甲状腺癌病人骨矿物质含量的研究

甲状腺癌病人在接受手术治疗和放射性碘清除残余甲状腺组织后，为了维持正常的甲状腺激素水平，必须接受激素替代治疗（HRT）。甲状腺激素能刺激骨骼的更新，加速骨质的形成和破坏，抑制剂量的甲状腺激素会引起骨矿物质的丢失。适当调整甲状腺癌病人的甲状腺激素替代治疗剂量，对于减少复发的可能和骨量的流失均十分重要。     

强直性脊柱炎患者的骨密度变化

目的 评价强直性脊柱炎患者的骨密度变化，探讨其骨代谢改变的病因和发病机理。方法 采用前瞻性健康对照研究方法，对67例强直性脊柱炎患者以双能X线吸收法测定腰椎、股骨颈、股骨粗隆和Ward三角区骨密度，同时检测骨钙素、降钙素、血钙及炎症急时相反应指标，并与健康对照组进行比较。结果 强直性脊柱炎骨密度与对照组比较：股骨颈、股骨粗隆和Ward三角区骨密度显著降低，早期患者的腰椎骨密度显著降低；血清骨钙素水平较对照组显著降低；骨密度指标与炎症急时相反应指标呈负相关。结论 强直性脊柱炎患者的骨密度降低，其原因应是免疫炎症反应、运动受限等多种因素作用的结果。     

内分泌治疗对乳腺癌患者骨密度影响的研究进展

雌、孕激素受体（ER、PR）阳性的浸润性乳腺癌患者,均应接受内分泌治疗。内分泌治疗疗效好,但有其相应的不良反应,骨密度（bone mineral density,BMD）降低是内分泌治疗的主要不良反应之一。本文主要介绍乳腺癌内分泌治疗对患者骨密度的影响方面研究进展。     

冠心病患者的骨密度分析

目的 探讨冠心病患骨密度变化。方法 研究了６５例冠心病患脚跟骨骨密度,以８０例年龄健康人作对照。结果 发现冠心病患较同年龄组健康对照骨密度降低（Ｐ〈０．０１）,合并骨质疏松率男性为３１．９％,女性为３９．４％。冠心病患随着病程增加骨密度降于显负相关（Ｐ〈０．０１）,合并骨质疏松的冠心病患心脏的收缩功能较不合并骨质疏松患差,且其心律失常发生率较不合并骨质疏松患高（Ｐ〈０．０１）。结论     

骨折病人的骨密度检测

目的 观察骨折病人骨折治疗前后的骨密度变化.方法对202例男性骨折病人和96例女性骨折病人在骨折后1w、1个月、3个月、6个月时进行数字X线骨密度测量(XBM),观察骨密度值的变化.结果 男、女骨折病人骨折后1个月时与骨折时比较,男:降低4.84%;配对t检验:t=6.134,P<0.001;女:降低5.71%;t=4.734,P<0.001;3个月时与骨折时比较,男:降低1.41%;配对t检验:t= 1.288,P>0.05;女:降低2.10%;t=1571,P>0.05;6个月时与骨折时比较,男:降低0.26%;配对t检验:t= 0.009,P>0.05;女:降低0.60%;t=0.288,P>0.05.结论 男、女骨折病人骨折后1个月时有非常显著的骨密度降低,3个月时骨密度有明显恢复,较骨折时已无显著性降低;6个月时基本恢复到接近正常水平,与骨折时比较没有显著性差异.     

