伊班膦酸钠可防治肾小球疾病患者糖皮质激素引起的骨密度减低

目的探讨伊班膦酸钠防治肾小球疾病患者糖皮质激素(GC)所致的骨密度减低的疗效和安全性，观察期1年。方法前瞻性自身对照研究16例骨量减少或骨质疏松患者，用强的松治疗半年后加用伊班膦酸钠，每3个月1mg，每3个月检测腰椎1～4(L1-4)和股骨近端骨密度(双能X线骨密度仪)。结果用GC治疗半年后各部位骨丢失(13．0—70．8)mg/cm^2，丢失率为1．4％～7．9％。加用伊班膦酸钠半年后L1-3和股骨粗隆骨量增加(5．2～26．2)mg／cm^2，增加率为1．0％～3．6％；L4、股骨颈和三角区继续骨丢失(0．5～6．9)mg/cm^2，丢失率0．1％～0．8％。2／16例出现能耐受的腰背部紧缩、酸沉和疼痛，48h内自行缓解。结论间断静脉用伊班磷酸钠防治肾小球疾病患者GC所致的骨密度减低有效且副作用小，耐受性好。     

Treatment with ibandronate preserves bone in experimental tumour-induced bone loss

Cancer-induced bone diseases are often associated with increased bone resorption and pathological fractures. In recent years, osteoprotective agents such as bisphosphonates have been studied extensively and have been shown to inhibit cancer-related bone resorption in experimental and clinical studies. The third-generation bisphosphonate, ibandronate (BM 21.0955), is a potent compound for controlling tumour osteolysis and hypercalcaemia in rats bearing Walker 256 carcinosarcoma. We have studied the effect of ibandronate given as an interventional treatment on bone strength and bone loss after the onset of tumour growth in bone. Our results suggest that it is capable of preserving bone quality in rats bearing Walker 256 carcinosarcoma cells. Since other bisphosphonates have produced comparable results in man after their success in the Walker 256 animal models our findings suggest that ibandronate may be a powerful treatment for maintaining skeletal integrity in patients with metastatic bone disease.     

伊班膦酸钠联合阿司匹林对冠心病合并骨质疏松症骨密度及骨代谢的影响

目的 观察伊班膦酸钠联合阿司匹林对绝经期冠心病患者骨密度及骨生化和代谢的影响。方法 89例绝经后冠心病患者,按随机数字表法将其分为治疗组(n=44)、对照组(n=45)。治疗组给予伊班膦酸钠联合阿司匹林治疗,治疗期12个月。对照组给予阿司匹林治疗。测定治疗不同时间段患者,腰椎L1~ 4、左股骨颈、Ward三角骨密度及血清钙(Ca)、血磷(P)、1,25-(OH)2D3、甲状旁腺激素(PTH)、I型胶原交联C末端肽(CTX)及骨特异性碱性磷酸酶(BALP)水平的变化情况。结果 治疗12个月后,两组患者的骨密度都有不同程度提高,治疗组腰椎L1~4、左股骨颈、Ward骨密度均显著高于同时期对照组(P <0.05);治疗12个月后,两组患者的血清CTX水平都有不同程度下降,BALP明显上升(P＜0.05),而治疗组改变明显高于同期对照组(P＜0.05),血清钙(Ca)、血磷(P)、1,25-(OH)2D3、甲状旁腺激素(PTH)无明显改变(P＞0.05)。结论 伊班膦酸钠联合阿司匹林能提升绝经期冠心病患者骨密度,改善骨生化和代谢状态。     

维持性血液透析及腹膜透析患者骨密度的评估

目的了解我院MHD及PD患者BMD状况,探讨BMD与临床资料、骨代谢指标及生化指标的相关性及危险因素分析。方法选择我院住院及门诊随访的MHD及PD患者,透析龄均超过3个月,收集患者临床资料及血尿标本。采用超声骨密度仪检测患者BMD状况,对骨量异常患者的BMD及患者一般临床及实验室资料进行相关性分析,并进一步分析透析患者骨量异常的危险因素。采用SPSS19.0软件包进行数据统计及分析。结果 MHD组及PD组骨量异常发生率分别为57.98%,48.54%,有显著统计学差异;随着透析龄的延长,透析患者BMD下降,透析龄3年以上的PD患者比MHD患者的TScore值相对较高,两组间也存在统计学差异。高龄、高透析龄、高BMI、高血磷及高ALP血症是透析患者发生骨量异常的危险因素。结论 MHD患者比PD患者更易发生骨量异常,且随着透析龄的延长,透析患者骨量异常发生率增高,高龄、高透析龄、高BMI、高血磷及高ALP血症是透析患者发生骨量异常的危险因素。     

Risk factors for reduced bone density in haemodialysis patients.

