20例糖尿患者骨代谢部分指标变化

对２０例糖尿病患者分别测定其腰椎骨密度（ＢＭＤ）、血清钙、磷、碱性磷酸酶、骨钙素（ＢＧＰ）、２４小时尿羟脯氨酸（ＨＯＰ）。结果：ＢＭＤ与糖尿病病程、血糖呈负相关；２０￣３９岁的女性和４０￣５９岁的男性患者，其ＢＧＰ低于正常对照组；１４例测定了２４小时尿ＨＯＰ，其中１１例高于正常对照组。提示：糖尿病患者的骨代谢紊乱既有骨矿化的异常，也有骨基质的改变。     

20例糖尿病患者骨代谢部分指标变化

对２０例糖尿病患者分别测定其腰椎骨密度（ＢＭＤ）、血清钙、磷、碱性磷酸酶、骨钙素（ＢＧＰ）、２４小时尿羟脯氨酸（ＨＯＰ）．结果：ＢＭＤ与糖尿病病程、血糖呈负相关；２０～３９岁的女性和４０～５９岁的男性患者，其ＢＧＰ低于正常对照组；１４例测定了２４小时尿ＨＯＰ，其中１１例高于正常对照组。提示：糖尿病患者的骨代谢紊乱既有骨矿化的异常，也有骨基质的改变。     

老年女性Graves病治疗前、后骨密度及钙磷代谢文化

２２例老年女性Ｇｒａｖｅｓ病患者治疗前血清钙、碱性磷酸酶（ＡＫＰ）及２４小时尿钙、磷排量均显著高于对照组（Ｐ＜０．０５），骨密度（ＢＭＤ）显著低于对照组（Ｐ＜０．０５）。经治疗２～３个月甲状腺机能亢进（甲亢）基本控制后，血清钙及２４小时尿钙、磷排量随之恢复正常，但血ＡＫＰ、ＢＭＤ直到治疗１２～１８个月才恢复正常。本文对老年女性Ｇｒａｖｅｓ病治疗前、后ＢＭＤ及钙、磷代谢的变化进行了初步讨论。     

2型糖尿病对骨代谢及相关激素的影响

目的 探讨２型糖尿病对骨代谢紊乱及相关激素的影响。方法 突兀 健康对照者和６０例２型糖尿病患者血甲状旁腺激素（ＰＴＨ）、降钙素（ＣＴ）、２５羟维生素Ｄ３（２５（ＯＨ）Ｄ３）、环磷酸腺苷（ＣＡＭＰ）和血、尿钙（ＣＡ）、磷（Ｐ）、镁（ＭＧ）、糖基化血红蛋白（ＨｂＡ１ｃ）、２４小时尿糖,Ｃ肽曲线下面积等指标。结果 （１）２型糖尿病患者血坑于对照组（Ｐ〈０．００１和Ｐ〈０．０１）,ＣＴ水平显著低于对照组Ｐ     

地方性氟骨症硼砂制剂治疗前后骨矿密度和血尿氟变化

１３２例地方性氟骨症病人分别给予硼砂片、复方硼砂片和安慰剂，共６个月。实验前后用单光子吸收法（ＳＰＡ）测定前臂骨矿密度（ＢＭＤ），同时测定血、尿赢（Ｆ－）。与天津市正常人比较，前臂ＢＭＤ女性降低。全部病人血、尿Ｆ－增高。治疗后实验两组前臂ＢＭＤ减低者ＢＭＤ明显增加，血Ｆ－下降，尿Ｆ－无变化。结果表明，氟骨症病人用硼砂制剂治疗后骨代谢异常有所好转。     

