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。     

多囊卵巢综合征患者血清25(OH)D3与糖脂代谢的相关性研究

目的观察多囊卵巢综合征(Polycystic ovary syndrome,PCOS)患者血清25羟维生素D_3[25 hydroxyvitamin D,25(OH)D_3]水平,探讨PCOS患者维生素D对糖脂代谢的影响。方法选取2015年12月至2016年9月我院住院及门诊新诊断的70例PCOS患者及70例年龄及体重指数均匹配的健康对照者。根据BMI分为四组:超重/肥胖PCOS组(OW/OB+PCOS组)36例,非肥胖PCOS组(PCOS组)34例,超重/肥胖对照组(OW/OB组)37例,非肥胖对照组(NC组)33例。测定血清25(OH)D_3、空腹血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)、糖化血红蛋白(Hb Alc)、空腹胰岛素(Fins)、性激素水平,采用稳态模型HOMA-IR指数评估胰岛素抵抗(Insulin resistance,IR)程度。结果 OW/OB+PCOS组25(OH)D_3、HDL-C均较OW/OB组显著降低,而TG、Fins、HOMA-IR均较OW/OB组显著增高(P0.05);(2)OW/OB+PCOS组25(OH)D_3、HDL-C均较PCOS组显著减低、而TG、Fins、HOMA-IR均显著增高(P0.05);(3)PCOS组25(OH)D_3、HDL-C较NC组均显著减低,而TG、Fins、HOMA-IR、LH、TES则均显著增高(P0.05);(4)相关分析示25(OH)D_3水平与BMI、FINS、HOMA-IR、TG呈负相关(r=-0.208,P=0.034;r=-0.918,P=0.000;r=-0.799,P=0.000;r=-0.683,P=0.002),与HDL-C呈正相关(r=0.585,P=0.001)。结论 PCOS患者血清25(OH)D_3水平减低与肥胖和脂代谢紊乱密切相关。     

阿仑膦酸钠对甲状腺功能减患者骨密度及骨生化、代谢影响的临床研究

目的观察阿仑膦酸钠对甲状腺功能减患者骨密度及骨生化、代谢影响的影响。方法初次诊断为未绝经的甲状腺功能减退女性患者64例,按随机数字表法将其分为治疗组32例,对照组32例。对照组给予左旋甲状腺素替代治疗,治疗组在对照组治疗的基础上给予阿仑膦酸钠70 mg/周,为期12个月。测定治疗不同时间段患者,腰椎1-4(L_(1-4))、左侧股骨颈BMD及血Ca~(2+)、血P~(3+)、1,25-(OH)_2D_3、碱性磷酸酶(ALP)、血清Ⅰ型胶原羧基端吡啶并啉交联肽(ICTP)以及血清骨钙蛋白(bone gla-protein,BGP)水平的变化情况。结果治疗前两组患者的骨密度及骨生化、代谢指标比较不具有统计学意义(P0.05);治疗12个月后,治疗组患者的腰椎1-4(L_(1-4))及股骨颈BMD均显著高于治疗前及同时期对照组(P0.05);治疗后12个月后,两组患者的血ALP、ICTP及BGP均有不同程度升高,治疗组的BGP升高程度明显大于对照组;而对照组的ALP及ICTP升高程度明显大于治疗组,比较有统计学意义(P0.05)。治疗前后两组患者血Ca~(2+)、血P~(3+)、1,25-(OH)_2D_3比较无明显差异(P0.05)。结论阿仑膦酸钠可以明显提升甲状腺功能减患者骨密度,改善骨生化和代谢状态。     

2型糖尿病患者HbA1C、25( OH )VD水平与骨密度的相关性研究

目的 观察2型糖尿病患者HbA1C、25 (OH)VD水平与骨密度(Bone Mineral Density,BMD)的相关性.方法 收集我院160例住院患者资料,以HbA1C水平分组,HbA1C<7%为组1(平均年龄52.47±11.39岁),HbA1C>8.5%为组2(平均年龄56.38±9.84岁),测定HbA1c、身高、体重、体重指数(Body Mass Index,BMI),采用美国Norland双能X线骨密度检测仪测定患者L2-4和左侧股骨近端(Neck、Troch、Ward's三角区)BMD,采用酶联免疫吸附法检测血清25(OH)VD,分析HbA1c、25(OH)VD、BMD三者的相关性.结果 两组患者身高、体重、BMI无显著性差异,2型糖尿病患者血清25(OH)VD水平与HbA1C呈负相关(r=-0.758,P<0.05),与腰椎骨密度无相关性(P>0.05),与髋部骨密度呈明显正相关(P＜0.05).结论 糖尿病患者血糖控制水平对25(OH)VD与骨密度有不良影响.     