BACKGROUND: Renal osteodystrophy may result in considerable morbidity for patients with end-stage renal disease. Secondary hyperparathyroidism, adynamic bone disease and osteomalacia, the main bony problems in chronic renal failure, may all be responsible for a reduction in bone mineral density (BMD). This can result in an increased fracture risk. By virtue of their age, post-menopausal status (in women), sedentary life-style and treatment (including previous corticosteroids), haemodialysis patients may be expected also to be at risk for developing osteoporosis, but little is known about the relative importance of these factors. METHODS: We report a prospective study examining the prevalence of reduced bone mineral density (BMD) and its association with a wide range of factors, in a heterogenous group of 88 chronic haemodialysis patients. Femoral neck and lumbar BMD were measured by dual-energy X-ray absorptiometry (DXA). Stepwise multiple linear regression analysis was used to identify risk factors associated with low bone mass. RESULTS: Forty three patients (48.9%) had reduced BMD, and in 17 (19.3%) BMD was below the fracture threshold as defined on DXA measurements by the World Health Organization (WHO). The BMD had significant negative associations with age, serum parathyroid hormone (PTH) levels, current gastric acid suppression therapy, female gender, age at menarche and history of previous fracture. Positive associations were found with weight, haemoglobin concentration, average serum phosphate, weekly heparin dose, oral calcium supplementation and history of parathyroidectomy. CONCLUSIONS: We have confirmed the importance of PTH-related bone disease in affecting BMD in haemodialysis patients, but have found that some other factors, which are known to be risk factors for osteoporosis, are also important.     

Effect of monthly ibandronate on hip structural geometry in men with low bone density

Summary  

Hip structural analysis (HSA) performed in a subset of participants from the STudy Researching Osteoporosis iN Guys (STRONG) demonstrated that 1 year of ibandronate treatment was associated with a significant improvement in some but not all parameters of hip geometry relative to placebo in men with low bone density.     

Bisphosphonates in children with hypercalciuria and reduced bone mineral density

Previous studies have demonstrated reduced bone mineral density (BMD) and biochemical changes of excessive bone resorption in some patients with idiopathic hypercalciuria (IH). Consequently, bisphosphonates have been successfully employed in research animals and adults with IH and reduced BMD. We evaluated the effect of treatment with bisphosphonates in seven patients ages 10–16 years with persistent IH and reduced BMD. In five children, preceding traditional therapy failed. All children received oral alendronate and one also IV Zoledronic acid for 6–18 (median 9.0, mean 10.7) months. With treatment, BMD Z scores in the lumbar spine improved from −2.0 ± 0.3 to −0.8 ± 0.8 (p = 0.002) and in the femoral neck from −1.8 ± 0.4 to −0.7 ± 0.9 (p = 0.01); urine N-telopeptides/creatinine decreased from 372 ± 289 to 72 ± 39 nmol/mmol (p = 0.05) and calcium/creatinine from 0.29 ± 0.12 to 0.13 ± 0.06 mg/mg (p = 0.009). Height Z scores, normal at baseline in all, remained unaffected, and no new stones or fractures were documented throughout the treatment period. Serum creatinine, electrolytes, calcium, phosphorus and parathyroid hormone remained normal as well. In summary, in children with IH and decreased BMD, treatment with bisphosphonates normalized urine calcium excretion, eliminated urinary symptoms, and significantly improved reduced BMD. These short-term beneficial effects indicate the need for larger prospective studies on the potential of bisphosphonates to serve as a new tool in treating children with IH and reduced BMD.     