益钙宁治疗绝经后骨质疏松的骨密度和骨转换指标的改变

目的为观察绝经后骨质疏松妇女应用益钙宁长期治疗４８周至７２周对骨密度（ＢＭＤ）及骨转换生化指标的影响。方法３３例患者应用益钙宁（２０单位／次，１次／周）加乳酸钙（元素钙，５００ｍｇ／日）治疗，另３５例患者单纯用乳酸钙（元素钙５００ｍｇ／日）治疗。结果应用益钙宁加钙治疗组患者腰椎２～４ＢＭＤ在治疗２４周始即有明显增加并持续至７２周；股骨近端的ＢＭＤ增加，Ｗａｒｄｓ三角区部位见于２４周到４８周；股骨颈部位见于４８周和７２周；大转子部位仅在７２周。血ＢＧＰ水平治疗２４周呈增高的改变，而血ＴＲＡＰ和尿ＨＹＰ／Ｃｒ比值的改变于治疗２４周、４８周和７２周均有明显的下降。单纯用钙对照组于治疗后与治疗前比较未见明显改变。结论本研究结果提示益钙宁长期治疗可抑制骨吸收并可能刺激骨形成，预防骨量丢失并增加骨量     

骨质疏松症患者骨密度和几种骨代谢参数的关系分析

目的探讨骨质疏松症（ＯＰ）患者骨密度（ＢＭＤ）和几种骨代谢参数相互关系及其在ＯＰ发病中的作用与诊断中的意义。方法随机选择绝经后妇女７４例，根据ＢＭＤ分为ＯＰ组、非ＯＰ组，以绝经前妇女３１例为对照组，将３组中ＢＭＤ与白细胞介素－６（ＩＬ－６），雌二醇（Ｅ２），骨钙素（ＢＧＰ），碱性磷酸酶（ＡＬＰ），血清钙（Ｃａ）和磷（Ｐ）等进行比较。结果ＢＭＤ与骨代谢参数的表现为：ＢＭＤ与ＩＬ－６、ＢＧＰ、ＡＬＰ呈负相关（ｒ分别为－０．５５８，－０．５３２，－０．４１９），与Ｅ２呈正相关（ｒ＝０．４０５），与Ｃａ和Ｐ无显著性相关关系（ｒ分别为０．０７３，０．０８０），结果显示：随血清雌激素水平下降ＢＭＤ减少，ＢＭＤ减少时，血清ＩＬ－６、ＢＧＰ、ＡＬＰ水平则升高。结论ＩＬ－６高表达与ＯＰ发病以及雌激素减少有关，血清雌激素水平下降可能导致ＩＬ－６分泌增多，ＩＬ－６水平升高，则可能是引起骨丢失原因之一     

不同药物对糖尿病骨质疏松的短期疗效比较

把糖尿病事并骨质疏松而血糖控制满意的患者分为单纯加用钙剂组（组１）、钙剂加维生素Ｄ２组（组２）、钙剂加钙全组（组３）、钙剂加密息组（组４）及单纯尿治疗组为对照组（组５），治疗三个月后进行疗效比较。结果组１、组５治疗前后骨密度、骨代谢指标（血钙、血磷、碱性磷酸酶（ＡＫＰ）、血甲主腺激素（ＰＴＨ）、尿羟脯氨酸（均无明显变化）（Ｐ〉０．０５）。组２治疗后ＰＴＨ明显降低（Ｐ〈０．０５）。组３、组４血ＰＴＨ     

甲状腺功能亢进患者骨代谢变化的研究

目的　进一步探讨甲状腺功能对骨代谢的影响。方法　本文对４４ 例甲状腺功能亢进症（ 甲亢） 患者及４７ 例健康志愿者采用酶联免疫法（ Ｅ Ｌ Ｉ Ｓ Ａ） 测定了尿脱氧吡啶啉（ Ｄ Ｐ Ｄ） ，放射免疫法（ Ｒ Ｉ Ａ） 测定 Ｆ Ｔ３ 、 Ｆ Ｔ４ ，双能 Ｘ 线吸收骨密度仪测定腰椎（ Ｌ２４ ） 、股骨颈（ Ｎｅｃｋ） 、 Ｗａｒｄ’ｓ 三角（ Ｗａｒｄ’ｓ） 、大转子（ Ｔｒｏｃｈ） 部位的骨密度（ Ｂ Ｍ Ｄ） ，以及骨代谢相关指标。结果　尿 Ｄ Ｐ Ｄ 水平为相应年龄对照组的６ 倍（ Ｐ＜ ０ ．００１） ，血清碱性磷酸酶（ Ａ Ｌ Ｐ） 活性为对照组２ 倍（ Ｐ＜ ０ ．００１） ，腰椎及股骨上端 Ｂ Ｍ Ｄ 与对照组同部位比较有不同程度降低，其骨量丢失发生率达５０ ％ 以上，且严重程度及发生率尚随年龄而增加。相关分析还表明，尿 Ｄ Ｐ Ｄ与 Ｆ Ｔ３ 、 Ｆ Ｔ４ 、 Ａ Ｌ Ｐ 之间呈正相关，与骨密度无相关性。结论　甲状腺激素可能直接参与加速骨转换过程，并以增加骨吸收过程为显著，由此导致骨量丢失。     