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。     

绝经后女性骨密度与骨代谢生化指标的相关性分析

目的分析绝经后女性骨密度(bone mineral density,BMD)与骨代谢生化指标的相关性。方法选取西南医科大学附属医院2017年1月至2018年12月收治的绝经后女性患者151例。根据骨密度T值将患者分为骨质疏松组(83例)、骨量低下组(47例)和骨量正常组(21例),比较三组患者骨代谢生化指标的差异,并对各项指标与BMD进行相关性分析。结果骨质疏松组甲状旁腺素(PTH)、Ⅰ型前胶原氨基末端前肽(P1NP)、Ⅰ型胶原羧基端肽β特殊序列(β-CTX)显著高于骨量低下组和骨量正常组(P0. 05),骨量低下组显著高于骨量正常组(P0. 05)。骨质疏松组体质量指数(bone mass index,BMI)、25(OH) D_3显著低于骨量低下组和骨量正常组(P0. 05),骨量低下组显著低于骨量正常组(P0. 05)。血钙、血磷、骨钙素(BGP)、血清的骨特异性碱性磷酸酶(BALP)在三组之间比较,差异无明显统计学意义(P0. 05)。Spearman相关分析显示,PTH、P1NP、β-CTX与骨密度呈负相关(r=-0. 538,-0. 520,-0. 462,P 0. 05),25(OH) D_3与骨密度呈正相关(r=0. 517,P0. 05),血钙、血磷、BALP、BGP与骨密度无相关性(P0. 05)。结论血清25(OH) D_3、PTH、P1NP、β-CTX与骨密度存在显著相关性,骨代谢生化指标监测有助于绝经后女性骨质疏松的早期诊断。     

胰岛素及降糖药物治疗对2型糖尿病骨密度的影响

目的 探讨胰岛素及降糖药治疗对2型糖尿病患者骨密度的影响。均测量身高、体重,同时分析病程、糖化血红蛋白、空腹胰岛素、血清C-肽、与2型糖尿病骨质疏松的关系,讨论其影响因素和可能的机制。方法 收集276例2型糖尿病患者,根据其治疗情况分为胰岛素（A）组及降糖药物(B)组,测定上述两组患者骨密度（BMD）、体重指数（BMI）、血清C-肽、空腹血糖、糖化血红蛋白、并按病程结合年龄分组对比。结果 （1）高龄段两组骨质疏松的发病率无统计学差异;（2）早期及长期使用胰岛素治疗组骨密度较降糖药治疗组高（P<0.01）,两组相差显著。（3）骨密度与糖化血红蛋白呈负相关、与空腹胰岛素及血清C-肽呈正相关。结论 胰岛素早期干预能延缓并减低患者的骨质疏松发病率及程度,对于高龄及病程大于15年糖尿病患者,胰岛素与降糖药对其骨质疏松的防治作用无明显差异。糖化血红蛋白、空腹胰岛素、血清C-肽对骨质代谢有一定影响。     