终末期肾脏病透析患者骨密度与冠脉钙化的相关性分析

目的探讨终末期肾脏病(end stage renal disease,ESRD)透析患者骨密度与冠状动脉钙化(coronary artery colcification,CAC)之间的相关性。方法本研究为横断面研究。纳入115例ESRD患者,收集相关人口学特征、原发病、实验室检查等资料,双能X射线评估腰椎、股骨颈及髋部骨密度,多层螺旋计算机断层扫描(MSCT)检查患者CAC发生情况。以钙化积分100为界,将患者分为高钙化组和低钙化组。结果高钙化组56例,占维持性透析患者48%,其中男性36例,占高钙化组人数64.3%。高钙化组年龄、透析龄及血清甲状旁腺激素、碱性磷酸酶、25(OH) D水平均明显高于低钙化组,而股骨颈骨密度、髋部骨密度、血清胆固醇水平明显低于低钙化组(P0.05);男性高钙化组股骨颈骨密度及髋部骨密度明显低于低钙化组,且其冠脉钙化积分与股骨颈骨密度(r=-0.34,P0.05)、髋部骨密度(r=-0.65,P0.01)呈负相关。多元线性回归分析校正了年龄、透析龄等因素后仍显示男性髋部骨密度与冠脉钙化积分呈负相关(β=-1870.47,P0.05)。但在女性患者中,高钙化组与低钙化组骨密度无明显差异。结论骨密度降低可能是男性维持性透析患者冠脉钙化风险增高的危险因素。     

长期维持血液透析患者腰椎QCT骨密度定量检测结果分析

目的：探讨长期维持性血液透析患者的骨质疏松症发病率,为临床诊断和治疗提供依据。方法整理在本院进行腰椎QCT骨密度测量中的透析患者45例,其中男25例、女20例,年龄25～77岁、平均56．1岁,透析时间20～134个月、平均56．3个月;随机选取健康人群45例,其中男17例、女28例,年龄30～78岁、平均49．2岁。按男女性别分为透析组与对照组。年龄、性别差异无统计学意义（ P＞0．05）。利用SPSS19．0对数据进行处理,计量资料采用方式表示,采用配对样本T检验、独立样本T检验,P＜0．05表示差异有显著性;计数资料采用卡方检验。结果长期维持血液透析患者的腰椎骨密度要低于健康人群的骨密度（ P＜0．05）;骨质疏松症发病率要高;骨密度改变与透析时间无统计学意义（ P＞0．05）。结论长期维持血液透析患者的腰椎骨密度低于健康人群,骨质疏松症的发病率高。     

伊班膦酸钠对糖皮质GCs诱导骨质疏松患者骨代谢指标的影响

目的观察伊班膦酸钠对糖皮质GCs诱导骨质疏松患者骨代谢指标的影响。方法以本院2017年1月至12月期间收治的48例糖皮质GCs诱导骨质疏松患者为受试对象。随机分为对照组(24例)和观察组(24例),两组患者均给予阿法骨化醇胶囊(0.5μg/次,2次/d,共12周)治疗,试验组加用伊班膦酸钠注射液(首次2 mg,此后3 mg/月,共3个月)静脉滴注治疗。比较两组患者治疗前后血清PTH、BALP、BGP、CTX-1、tPINP等骨代谢指标差异。结果对照组和试验组患者治疗前的PTH、BALP、BGP、CTX-1、tPINP表达水平比较无差异性(P均0.05)。与治疗前比较,试验组和对照组患者治疗后的BALP、PTH表达水平显著上调,BGP、CTX-1、tPINP表达水平均显著下调(P均0.05)。与对照组治疗后比较,试验组患者治疗后的BALP、PTH表达水平上调幅度更大,BGP、CTX-1、tPINP表达水平下调幅度更大(P均0.05)。结论伊班膦酸钠治疗糖皮质GCs诱导骨质疏松患者,可显著改善患者血清PTH水平的异常表达,促进骨吸收和骨形成,这可能是伊班膦酸钠治疗糖皮质GCs诱导骨质疏松临床机制中的靶点。改善糖皮质GCs诱导骨质疏松患者生活质量和治疗预后均有重要的意义。     

Decreased osteogenic differentiation of mesenchymal stem cells and reduced bone mineral density in patients with adolescent idiopathic scoliosis

Generalized low bone mass and osteopenia in both axial and peripheral skeletons have been reported in adolescent idiopathic scoliosis (AIS). However, the mechanism and causes of bone loss in AIS have not been identified. Therefore, this study examined the relationship between the osteogenic and adipogenic differentiation abilities of mesenchymal stem cells (MSCs) and bone mass in 19 patients with AIS and compared these with those of 16 age- and gender-matched patients with lower leg fracture. Mean lumbar spinal bone mineral density (LSBMD) in AIS patients was found to be lower than in controls (P = 0.037) and the osteogenic differentiation abilities and alkaline phosphatase activities of MSCs from patients were also found to be lower than those of controls (P = 0.0073 and P = 0.001, respectively), but the abilities of the MSCs of patients and controls to undergo adipogenic differentiation were similar. The osteogenic differentiation ability was found to be positively correlated with alkaline phosphatase activity in the AIS group. However, the osteogenic and adipogenic abilities were not found to be correlated with LSBMD in either patients or controls. These findings suggest that the decreased osteogenic differentiation ability of MSCs might be one of the possible mechanisms leading to low bone mass in AIS. However, we did not determine definite mechanisms of low bone mass in AIS. Therefore, further study with large scale will be needed to identify the mechanism involved.     