女性类风湿关节炎患者骨密度的研究

目的探讨女性类风湿关节炎(RA)患者骨密度(BMD)的变化和骨质疏松(OP)的发生情况及其与临床指标的相关性.方法采用双能X线骨密度仪,测量了45例女性RA患者和45例女性正常人的前臂、腰椎2～4以及股骨颈、Ward区和大转子的骨矿含量,并同时测定握力、关节功能、X线分期、关节压痛数和肿胀数、日常生活能力评估(以健康评估表HAQ积分表示)和血沉、血清类风湿因子、C反应蛋白、钙、磷、碱性磷酸酶等指标.结果女性RA患者中除股骨Ward区骨量丢失较对照组差异有显著性(P＜0.05)外,其余各测定部位的BMD与对照组间差异无显著性(P＞0.05).45例女性RA患者中发生骨质疏松较非骨质疏松组年龄更大(P＜0.005),关节功能更差(P＜0.01),HAQ积分更高(P＜0.05),握力更低(P＜0.05),CRP更高(P＜0.05).女性RA患者中服用糖皮质激素组与未服用糖皮质激素组间BMD及OP发生情况的差异无显著性(P＞0.05).绝经后女性RA患者的骨量丢失较绝经前明显(P＜0.05);除桡骨远端外,绝经后患者各测定部位BMD均低于绝经前患者(P＜0.05).Logistic Regression分析显示年龄:OR=1.085[(1.019-1.156),P=0.011]和关节功能:OR=4.828[(1.368-17.039),P=0.014]为RA患者骨质疏松发生的相关因素.结论女性RA患者的总体骨量变化与正常人相近,但股骨Ward区的骨量丢失明显高于正常人.其BMD的降低和OP的发生与年龄、绝经和关节炎的严重程度有关.     

Bone mineral density in pediatric patients with idiopathic hypercalciuria

It is well known that some patients with renal lithiasis due to idiopathic hypercalciuria (IH) may exhibit decreased bone mineral density (BMD). We have studied a large group of children with IH and related their BMD values to several renal function parameters and calcium and bone metabolism markers. Children with IH had higher osteocalcin and calcitriol levels and higher urinary excretion of magnesium and prostaglandin E₂, as well as lower tubular reabsorption of phosphate, urinary excretion of ammonium, maximum urinary PCO₂, and BMD compared with control group of children. In children with IH we observed a negative correlation between BMD and age. We found osteopenia in 22 of 73 children with IH (30.1%); these children showed lower citraturia levels and higher fractional excretion of uric acid than children with normal BMD. In osteopenic children there was a negative correlation between BMD and calcitriol levels. Several possible pathogenetic factors have been proposed for the bone mass loss. Our results demonstrate that, at least in some cases, it may be related to high levels of calcitriol, which has a well-known resorption ability. Whether a certain degree of intracellular acidosis or a higher production of prostaglandin E₂ could play a role in some cases is still an open question. In children with normal BMD we observed a direct correlation between osteocalcin and tartrate-resistant acid phosphatase levels; this correlation did not hold for children with osteopenia. Received February 7, 1996; received in revised form and accepted March 25, 1997     

Bone mineral density and bone turnover in patients with Bartter syndrome

The aim of this investigation was to evaluate bone mineral density (BMD), by use of DXA, and bone turnover, in patients with Bartter syndrome (BS). Ten patients (2 with BS type II and 8 with BS type III) were included in the procedure. Age at study varied between 2 and 30 years. During the studies usual treatment with indomethacin, spironolactone, and potassium chloride was maintained. Results were compared with those obtained in the 20 asymptomatic parents. Height of the patients at the time of the study did not differ from reference values (Z-score –1.2 to +0.8). Three patients (1 with BS type II and 2 with BS type III) presented reduced lumbar spine BMD or overt osteopenia (BMD Z-scores: –2.3, –1.3, and –1.1). BMD did not correlate significantly with age. Paternal and maternal femoral neck BMD values correlated significantly with lumbar spine BMD of the patients (r=0.65, P<0.05, and r=0.80, P<0.01). Lumbar spine BMD Z-scores correlated negatively with urinary Ca excretion when values both from patients and parents were jointly analyzed (r=–0.43, P<0.05). Plasma calcium concentration was significantly higher (P<0.001) and plasma phosphate Z-score was significantly lower (P<0.05) in the patients than in the parents. However, no significant differences were observed in values for intact PTH, 1,25 (OH)₂D₃ and 25 (OH)D₃. Intact PTH values correlated positively with BMD Z-scores at lumbar spine (r=0.45, P<0.05) and at femoral neck (r=0.63, P<0.01). Age-corrected biochemical markers of bone formation (plasma alkaline phosphatase and osteocalcin concentrations) were normal whereas age-corrected markers of bone reabsorption (urinary PYD and DPD excretion) were significantly higher than parental values (P<0.01 and <0.05, respectively). We conclude that: (1) reduced BMD is not an exclusive feature of neonatal BS and it can be also observed in classic BS; (2) the loss of bone mineral is not progressive, probably because of the hypocalciuric effect of indomethacin therapy; and (3) this study did not determine whether loss of bone mass is the cause or the consequence of hypercalciuria although the beneficial effect of indomethacin therapy implies the latter.     