维生素D对糖尿病合并骨质疏松患者血清骨保护素、趋化素水平的影响

目的观察维生素D(Vit D)对2型糖尿病(type 2 diabetes mellitus,T2DM)合并骨质疏松(osteoporosis,OP)的患者血清骨保护素(osteoprotectin,OPG)及趋化素(Chemerin)水平的影响,初步探讨两者在疾病进展中的作用。方法选取2020年7～12月于我院就诊的新诊断T2DM合并OP的患者123例,根据患者血清中25-羟基维生素D[25(OH) D]水平将其分为3组,分别为Vit D正常组(40例)、Vit D不足组(42例)和Vit D缺乏组(41例),同期选取我院体检中心健康人员40例作为对照(NC组)。Vit D不足组及Vit D缺乏组分别给予Vit D2注射液15 mg,肌肉注射,每4周1次,连续治疗12周。收集患者一般资料,检测治疗前后血清中TC、TG、HDL-C、LDL-C、25(OH) D、FPG、FINS、Hb A1c、OPG及Chemerin水平,同时利用双能X线骨密度仪检测治疗前后患者股骨颈骨密度(bone mineral density,BMD),并分析各因素与股骨颈BMD之间的相关性。结果治疗12周时,Vit D不足组及Vit D缺乏组血清TG、Hb A1c、OPG、Chemerin均较治疗前显著降低,而HDL-C、25(OH) D、股骨颈BMD均较治疗前显著升高(P0.05)。Vit D不足组中,治疗4周时血清Hb A1c、25(OH) D水平及股骨颈BMD较治疗前无显著变化(P0.05),TG、OPG、Chemerin较治疗前显著降低(P0.05),HDL-C较治疗前显著升高(P0.05)。在Vit D缺乏组中,治疗4周时患者血清中HDL-C、25(OH) D水平及股骨颈BMD均较治疗前显著升高(P0.05),血清TG、OPG、Chemerin水平均较治疗前显著降低(P0.05)。血清TG、LDL-C、Hb Alc、25(OH) D、OPG及Chemerin是股骨颈BMD的影响因素(P0.05)。结论Vit D可能通过升高血清Vit D水平,降低OPG、Chemerin而影响T2DM合并OP患者的骨密度。     

老年男性2型糖尿病患者胰岛素抵抗与 骨质疏松关系的研究

目的 探讨老年男性2型糖尿病(T2DM)患者骨代谢指标及骨密度(BMD)的临床特点,2型糖尿病危险因素与骨密度之间的关系.方法 入选老年男性T2DM患者116例,其中糖尿病肾病(DN)50例,分为T2DM组和DN组,另设老年男性健康对照组50例,记录年龄、体重指数(BMI)、DM病程,均行双能X线骨密度测定检查,并抽血检测空腹血糖(FPG)、糖化血红蛋白(HbA1C)、空腹胰岛素(Fins)、骨代谢、生化等指标的变化,计算稳态胰岛素评估模型胰岛素抵抗(HOMA-IR)指数.结果 (1)T2DM组、DN组年龄和BMI匹配的对照组比较无显著差异(P＞0.05);DN组病程长于T2DM组,两组比较有统计学意义,(P＜0.05);(2)T2DM组、DN组的BMD和骨矿含量(BMC)、25-羟基维生素D、睾酮(T)和骨钙素(BGP)水平较对照组降低,差异有统计学意义(P＜0.001与P＜0.05);DN组较T2DM组更低,两组比较差异有统计学意义(P＜0.05);(3) T2DM组和DN组的甲状旁腺激素(PTH)、B-胶原系列(B-CL)水平高于对照组,差异有统计学意义(P＜0.001与P＜0.05);然而DN组又高于T2DM组,差异显著(P＜0.05);(4)T2DM组、DN组存在胰岛素抵抗(IR),DN组IR尤其显著.HOMA-IR指数与BMD水平呈负相关(P＜0.05).结论 老年男性糖尿病患者DM病程及IR程度均与骨质疏松程度牟正相关,改善老年男性2型糖尿病患者IR对预防其OP的发生和发展有重大意义.     

阿仑膦酸钠联合阿法骨化醇对糖皮质激素性骨质疏松的疗效

目的观察阿仑膦酸钠联合阿法骨化醇对糖皮质激素性骨质疏松（GIOP）的疗效。方法将54例GIOP患者分成A、B组。A组30例给予阿仑膦酸钠70mg,1次／周,阿法骨化醇0．25g,2次／d,碳酸钙750mg,2次／d;B组24例,在A组给药基础上减去阿仑膦酸钠。疗程共6个月。比较2组治疗前后骨密度（BMD）、血钙和血磷,同时比较2组疼痛评分。结果A组治疗后BMD、疼痛评分较治疗前均明显改善（P〈0．05）;B组无明显变化（P〉0．05）。A组上述结果与B组比较,差异均有统计学意义（P〈0．05）。2组治疗前后血钙、血磷变化均无统计学差异（P〉0．05）。结论阿仑膦酸钠与阿法骨化醇联合治疗GIOP疗效优于单用阿法骨化醇。     

