椎、股骨颈BMD较高(P<0.05),△BMD差异有统计学意义(P<0.001);协方差校正股骨粗隆BMD及△BMD两组间比较差异有统计学意义(P<0.05);观察组治疗前BMD同治疗后BMD水平呈线性相关(P<0.001),BMD水平治疗前、后回归线斜率(b)不同。新发骨折率及不良反应率组间对比差异无统计学意义(P>0.05)。结论①维生素K2及咪达普利对合并高血压的老年女性骨质疏松患者联合用药效果有叠加作用,对骨代谢及骨密度有更好的改善作用;②联合用药对身体各处骨密度改善水平并不一致,骨密度基线水平可能对骨密度改善的曲线存在影响。     

Effects of strontium ranelate on bone mass and bone turnover in women with thalassemia major-related osteoporosis

Subjects affected by thalassemia major (TM) often have reduced bone mass and increased fracture risk. Strontium ranelate (SrR) is an effective treatment for postmenopausal and male osteoporosis. To date, no data exist on the use of SrR in the treatment of TM-related osteoporosis. Our aim was to evaluate the effects of SrR on bone mineral density (BMD), bone turnover markers and inhibitors of Wnt signaling (sclerostin and DKK-1). Twenty-four TM osteoporotic women were randomized to receive daily SrR 2 g or placebo in addition to calcium carbonate (1,000 mg) and vitamin D (800 IU). BMD at the lumbar spine and femoral neck, bone turnover markers (C-terminal telopeptide of procollagen type I [CTX], bone-specific alkaline phosphatase [BSAP]) and insulin-like growth factor-1 (IGF-1), sclerostin and DKK-1 were assessed at baseline and after 24 months. Back pain was measured by visual analog scale (VAS) every 6 months. After 24 months, TM women treated with SrR had increased their spine BMD values in comparison to baseline (p < 0.05). Moreover, they also exhibited a reduction of CTX and sclerostin levels (but not DKK-1) and exhibited an increase of BSAP and IGF-1 (p < 0.05); however, no significant changes were observed in the placebo group. In the SrR group, a reduction of back pain was observed after 18 months in comparison to baseline (p < 0.05) and after 24 months in comparison to placebo (p < 0.05). Our study reports for the first time the effects of SrR in the treatment of TM-related osteoporosis. SrR treatment improved BMD and normalized bone turnover markers, as well as lowering sclerostin serum levels.