辅助化疗对乳腺癌患者骨密度的影响

目的观察辅助化疗对乳腺癌患者骨密度的影响。方法选取2015年3月至2016年3月就诊宣武医院普外科并行辅助化疗的乳腺癌患者71名,绝经前32人,绝经后39人,根据疾病采用不同化疗方案(EC、FEC、TC、EC-T),患者化疗前均进行骨密度的检查,同时在化疗结束后再进行骨密度的检查。结果在绝经前患者,化疗导致患者腰椎骨密度下降,且患者基础BMI越高,骨密度下降越快;在绝经后患者,化疗导致患者股骨骨密度的下降,与患者的基础BMI关系不大。结论化疗使乳腺癌患者骨密度下降,骨健康受损,且与绝经前患者的BMI相关。     

北京城区10?12岁女孩骨密度的研究

目的 观察10－12岁女孩骨密度（BMD）的变化。方法 对375例健康女孩行全身扫描和左前臂扫描，按首位（10岁）平均体重指数（BMI）分组为超重组（BMMI＞19．6）、正常组（BMI＝14．2－19．6）、偏轻组（BMI＜14．2）。1年和2年后，利用同台双能X线骨密度仪再次扫描，连续3年追踪观察该年龄段女孩每年BMD的变化。结果 全身各部位的BMD值和全身总的骨矿含量（BMC）值第2年明显高于第1年（P＜0．01－0．001）。第3年（12岁）与第2年（11岁）相比：仅前臂远端1／10处BMD值有明显增加（P＜0．001），前臂远端1／3处BMD值和全身总的BMD值无增加，且全身总的BMD值略有下降（P＞0．05）；但全身总的BMC值有明显增加（P＜0．001）。BMD、BMC值均以超重组最高，正常组次之，偏轻组最低。结论 青春期女孩不同部位的BMD值年增长率快慢不一，但全身总的BMC值总是随着年龄增长而增加。     

儿童骨质密度不足相关研究概况

伴随诊断和治疗技术的发展,在儿童期发生的骨质密度减低逐渐引起了人们的重视。儿童低骨密度是由多种原因造成的,其中儿童在青春期生长高峰时,钙与维生素D摄入量不足是造成骨量减低的主要原因之一;导致骨量减低的其他临床相关因素还包括：成骨不良、佝偻病、少年类风湿、慢性关节炎,神经肌肉异常相关性骨量降低和特发性骨质疏松等疾病。为能够让临床医师早期认识与处理上述导致儿童期低骨质密度的问题,对儿童骨量降低提供有效的治疗,本文将对正常骨骼矿化过程、骨质密度测量技术,骨质降低的病理生理学机理和治疗方式选择的评估等方面展开综合性论述。     

Bone mineral density in hyperandrogenic amenorrhoea

Summary The authors assessed bone mineral density in antrogenized amenorrheic (group A; n=9_ and androgenized nonamenorrheic patients (group B; n=30) and compared it with controls (n=22). Bone mineral density of group A patients (1.023±0.045 g/cm²) did not differ from controls 1.047±0.83 g/cm²); both groups had significantly lower values than group B women (1.099±0.085 g/cm²). Of the hormonal variables explaining bone mineral density in antrogenized women, only dehydroepiandrosterone sulfate had a significant negative correlation (r=-0.45). In contrast to other forms of amenorrhea, women with hyperantrogenic amenorrhea seem to be spared from osteopenia.     