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。     

Randomized Controlled Trial of the Effects of Calcium With or Without Vitamin D on Bone Structure and Bone‐Related Chemistry in Elderly Women With Vitamin D Insufficiency

There are few data on the relative effects of calcium supplementation with or without extra vitamin D on BMD in patients selected for low vitamin D status. The aim of this study is to evaluate the relative importance of vitamin D and calcium treatment on BMD and bone‐related chemistry in elderly women with vitamin D insufficiency. Three hundred two elderly women (age, 77.2 ± 4.6 yr) with serum 25(OH)D concentrations <60 nM participated in a 1‐yr randomized, double‐blind, placebo‐controlled trial. All subjects received 1000 mg calcium citrate per day with either 1000 IU ergocalciferol (vitamin D₂) or identical placebo (control). The effects of time and time treatment interactions were evaluated by repeated‐measures ANOVA. At baseline, calcium intake was 1100 mg/d, and 25(OH)D was 44.3 ± 12.9 nM; this increased in the vitamin D group by 34% but not the control group after 1 year (59.8 ± 13.8 versus 45.0 ± 13.3 nM, p < 0.001). Total hip and total body BMD increased significantly, and procollagen type I intact N‐terminal propeptide (PINP) decreased during the study with no difference between the treatment groups (hip BMD change: vitamin D, +0.5%; control, +0.2%; total body BMD change: vitamin D, +0.4%; control, +0.4%; PINP change: vitamin D, ?3.9%; placebo, ?2.8%). Although the fasting plasma and urine calcium increased in both groups equally, there was no detectable change in serum PTH. The increase in 25(OH)D achieved with vitamin D supplementation had no extra effect on active fractional intestinal calcium absorption, which fell equally in both groups (vitamin D, ?17.4%; control, ?14.8%). In patients with a baseline calcium intake of 1100 mg/d and vitamin D insufficiency, vitamin D₂ 1000 IU for 1 year has no extra beneficial effect on bone structure, bone formation markers, or intestinal calcium absorption over an additional 1000 mg of calcium. Vitamin D supplementation adds no extra short‐term skeletal benefit to calcium citrate supplementation even in women with vitamin D insufficiency.     

Abnormal calcium homeostasis in disabled stroke patients with low 25-hydroxyvitamin D

Disabled elderly stroke patients occasionally have very low serum 25-hydroxyvitamin D (25-OHD), which may be due to sunlight deprivation and malnutrition. Many of such patients have very low level of serum 1, 25-dihydroxyvitamin D (1, 25-[OH]2D; calcitriol), and immobilization-induced hypercalcemia may be responsible for inhibition of renal synthesis of calcitriol. To elucidate determinants of serum 1, 25-[OH]2D levels in elderly poststroke patients, we measured serum indices of bone and calcium metabolism and metacarpal bone mineral density (BMD). Patients whose serum 1, 25-[OH]2D concentration was below the mean-3 SD of normal control subjects were defined as the low 1, 25-[OH]2D group and the rest of the patients were designated as the normal group. Mean illness duration was 59 months in the normal group and 20 months in the low group. The Barthel index (BI), which predicts the degree of immobilization, was significantly lower in the low group than in the normal group. Mean serum 1, 25-[OH]2D and 25-OHD concentrations in the normal group were 36.7 pg/ml and 4.4 ng/ml, respectively; and those in the low group were 14.2 pg/ml and 1.8 ng/ml, respectively. Multiple regression analysis identified illness duration and calcium level as independent determinants of 1, 25-[OH]2D in both groups, and PTH in the normal group and 25-OHD in the low group were additional independent determinants. BMD in stroke patients was significantly lower than that in controls, and BMD in the normal group was lower as compared to the low group. BMD correlated negatively with 1, 25-[OH]2D and PTH in the normal group, and hyperparathyroidism may contribute to reduced BMD. These results suggest that treatment of decreased bone mass in stroke patients has to be individualized according to vitamin D status and calcium homeostasis.     

Relation between vitamin D insufficiency, bone density, and bone metabolism in healthy postmenopausal women.