甲亢患者骨密度和血清骨代谢指标的变化

目的观察甲亢患者骨密度和骨代谢的变化。方法采用双能Ｘ线吸收法（ＤＥＸＡ）测量了８１例甲亢患者和与患者年龄、性别和月经状况相匹配的８１例健康对照者腰椎２４（Ｌ２Ｌ４）和股骨近端（股骨颈、大转子和Ｗａｒｄ’ｓ三角区）的骨密度（ＢＭＤ），并同时检测其血清骨代谢指标，如骨特异性碱性磷酸酶（ＢＡＰ）、骨钙素（ＯＳＣ）和血清Ｉ型前胶原羧基末端前肽（ＰＩＣＰ）、Ｉ型胶原交联羧基末端肽（ＩＣＴＰ）、ＰＴＨ和２５羟维生素Ｄ。结果甲亢患者Ｌ２Ｌ４和股骨近端的ＢＭＤ测量值明显低于正常对照组。甲亢患者成骨细胞活性指标（血清ＰＩＣＰ、ＢＡＰ和ＯＳＣ）和破骨细胞功能指标（血清ＩＣＴＰ）检测水平明显高于正常对照组，而其血清ＰＴＨ和２５羟维生素Ｄ水平正常。甲亢患者成骨细胞活性指标之间以及它们与破骨细胞功能指标之间呈显著正相关。甲亢患者骨密度的Ｚｓｃｏｒｅ与血清骨代谢指标之间无显著相关。结论甲亢患者破骨细胞功能增强，同时伴有成骨细胞活性增高，无继发性甲状旁腺功能亢进和维生素Ｄ代谢异常。     

Short-term treatment with troglitazone decreases bone turnover in patients with type 2 diabetes mellitus

Poorly controlled type 2 or non-insulin dependent diabetes mellitus (NIDDM) patients exhibit high bone turnover, which decelerate with treatment according to the degree of improvement in glycemic control. In adults, higher bone turnover results in rapid bone loss. Therefore, deceleration of bone turnover is beneficial for bone. Troglitazone (Tro), a new anti-diabetic drug, is a thiazolidinedione (TZD) which promotes adipocyte differentiation by activating peroxisome proliferator activated receptor gamma (PPARgamma). Because, in the bone marrow, adipocytes and osteoblasts originate in common mesenchymal stem cells that are also essential for osteoclastogenesis, TZDs may directly affect bone metabolism. Thus, we examined the effects of Tro on metabolic bone markers in type 2 DM patients. Tro (400 mg/day) was administered to 33 type 2 DM patients for four weeks. The day before and four weeks after starting Tro, serum and urine samples were collected after overnight fasting. Metabolic bone markers and glycemic indices were assessed. As bone resorption markers, urinary free and total deoxypyridinoline as well as urinary collagen type I C-terminal telopeptide were measured; as bone formation markers, serum bone type and total alkaline phosphatase (BALP and ALP) levels along with osteocalcin (OC) were used. No significant changes in fasting plasma glucose or HbA1c levels were observed in our short-term treatment with Tro. All the bone resorption markers, BALP and ALP were significantly decreased. OC was not significantly changed. The discrepant changes of OC from all the other metabolic bone markers suggest limitation of the use of OC as a reliable bone formation marker in diabetics. Our results that Tro decreased metabolic bone markers before significantly improving glucose metabolism suggest that it has direct effects on bone and decreased bone turnover. TZDs may spare bone mass in NIDDM subjects through its dual effects on glucose and bone metabolism.     