Bone mineral density in children with nocturnal enuresis

In enuretic children there is a significantly higher incidence of fine and gross motor clumsiness, delayed developmental milestones, slower and poor linear growth, and these patients are shorter than normal children. Skeletal maturation of enuretic children has been determined with bone age in only two studies before, but to our knowledge bone mineral content of enuretic children has not previously been determined by bone mineral density measurement. Bone mineral density was measured by the dual-energy x-ray absorptiometry method in children with nocturnal enuresis and compared with that of a control group to detect whether there were any delay in bone development and any decrease in bone mass. Thirty enuretic children were compared with a control group of 40 healthy children with respect to body height and weight measurements, daily calcium intake, serum calcium, phosphorus and ALP levels, chronological and bone ages, and bone mineral density measurements. Of the parameters compared, bone age was significantly retarded, and bone mineral density was significantly reduced in children with enuresis (8.3 +/- 1.9 vs 9.7 +/- 2.3 years; p = 0.01, and 0.5476 +/- 0.07 vs 0.6077 +/- 0.05 g/cm2; p = 0.001, respectively). Chronological ages demonstrated a significant correlation with the bone ages in both the study and control groups (r = 0.852, p < 0.001, and r = 0.844, p < 0.001, respectively). However, the mean chronological age was significantly greater than the mean bone age in the study group (p < 0.001), whereas the mean chronological age was not significantly different from the mean bone age in the control group (p = 0.514). To clarify the exact mechanism responsible for these manifestations of skeletal maturation retardation, the relationship between the maturational delay of the central nervous system connections or the effect of any perinatal insult and the retardation in skeletal maturation remains to be determined.     

Bone mineral density of the proximal femur and lumbar spine in glucocorticoid-treated asthmatic patients

The importance of the proximal femur as a site of osteoporotic fractures, the development of techniques for bone mineral density (BMD) measurement at this site and the apparent selectivity of the osteopenic effects of glucorticoids have focused attention on the assessment of proximal femoral BMD in steroid-treated subjects. We have, therefore, measured BMD (Lunar DPX) in the lumbar spine and proximal femur of 31 asthmatic patients receiving long-term glucocorticoid therapy (mean ± SEM dose 16 ± 1 mg prednisone/day, mean duration 10 ± 2 years). BMD values expressed as the percentage of normal age- and sex-appropriate mean values, after weight adjustment, were as follows: lumbar spine 80 ± 2%, femoral neck 83 ± 2%, Ward's triangle 78 ± 3% and trochanter 86 ± 2%. All these values were significantly less than control (p<0.0001) and the decrement in BMD was more marked in Ward's triangle than at the other two femoral sites (p<0.05). In all regions BMD was unrelated to dose or duration of steroid treatment. It is concluded that there are reductions in the BMD of the lumbar spine and proximal femur in glucocorticoid-treated asthmatics, probably reflecting the mixed cortical/trabecular makeup of both regions.     

早孕期骨密度正常妇女产褥期骨密度分析

目的分析早孕期骨密度正常妇女产褥期骨密度情况,分析产前、产时、产后各种因素对产褥期骨密度的影响。方法对210名在海淀妇幼保健院建档并住院分娩的早孕期桡骨骨密度正常的妇女在产褥期进行超声骨密度测定,分析孕前体重指数、孕期体重增长、分娩方式、胎儿体重、产后出血、产后喂养方式、产后补钙情况、产后户外活动等对产褥期骨密度的影响。结果早孕期骨密度正常的妇女在产褥期骨密度正常者占90.5%,骨量减少占9.5%,骨质疏松0%。210名妇女产褥期骨密度较早孕期减少,差异有统计学意义(P0.05)。产后出血量多于500m L,孕期体重增加超过12.5kg,产后未补钙及产后户外活动少的产妇,产褥期骨密度较低,差异有统计学意义(P0.05)。而孕前体重指数、分娩方式、胎儿体重、产后喂养方式对产褥期骨密度无影响(P0.05)。结论产褥期骨密度较早孕期下降,孕期控制体重增长、产褥期补钙、适当户外活动,可减少骨量流失。     