Although only few postmenopausal women exhibit biochemical signs of hypovitaminosis D, vitamin D insufficiency has been shown to have adverse effects on bone metabolism and could be an important risk factor for osteoporosis and fracture. We determined serum levels of 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone (iPTH), bone turnover markers, dietary calcium intake, and bone mineral density (BMD; measured by dual X-ray absorptiometry) in 161 consecutive ambulatory women, healthy except for osteoporosis, referred to a bone metabolic unit. The prevalence of vitamin D insufficiency [25(OH)D < or = 15 ng/ml] was 39.1%. 25(OH)D was lower in the osteoporotic subjects (15.7 +/- 5.3 ng/ml vs. 21.8 +/- 9.7 ng/ml; p < 0.001). After controlling for all other variables, lumbar spine (LS) BMD was found to be significantly associated with 25(OH)D, body mass index (BMI), and years after menopause (YSM) (R2 = 0.253; p < 0.001). For femoral neck (FN), significant independent predictors of BMD were YSM, BMI, iPTH, and 25(OH)D (R2 = 0.368; p < 0.001). The probability of meeting osteoporosis densitometric criteria was higher in the vitamin D insufficiency group (odds ratio [OR], 4.17, 1.83-9.48) after adjusting by YSM, BMI, iPTH, and dietary calcium intake. Our study shows that vitamin D insufficiency in an otherwise healthy postmenopausal population is a common risk factor for osteoporosis associated with increased bone remodeling and low bone mass.     

活性维生素D对骨量减少的强直性脊柱炎患者骨代谢指标及病情的影响

目的探讨补充活性维生素D对于骨量减少的强直性脊柱炎(AS)患者骨代谢标志物、骨密度及炎性指标的影响。方法选取骨量减少的AS患者60例为研究对象,同期健康体检者20例作为健康组,比较两组受试者血清骨特异性碱性磷酸酶(BALP)、抗酒石酸酸性磷酸酶异构体-5b(TRACP-5b)、25-(OH)D3的水平。将上述AS患者随机分为治疗组和对照组,每组30例,对照组口服美洛昔康、柳氮磺吡啶、碳酸钙,治疗组在此基础上加用骨化三醇口服。比较2组治疗前后BALP、TRACP-5b、25-(OH)D3,骨密度(BMD)以及红细胞沉降率(ESR)、C反应蛋白(CRP)等指标的变化水平。结果 AS组BALP、TRACP-5b高于健康组,25-(OH)D3低于健康组(P0.05)。治疗组和对照组治疗后血清BALP、25-(OH)D3水平均有升高(P0.05),TRACP-5b水平均有下降(P0.05);治疗组BALP及25-(OH)D3治疗前后差值高于对照组(P0.05)。6个月后治疗组复查腰椎、大转子、转子间BMD较对照组均有不同程度的提升(P0.05),5例骨量恢复正常;对照组6个月后BMD变化不明显;治疗组治疗前后腰椎、大转子、转子间BMD变化差值均高于对照组(P0.05);治疗组与对照组ESR、CRP及BASDAI评分较前均有所降低(P0.05),其中治疗组ESR下降水平较对照组差异具有统计学意义(P0.05)。结论活性维生素D可以改善骨量减少的强直性脊柱炎患者的骨代谢指标并降低疾病活动度。     

The Effect of Low-Dose Cholecalciferol and Calcium Treatment on Posttransplant Bone Loss in Renal Transplant Patients: A Prospective Study

Background/Aim. Posttransplant steroid doses have been reduced with the use of new and potent immunosuppressive agents. However, posttransplant osteoporosis is still a serious problem. Our aim in this study was to investigate the effect of low-dose cholecalciferol and calcium supplementation on bone loss after transplantation in renal transplant patients. Methods. Fifty-eight renal transplantation patients were included in the study. Fourteen newly transplanted patients (group 1) and 44 renal transplantation patients with a graft age of at least six months (group 2) were involved. All patients received 400 IU/day orally cholecalciferol (vitamin D3) and 600 mg/day orally calcium replacement starting from the second day posttransplantion. All patients baseline serum and urine biochemistry, serum 25-hydroxy vitamin D3 (25 (OH)D3), and bone mineral density (BMD) tests were performed. Also, the same measurements were performed at the 12th month in group 1. Results. After one year of treatment, BMDs were improved in group 1. Patients in group 1 had a nonsignificant increase of lumbar spine (8.12 ± 18.64% of baseline BMD) and femoral total (7.10 ± 13.48% of baseline BMD) BMD at the end of the first year. On the other hand, there was a significant increase in femoral neck (10.06 ± 15.70% of baseline BMD, p < 0.05) measurements. The baseline results of group 2 were similar to group 1. In group 1, 25 (OH)D3 levels were increased while PTH levels were decreased at the end of the year. Conclusion. In renal transplant patients who use low-dose metilprednisolon and new immunosuppressive agents together, low doses of vitamin D3 and calcium replacement for one year provides a reduction in lumbar spine, femoral neck, and femoral total bone loss and prevents bone loss in group 2. In addition, it contributed to the normalization of PTH levels.     