牙周炎患者下颌骨骨密度的分析研究

采用双能Ｘ线骨密度仪分析测定，选择了全身骨密度正常者４２人，其中牙周炎患者１８人，牙周组织正常者２４人。并对他们的下颌骨进行Ｘ线平行投照，用计算机图像定量分析系统分析处理，测量了牙周炎组与非牙周炎组下颌骨光密度。分析结果表明，全身骨密度正常的牙周炎组与非牙周炎组，两者在下颌骨骨密度上未见明显异常。     

Treatment of osteoporosis after liver transplantation with ibandronate

Osteoporosis is a major side‐effect after liver transplantation (LTX). Therefore, the objective of the study was to evaluate the efficacy of ibandronate to reduce fractures after LTX. Seventy‐four patients after LTX were included in the study and measurements of bone mineral density (BMD) of lumbar spine and proximal femur using dual energy X‐ray absorptiometry (DEXA) were performed prior to and 3, 6, 12 and 24 months after surgery. The study group (IBA) consisted of 34 patients who received calcium (1 g/day), vitamin D3 (800–1000 IE/day) and ibandronate 2 mg every 3 months intravenously for 1 year. The control group consisted of 40 patients (CON) who received calcium and vitamin D3 at the same dosages. Prevalence of new fractures was predefined as primary endpoint. Changes of BMD and biochemical markers of bone metabolism were also investigated. In all patients, we found a reduction of BMD in the first few months after LTX. In the lumbar spine and the proximal femur the maximum reduction occurred 3 and 6 months post‐LTX. One and 2 years after transplantation, the group receiving ibandronate demonstrated a better recovery from loss of BMD and a significantly lower prevalence of fractures (IBA 2 vs. CON 10 P < 0.04, χ²). Ibandronate with calcium and vitamin D3 reduces the BMD‐loss after LTX and decreases the rate of bone fractures significantly.     

Monthly ibandronate for the prevention of bone loss in patients after liver transplantation

Background

Osteopenia and osteoporosis are diseases frequently occurring after liver transplantation (OLT).

Purpose

In a prospective study, we have investigated the effect of ibandronate, vitamin D₃, and calcium on the prevention and treatment of posttransplant osteopenia and osteoporosis.

Methods

The bone mineral density (BMD) of the lumbar spine (LS) and of the femoral neck (FN) were measured in 74 patients prospectively pre- and post-OLT.

Results

Postoperatively the study group showed a consistent percentage increase in BMD (g/cm²) and a significantly increased BMD after 12 and 24 months in the LS (12 months: 1.05 ± 0.21 g/cm²; P < .001 24 months: 1.11 ± 0.19 g/cm²; P < .001) and the FN (12 months: 0.88 ± 0.16 g/cm²; P < .002 24 months: 0.90 ± 0.15 g/cm²; P < .001) in comparison with baseline pre-OLT (LS pre-OLT 0.98 ± 0.19 g/cm², FN 0.86 ± 0.14 g/cm²). The overall bone fracture rate was 5.4% up to 24 months.

Conclusion

Ibandronate once monthly per os significantly increased the BMD in the LS and FN after OLT at 12 and 24 months. The increased BMD limits the risk of fracture.     

Dental malocclusion is associated with reduced systemic bone mineral density in adolescents.

There is no published data about associations between the state of dentition and bone mass in adolescents. The objective of this study was to investigate whether the prevalence of caries and dental malocclusion is associated with bone mass during growth. In 123 healthy Caucasian subjects (72 males, 51 females) aged 14-18 yr, DMFT figures (decayed teeth, missing teeth, filled teeth) and presence of malocclusion, according to Angle classification, were determined. Participants completed a questionnaire regarding dental hygiene, physical activity level, and consumption of sweets. Anthropometry and pubertal stages were examined. Bone mineral density (BMD) was examined using dual energy X-ray absorptiometry (DXA) in the total body, head, and lumbar spine. No association was found between DMFT (mean+/-SD: 8.33+/-3.9) and BMD or Z-scores for BMD. Malocclusion was found in 49 subjects (39.8%) and was more prevalent in females than males. Malocclusion was associated with lower total BMD independently of body size (p=0.001; Z-scores: -0.21+/-0.27 vs +0.33+/-0.17; p=0.1) in males (but not females), producing odds ratio 1.6 (95% confidence interval: 1.09-2.34%; p=0.02). Head BMD was also lower in the males with malocclusion than in those without (p=0.004). Neither caries nor the tooth loss appear to be associated with BMD during growth. Boys with malocclusion are at higher risk of reduced BMD. This suggests that inadequate bone mass accrual in males coexists with impaired growth of the masticatory system in childhood and adolescence, however, the causal pathway is unknown. Factors that produce malocclusion may also affect bone mass or size but further prospective studies are needed to evaluate the relationship.     