观察低雌激素闭经患者骨密度情况及性激素治疗对其骨密度的影响

目的了解年龄16~40岁低雌激素闭经患者骨密度情况及激素替代治疗(HRT)对其骨密度的影响。方法回顾性分析在北京协和医院妇科内分泌中心就诊的低雌激素闭经病例共86例,其中原发性闭经患者40例、继发性闭经患者46例;选择同期的社区志愿者中月经正常者52例作为对照组。采用双能X线法测量三组的骨密度。对18例原发性闭经患者及12例继发性闭经患者,进行HRT治疗,1年后复查骨密度。结果原发性闭经组和继发性闭经组与对照组比较,普遍存在腰椎和股骨骨密度显著性降低(P0.01),Z值的均值示骨量减少,且原发性闭经组降低尤为明显。经HRT治疗1年后原发性闭经组骨密度增加(0.034±0.046)g/cm2,Z值增加(1.08±0.81);继发性闭经组骨密度增加(0.017±0.048)g/cm2,Z值增加(0.75±0.91),较治疗前均有显著性增加(P0.05)。按卵泡刺激素(FSH)水平分组,高促性腺素组和正常(或)低促性腺素组的骨密度均显著低于对照组(P0.01),但促性腺素分组之间骨密度无显著性差异。结论低雌激素闭经患者的骨密度均明显降低;HRT可增加骨密度,在原发性闭经组疗效尤为明显。     

中老年女性骨关节炎患者骨密度的特点

目的　通过测量骨关节炎患者腰椎和髋部骨密度 ,探讨骨关节炎患者骨密度的特点及骨关节炎与骨质疏松症的关系。方法　本组研究对象均为中老年女性膝关节骨关节炎患者 ,其中 5 9例测量了腰椎和髋部骨密度 ,12例仅测量了腰椎骨密度。所有患者均按Kellgren分级标准对膝关节进行了评分。结果　绝经后妇女膝关节X线评分随Kellgren分级级数的增高患者腰椎骨密度均值逐渐增高 ,4级骨关节炎患者腰椎骨密度均值明显高于 2级患者 (P <0 0 5 ) ,而髋部骨密度均值随Kellgren分级级数的增高差异无显著性。如以低于同性别同部位峰值骨量的 2 0SD为骨质疏松诊断标准 ,腰椎和髋部符合骨质疏松症诊断的分别为 4 3 7%和 77%。在控制年龄和骨关节炎的影响后 ,股骨颈骨密度与体重指数的偏相关系数为 0 4 0 7(P <0 0 1)。结论　中老年女性骨关节炎患者中同时患有骨质疏松症的比例较高 ,同髋部骨密度测量相比 ,腰椎骨密度测量受骨关节炎影响较大。     

Bone mineral density in patients with predialysis chronic kidney disease

Abstract

Background: There is limited data available especially in Indian Population about prevalence of reduced bone mineral density (BMD) and various factors associated with it in CKD patients not on dialysis. Material: This study included 75 adult patients. Patients were divided into three groups depending upon GFR. Serum creatinine, albumin, calcium, phosphate (PO4), alkaline phosphatase, iPTH and Vitamin D were measured at baseline. BMD was measured by dual energy X-ray absorptiometry. Results: There were 51 male and 24 female patients. The mean serum phosphate, alkaline phosphatase and iPTH levels increased steadily as CKD progressed. On the other hand, mean corrected serum calcium and Vitamin D levels decreased progressively in group A, B and C. The mean serum PTH values in group A, B and C were 137.16?±?109.85, 265.02?±?132.03 and 328.14?±?119.23?pg/mL, respectively and there was significant increase in mean PTH level from group A to group C (p?<?0.05). The mean level of vitamin D showed a trend of declination from group A to C (p?<?0.05). Z-score for group A, group B and group C was 1.11?±?2.39, 0.87?±?2.66 and ?0.92?±?1.59, respectively. Similarly, T score for the three groups were 0.47?±?2.34, ?0.4?±?2.00 and ?1.524?±?1.42. Both T-score and Z-score positively correlated with GFR. There was negative correlation between Z-score and iPTH, and positive correlation with Vitamin D. Conclusion: Reduced bone density was seen early in the course of CKD as estimated from reduced BMD levels, increased prevalence of osteoporosis and increased fracture risk and it worsened with the progression of CKD.     