T2DM伴骨质疏松Cys-C、25(OH)D3、BGP变化及临床意义

目的 探究老年2型糖尿病（T2DM）伴骨质疏松患者血清胱抑素C（Cys-C）、25羟维生素D3[25(OH)D3]、骨钙素（BGP）水平变化，并分析其对骨质疏松性骨折的预测价值。方法 选取2020年2月至2022年5月本院88例老年T2DM伴骨质疏松患者作为研究组，另选同期88例老年T2DM骨量减少患者作为对照A组，88例老年T2DM骨量正常患者作为对照B组。比较各组血清Cys-C、25(OH)D3、BGP水平、血糖指标、血脂指标、骨矿物质密度（BMD），分析研究组血清各指标水平与血糖指标、血脂指标、BMD的相关性。研究组均行常规对症治疗6个月，依据是否发生骨质疏松性骨折分为发生者、未发生者，比较治疗前后血清各指标水平及变化值，分析其对骨折的预测价值。结果 研究组血清Cys-C水平高于对照A组、对照B组，25(OH)D3、BGP水平低于对照A组、对照B组（P＜0.05）；Cys-C水平与BMD呈负相关，25(OH)D3、BGP水平与BMD呈正相关（P＜0.05）；发生者治疗前后血清Cys-C水平高于未发生者，25(OH)D3、BGP水平低于未发生者，各指标变化值低于未发生者（P＜0.05）；血清各指标变化值降低可增加骨质疏松性骨折发生风险（P＜0.05）；治疗3个月后血清各指标变化值联合预测骨质疏松性骨折的AUC大于治疗1个月后（P＜0.05）。结论 老年T2DM伴骨质疏松患者血清Cys-C水平升高，25(OH)D3、BGP水平降低，联合检测其水平变化对骨质疏松性骨折具有一定预测价值。     

Higher response with bone mineral density increase with monthly injectable ibandronate 1 mg compared with oral risedronate in the MOVER study

We examined response to bone mineral density (BMD) gains in the MOVER study following treatment with intravenous (IV) ibandronate 1 mg/month, and investigated the characteristics of a non-responder group. At 1 year, responder rates for patients with BMD increases >0 % were similar with IV ibandronate 0.5 or 1 mg/month and oral risedronate 2.5 mg/day. However, after 3 years, responder rates with BMD increases ≥3 % were highest with ibandronate 1 mg at all bone sites (>80 % at the lumbar spine [L2–L4] and >50 % at all femur sites, which was significantly higher than with risedronate). Non-responders were defined by BMD increases ≤3 % at L2–L4 or ≤0 % at total hip, and ≤50 % reduction in creatinine-corrected urinary collagen type 1 cross-linked C-telopeptide (uCTX) from baseline to 1 year. There were a small number of non-responders in the ibandronate 1 mg group: 3.3 % (10/299) with ≤0 % total hip BMD increase and ≤50 % uCTX reduction from baseline. These non-responders had lower 25-hydroxyvitamin D (25[OH]D) levels than responders, but no differences in kidney function, L2–L4 BMD or bone turnover marker baseline values. Throughout the study, non-responders failed to show any increases in BMD. Our analysis demonstrates significantly higher responder rates with IV ibandronate 1 mg/month than with risedronate at 3 years. A small number of non-responders in the ibandronate group had lower 25(OH)D baseline levels than responders, suggesting that 25(OH)D levels could be a useful indicator of BMD response to therapy.