The effect of methotrexate on bone metabolism markers in patients with rheumatoid arthritis

The aim of the present study was to evaluate the influence on urinary excretion levels of N-telopeptide of type I collagen (NTX) and deoxypyridinoline (DPD) as a useful marker for bone resorption, and on serum-bone alkaline phosphate (BAP) levels as a useful marker for bone formation and an early marker of osteoblast differentiation in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX). Thirty patients with RA, diagnosed according to the criteria of the American College of Rheumatology, were involved in this study between March 2003 and January 2005. None of the patients had a history of hormone (estrogen) replacement therapy. All patients were treated with MTX. Methotrexate was administered perorally at a dosage of 4–10 mg/week. All patients underwent general and physical examinations and routine blood and urinary analysis at the baseline, 3 months and 6 months after the initial treatment. Then the levels of NTX and DPD in urine and BAP in serum were measured in all patients. For comparison with the effect of other DMARDs on bone metabolism markers in RA patients, we measured the levels of NTX and DPD in urine and BAP in serum of RA patients, 13 patients treated with salazosulfapyridine (SASP), and 14 patients treated with actarit (ACT). In patients treated with MTX, NTX levels decreased significantly at 3 months after the initial treatment and remained low at 6 months after the initial treatment, and DPD levels significantly decreased at 6 months after the initial treatment. The mean serum BAP levels changed without significant differences from the baseline at 3 months and 6 months. In patients treated with SASP and ACT, all bone metabolism markers had not changed significantly at the three time points. On disease activity erythrocyte sedimentation rate, C-reactive protein, the number of swollen joints and tender joints, and mHAQ score decreased significantly at 3 months after the initial treatment, and remained at low levels at 6 months after the initial treatment with MTX. Methotrexate therapy looks promising in inhibiting generalized bone loss in patients with RA. In addition, NTX is a more sensitive marker than DPD.     

In Process Citation

Urinary bone resorption marker, deoxypyridinoline (DPD), and serum bone formation marker, bone alkaline phosphatase (BAP), were determined in three cases of osteoporotic patients with alendronate therapy. DPD decreased significantly at 1 month after start of treatment in two cases, and at 2 months in the other case. BAP gradually decreased by 30-40% at 3 months in all cases. The result shows that the determination of bone markers is useful for drug selection and early assessment of treatment efficacy in osteoporosis.     

The effect of infliximab on bone metabolism markers in patients with rheumatoid arthritis

OBJECTIVE: The aim of this study was to evaluate urinary excretion of N-telopeptide of type I collagen (NTX) and deoxypyridinoline (DPD), markers of bone resorption, and serum bone alkaline phosphatase (BAP) level, a marker of bone formation and an early marker of osteoblast differentiation, in patients with rheumatoid arthritis (RA) treated with infliximab. METHODS: Seventeen male and female patients (age 60.7+/-2.53 yr; mean disease duration 12.9+/-3.01 yr; Steinbrocker's class II-IV) with RA, diagnosed according to the criteria of the American College of Rheumatology (ACR), took part in the study between March 2003 and January 2005. None of the patients had a history of oestrogen replacement therapy. All patients were treated with infliximab combined with methotrexate. Infliximab was infused intravenously at 3 mg/kg at baseline, 2 and 6 weeks, then every 8 weeks. To evaluate disease activity, ESR, CRP, the numbers of swollen and tender joints, modified Stanford Health Assessment Questionnaire (mHAQ) score and ACR score were measured. Levels of NTX and DPD in urine and BAP in serum were measured in all patients. RESULTS: ESR, CRP, the number of swollen joints and tender joints, and mHAQ score had decreased significantly 6 weeks after initial treatment and were still low 6 months after initial treatment. NTX levels had decreased significantly 6 weeks after the initial treatment and were still low 6 months after initial treatment. DPD levels had decreased 6 months after initial infusion. Mean serum BAP level did not differ significantly among the three time points. NTX levels were statistically corresponding with the number of swollen joints and mHAQ scores. DPD levels were statistically lower corresponding with ESR. CONCLUSION: Infliximab therapy may inhibit generalized bone loss in patients with RA. NTX is a more sensitive marker than DPD.     