Effects of oral clodronate on bone mineral density in patients with relapsing breast cancer

The high prevalence of bone metastases in breast cancer and the risk that spinal and femoral osteoporosis may add further morbidity provide a rationale for bisphosphonate therapy in patients with skeletal metastases from mammary carcinoma. We investigated the effects of oral clodronate given during 9 months, with a 24-month follow-up, on bone mineral density (BMD), on biochemical markers of bone remodeling, and on osseous complications in 67 women with documented relapsing breast cancer, aged 58.7 ± 1.5 years (x ± SEM). Patients with active cancer disease were randomly allocated to two groups, with or without clodronate treatment (1600 mg/day, orally). Twenty-six women considered in complete remission (52.4 ± 2.4 years) were also studied. Expressed in deviation from gender- and age-matched normals (z score), base-line BMD at the levels of lumbar spine (LS), femoral neck (FN), and midfemoral shaft (FS) was +0.10 ± 0.22 vs. −0.12 ± 0.25, +0.03 ± 0.19 vs. −0.54 ± 0.24, and +0.08 ± 0.14 vs. −0.02 ± 0.22, in patients with active breast cancer and in subjects in remission, respectively. After 9 months of treatment, fasting urinary calcium to creatinine ratio was lower (0.26 ± 0.04 vs. 0.40 ± 0.04 mmol/mmol creatinine, p < 0.02) and serum osteocalcin was stabilized (−2.1 ± 1.1 vs. +7.0 ± 3.3 μg/L, as compared with pretreatment values, p < 0.02), in the clodronate-treated group. The rate of osseous complications (pathological fracture, hypercalcemic episode, scintigraphic or radiological evidence of metastasis development, chemo- or radiotherapy for bone disease progression) was 28.8 events per 100 patient-year in the clodronate-treated group vs. 39.0 in controls, and 31.5 vs. 40.5, after 9 and 15 months of follow-up, respectively. In 15 women without evident LS bone metastasis (7 clodronate-treated and 8 controls), LS BMD increased in the clodronate-treated group by +5.2 ± 2.5% vs. −0.3 ± 1.4%, and +8.1 ± 4.7 vs. −0.9 ±1.7, after 10.3 ± 0.4 and 17.3 ± 1.2 months, respectively (p < 0.01), as compared with pretreatment values. These results indicate that clodronate treatment decreased bone turnover and attenuated cancer-related bone morbidity. In addition, clodronate increased LS BMD in apparently unaffected bone of women with relapsing breast cancer.     

高血压患者用血管紧张素转换酶抑制剂治疗时的骨密度

目的 探讨血管紧张素转换蘸抑制剂(ACEI)对人体中轴骨骨量的影响。方法 我们将128例绝经后妇女分为4组：A组;正常血压组46例;B组：高血压ACEI短程(<5年,中位数为3年)治疗组18例;C组：高血压ACEI长程(≥5年．中位数7．5年)治疗组30例;D组：高血压心痛定治疗组34。采用双能X线吸收法测量其腰椎正侧位(APL2-4、LatL2-4)和左股骨近端各区(包括Neck、Troch、Inter、Total和Ward's)的骨密度,并检测了部分患血清BGP和晨尿羟脯氨酿(Hop／Cr)等生化指标。结果 B组和C组APL2-4．骨密度分别明显高于D组;B组和C组股骨近端除Troch外其他各区骨密度均分别明显高于D组,且C组尚显高于A组,有显差异(P<0．05);同A组和D组相比,B组和C组Troch和LatL2-4骨密度亦有增加趋势。此外,C组骨密度比B组有增高趋势,但差异无显意义。B组和C组血清BGP和晨尿HOP水平分别明显低于A组或D组(P<0．05),但B、C二组间无显差异;各组间血清钙、磷、ALP水平无显差异,结论 ACEI对骨量具有一定的保持作用．特别适用于老年女性高血压患。