Bone mineral density in patients on maintenance dialysis

Disorders of bone and mineral metabolism affect almost all patients with advanced chronic kidney disease (CKD). High prevalence of decreased bone mineral density has been reported in this population; however, the role and diagnostic utility of bone density measurements are not well established. The incidence of bone fractures is high in patients with ESRD, but the association between fractures and bone density is not obvious. A recent meta-analysis suggested that decreased density at the radius might be associated with higher overall fracture risk. Changes in bone mineral density reflect several underlying pathological processes, such as vitamin D deficiency, estrogen deficiency and changes in bone turnover. The response of bone to these factors and processes is not uniform: it can vary in different compartments of the same bone or in different bones of the skeleton. Therefore, it is important to differentiate between the various types of bone. This may be possible by proper selection of the measurement site or using methods such as quantitative bone computed tomography. Previous studies used different methods and measured bone mineral density at diverse sites of the skeleton, which makes the comparison of their results very difficult. The association between changes in bone mineral metabolism and cardiovascular mortality is well known in ESRD patients. Studies also suggest that low bone density itself might be an indicator for high risk of cardiovascular events and poor overall outcome in this population. Some of the risk factors of low bone mineral density, such as vitamin D or estrogen deficiency, are potentially modifiable. Further studies are needed to elucidate if interventions modifying these risk factors will have an impact on clinical outcomes. In this review, we discuss the options for and problems of assessment of bone density and summarize the literature about factors associated with low bone density and its link to clinical outcomes in patients on maintenance dialysis.     

Bone mineral density and bone histomorphometry in children on long-term dialysis

Bone mineral density (BMD) at the lumbar vertebrae (L(1)-L(4)) was assessed by dual-energy X-ray absorptiometry (DXA) in 20 children with chronic kidney disease (CKD) on dialysis, and its results were compared with bone biopsy and biochemical parameters. Biopsy specimens provided evidence of hyperparathyroid bone disease in eight cases (40%), and low bone turnover in 12 (60%). For BMD, expressed as Z-scores relative to normal, median Z-scores were -1.05 (range -2.36 to 1.06) for hyperparathyroid patients and -1.05 (range -4.40 to -0.03) for low bone turnover patients, with no statistical differences between groups (P = 0.512). In relation to BMD, of the whole sample, five (25%) had a Z-score under -2.0. When it was corrected for height, BMD was in the normal range. Additionally, there were no significant differences in single samples of serum calcium, alkaline phosphatase, phosphorus and intact parathyroid hormone (PTH) between groups with high or low bone turnover. Assessment of nutritional status, through height/age, showed that ten patients had Z-scores below -2.0 (median -2.12, range -7.13 to 0.73). In conclusion, renal osteodystrophy (ROD) seems to have a high prevalence among CKD pediatric patients, although only approximately a quarter of them developed changes in BMD. In children with CKD, measurements of bone mineral density may not be used for classification of various forms of ROD.     

Treatment of premenopausal women with low bone mineral density

Interpretation of bone mineral density (BMD) results in premenopausal women is particularly challenging, because the relationship between BMD and fracture risk is not the same as for postmenopausal women. Z scores rather than T scores should be used to define “low BMD” in premenopausal women. The finding of low BMD in a premenopausal woman should prompt an evaluation for secondary causes of bone loss. If a secondary cause is found, management should focus on treatment of this condition. In some cases in which the secondary cause cannot be addressed, such as glucocorticoid therapy or cancer chemotherapy, treatment with a bone-active agent to prevent bone loss should be considered. In women with no fractures and no known secondary cause, low BMD may not signify compromised bone strength. BMD is likely to remain stable in these women, and pharmacologic therapy is rarely justified. Assessment of markers of bone turnover and follow-up bone density measurements can help to identify those with an ongoing process of bone loss that may indicate a higher risk for fracture, and possible need for pharmacologic intervention.