The effect of methotrexate on bone metabolism markers in patients with rheumatoid arthritis

Abstract

The aim of the present study was to evaluate the influence on urinary excretion levels of N-telopeptide of type I collagen (NTX) and deoxypyridinoline (DPD) as a useful marker for bone resorption, and on serum-bone alkaline phosphate (BAP) levels as a useful marker for bone formation and an early marker of osteoblast differentiation in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX). Thirty patients with RA, diagnosed according to the criteria of the American College of Rheumatology, were involved in this study between March 2003 and January 2005. None of the patients had a history of hormone (estrogen) replacement therapy. All patients were treated with MTX. Methotrexate was administered perorally at a dosage of 4–10?mg/week. All patients underwent general and physical examinations and routine blood and urinary analysis at the baseline, 3 months and 6 months after the initial treatment. Then the levels of NTX and DPD in urine and BAP in serum were measured in all patients. For comparison with the effect of other DMARDs on bone metabolism markers in RA patients, we measured the levels of NTX and DPD in urine and BAP in serum of RA patients, 13 patients treated with salazosulfapyridine (SASP), and 14 patients treated with actarit (ACT). In patients treated with MTX, NTX levels decreased significantly at 3 months after the initial treatment and remained low at 6 months after the initial treatment, and DPD levels significantly decreased at 6 months after the initial treatment. The mean serum BAP levels changed without significant differences from the baseline at 3 months and 6 months. In patients treated with SASP and ACT, all bone metabolism markers had not changed significantly at the three time points. On disease activity erythrocyte sedimentation rate, C-reactive protein, the number of swollen joints and tender joints, and mHAQ score decreased significantly at 3 months after the initial treatment, and remained at low levels at 6 months after the initial treatment with MTX. Methotrexate therapy looks promising in inhibiting generalized bone loss in patients with RA. In addition, NTX is a more sensitive marker than DPD.     

Increased formation of 8-iso-prostaglandin F(2alpha) is associated with altered bone metabolism and lower bone mass in hypercholesterolaemic subjects

OBJECTIVES: To investigate the relationship of 8-iso-prostaglandin (PG) F(2alpha) levels, a reliable marker of in vivo oxidative stress and lipid peroxidation, with bone mineral density (BMD), bone turnover markers, osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) in hypercholesterolaemia. DESIGN: Cross-sectional study. SETTING: University hospital centre. METHODS: Serum 8-iso-PGF(2alpha) levels were measured in 173 hypercholesterolaemic subjects and in 152 age- and sex-matched normocholesterolaemic controls. Femoral neck and lumbar spine BMD, serum bone-specific alkaline phosphatase (BAP), osteocalcin (OC), OPG and RANKL levels, as well as urinary levels of C-terminal telopeptides of type I collagen (CTX-I), were also assessed. RESULTS: Hypercholesterolaemic subjects showed higher (P < 0.0001) serum 8-iso-PGF(2alpha) levels than controls. They also had decreased (P < 0.0001) femoral neck and lumbar spine BMD, and lower (P < 0.0001) serum BAP and OC levels. No significant differences between hypercholesterolaemic and control subjects were found when comparing urinary CTX-I levels, or serum OPG and RANKL levels. In multivariate linear regression analysis, serum 8-iso-PGF(2alpha) was the only negative predictor for femoral neck BMD and serum BAP and OC levels in hypercholesterolaemic subjects. No significant correlation (all P > 0.25) was present between serum 8-iso-PGF(2alpha) levels and urinary CTX-I levels, or serum OPG and RANKL levels, in hypercholesterolaemic subjects. CONCLUSIONS: We found an association between increased serum 8-iso-PGF(2alpha) levels and lower bone mass and reduced serum BAP and OC concentrations in hypercholesterolaemic subjects. These results would suggest a possible role for oxidative stress in the development of lower bone mass in hypercholesterolaemia.     

Biological variability of biochemical markers of bone turnover in healthy women

To investigate day-to-day biological change of biochemical makers of bone turnover, we measured eight markers for 5 days in 10 healthy women. They aged 26-41 years (mean age; 31.1 years old), and had regular menstrual cycles. Fasting second void urine and blood was collected from them on five successive days. As serum marker, Estradiol (E2), intact PTH (i-PTH), Bone-specific alkaline phosphatase (BAP), and serum C-telopeptide (S-CTX) were measured. As urinary markers, urinary CTX (U-CTX), N-telopeptide (NTX), pyridinoline (Pyr) and deoxypyridinoline (Dpyr) were measured. Day-to-day physiological variations were different between bone markers. Variability of serum markers was less than that of urinary markers. Moreover, in the comparison of the same molecular marker, CTX, the variability of S-CTX was less than U-CTX. One should consider physiological variation of the marker to evaluate whether the change of the biochemical marker of bone turnover is significant or not.     

Reduction of urinary levels of pyridinoline and deoxypyridinoline and serum levels of soluble receptor activator of NF-kappaB ligand by etanercept in patients with rheumatoid arthritis

The effects of soluble TNF-α receptor, etanercept, on bone metabolism were investigated in patients with rheumatoid arthritis (RA). Thirty RA patients were administered etanercept once or twice a week for more than 6 months. We evaluated clinical and laboratory parameters and measured urinary excretion levels of pyridinoline (PYD), deoxypyridinoline (DPD), cross-linked N-telopeptides of type I collagen (NTX), and serum levels of bone alkaline phosphatase (BAP), osteoprotegerin (OPG), and soluble receptor activator of NFκB ligand (sRANKL) at the baseline and at 3 and 6 months after initial treatment with etanercept. Etanercept treatment resulted in an improvement of symptoms due to RA and in a reduction of urinary excretion levels of PYD and DPD as well as serum sRANKL levels, with a significant difference at 6 months, and an increase of serum BAP levels at 3 and 6 months after the initial treatment with etanercept. Urinary NTX and serum OPG levels did not show a significant change at 3 and 6 months after the initial treatment, but serum OPG levels did show a reverse correlation with serum CRP levels, suggesting that the regulation of inflammation in RA may result in an induction of OPG production. Etanercept may have the ability to reduce the levels of bone resorption markers and to increase the levels of a bone formation marker while reducing sRANKL formation in RA patients.     

Study of bone loss in diabetes mellitus type 1

While people with type 1 diabetes mellitus (DM) often have bone deficiency, the relation between this deficiency and the duration or control of diabetes remains controversial. To assess the possibility of such an interrelationship, we studied parameters relating to mineral metabolism (Ca, P, alkaline phosphatase, Mg, PTH, and hydroxyproline (OHP)); bone remodeling (osteocalcin); diabetic control (HbA1c); and radiological study of the second metacarpal of the left hand and of bone age in 87 children with type 1 DM. The mineral parameters were not abnormal among the diabetics. Diabetic children had similar levels of fasting osteocalcin as normals (10.05 +/- 4.9 vs. 9.79 +/- 3.34 ng/ml, mean +/- SD); this did not differ by sex. The bone age fell within two standard deviations of the mean, and 9.5% of the diabetics had a bone mass deficit (less than the mean cortical thickness) greater than 2 SD. There was no correlation between osteocalcin and Ca, P, glycemia, HbA1c, PTH, Mg, or OHP. Our results do not support any association between bone mass loss and the severity or duration of type 1 diabetes. Bone turnover, measured by serum osteocalcin, was normal. Therefore the pathogenesis of osteopenia in type 1 DM remains unclear, and requires further investigation.     

左旋甲状腺素替代治疗对甲状腺功能低减患者骨矿代谢的影响

目的 了解甲状腺素短期替代治疗对甲状腺功能低减（甲减）患骨矿代谢的影响。方法 对２９例原发甲减患治疗前及左旋甲状腺素替代治疗（１１．５±２．５）个月,临床症状缓解,血清学指标恢复正常后,采用ＥＬＩＳＡ法测定尿脱氧吡啶啉（ＤＰＤ）,ＲＩＡ法测定血清降钙素（ＣＴ）、甲状旁腺素（ＰＴＨ－Ｍ）、骨钙素（ＢＧＰ）等,应用双能Ｘ线吸收法测定第２￣４腰椎（Ｌ２－４）和股骨颈、大转子、Ｗａｒｄ三角骨密度（ＢＭ