慢性肝病患者血清VitD3水平与骨代谢的关系

检测了部分慢性乙型肝炎(下简称慢乙肝)及肝硬化患者的血清1,25(OH)2D3、骨钙素(BGP)、甲状旁腺素(PTH)、钙、磷及尺桡平均密度(BMD),并与对照组比较.结果两组患者血清1,25(OH)2D3、BGP及BMD值均明显下降,肝硬化组下降尤为显著.肝硬化组血清PTH显著升高.两组患者血钙明显降低,而血磷三组间无差异.1,25(OH)2D3水平与BGP、BMD呈显著正相关;PTH与血钙、BMD无相关性.提示慢性肝病患者存在以骨形成减少为主的骨代谢紊乱,其中血清1,25(OH)2D3减少为关键因素,PTH虽升高,但与肝病患者骨密度变化无相关.     

慢性乙肝性肝硬化症男性患者血清性激素、钙调节激素和骨转移指标的变化

目的 慢性严重肝脏损害常合并肝性骨病，为了探讨终末期肝病患者的钙调节激素变化和骨转移率状态，我们回顾性分析了17例乙肝后肝硬化失代偿的男性患者，并和年龄，身高、体重相匹配的健康男性进行对照研究，方法 肝硬化组和对照组均检测其血清性激素[雄激素（T），雌激素（E2）]，钙调节激素[甲状旁腺素（PTH），降钙素（CT）和25羟维生素D3（25-OHVD3）]和骨转换指标[血清骨钙素（BGP）和尿脱氧吡啶啉/肌酐比值（Dpd/Cr)]以及钙（Ca^2 )，磷（PO^3-)和碱性磷酸酶（ALP）。结果 显示与对照组相比，肝硬化组血清T明显降低，E2水平和E2/T比值显著升高；血清PTH显著升高，25-OHVD3明显降低，而CT差异不大，其中E2升高和25-OHVD3降低有极显著意义，肝硬化组血清BGP和Ca^2 水平明显降低，尿Dpd/Cr比值和尿Ca^2 /Cr比值明显升高。而血清CT和PO^3-差异不大。结论 我们认为慢性严重肝硬化患者骨量减低，呈现出骨形成降低，骨吸收增强之特征，与维生素D和性激素代谢异常有关，而PTH升高乃继发性改变。     

原发性肾病综合征患者血清胰岛素样生长因子1的变化及其与骨代谢的关系

目的 探讨原发性肾病综合征（PNS）患者血清胰岛素样生长因子1（IGF-1）的变化及其与骨代谢指标之间的关系。评价IGF-1在PNS患者骨代谢异常机制中的临床价值。方法 随机选取2008年1月至2009年5月临床资料完整的慢性肾脏病（CKD）1、2期PNS患者30例为对象;健康体检者61例为健康对照组。测定血清IGF-1、钙、磷、PTH、25羟基维生素D3[25-（OH）D3]、骨钙素（BGP）、I型胶原吡啶交联C终端肽（CTx）及尿钙/尿肌酐（UCa/Cr）。双能X线骨密度仪检测患者骨密度（BMD）。 结果 与健康对照组比较,PNS组血Ca、25-（OH）D3及BGP水平显著降低;血CTx水平及UCa/Cr比值显著增高（均P < 0.05）;BMD水平降低[（1.078±0.090） g/cm2 比（1.090±0.062） g/cm2,P > 0.05],但差异无统计学意义。PNS组血清IGF-1水平显著低于健康对照组,差异有统计学意义[（155.75±17.48） μg/L比（223.17± 16.44） μg/L,P < 0.05],且与24 h尿蛋白量及CTx呈负相关（r = -0.757和r = -0.786,均 P < 0.05）;与血BGP和BMD呈正相关（r = 0.861和r = 0.584,均P < 0.05）。 结论 PNS患者（CKD 1、2期）存在骨代谢异常,表现为骨形成减少、骨吸收增加。血清IGF-1与血BGP、CTx及BMD相关,可作为反映PNS患者骨代谢改变的临床指标之一。     

慢性肾脏病患者骨代谢与尿蛋白量的关系

目的 研究慢性肾脏病（CKD）患者骨代谢状况与尿蛋白量的关系。 方法 随机挑选2008年1月至2009年5月在本院肾活检证实为原发性肾小球疾病的CKD患者71例为对象。按尿蛋白量分为3组：A组25例,尿蛋白量<1.0 g/24 h;B组16例,尿蛋白量 （1.0~<3.5） g/24 h;C组30例,尿蛋白量≥3.5 g/24 h。健康体检者58例为健康对照组。常规测定血清白蛋白、24 h尿蛋白量及血清钙、磷、PTH、25羟基维生素D3[25-(OH)D3]、骨钙素（BGP）、I型胶原吡啶交联C终端肽（CTx）及尿钙/肌酐（UCa/Cr）等骨代谢指标。双能X线骨密度仪检测患者骨密度（BMD）。对各因素间进行Pearson相关分析。 结果 与健康对照组比较,A、B、C组CKD患者血钙分别为（2.23±0.08）、（2.13±0.09）、（2.04±0.06）比 （2.37±0.12） mmol/L;血25-（OH）D3分别为（50.19±6.58）、（47.78±6.69）、（42.42±10.85）比（56.34±8.34） nmol/L（均P < 0.05）;而UCa/Cr显著升高,分别为0.25±0.11、0.34±0.13、0.41±0.05比0.14±0.06（均P < 0.05）。B、C组血BGP分别为（18.69±7.35）、（16.13±5.76） μg/L,显著低于健康对照组的（22.88±6.21） μg/L;血CTx分别为（413.59±114.93）、（516.21±314.25） ng/L,显著高于健康对照组的（304.53±234.15） ng/L（均P < 0.05）。A、B两组BMD与健康对照组差异无统计学意义;C组BMD显著低于健康对照组[（1.028±0.090）比（1.090±0.062） g/cm2,P < 0.05]。Pearson相关分析显示,24 h尿蛋白量与血钙、血 25-(OH)D3呈负相关,与UCa/Cr 呈正相关;UCa/Cr与血CTx 呈正相关,与血BGP呈负相关;25-(OH)D3与BGP呈正相关,与CTx呈负相关。 结论 原发性肾小球疾病CKD患者的骨代谢异常主要表现为骨形成降低,骨吸收增加,其变化与蛋白尿程度相关,而大量尿蛋白患者骨代谢显著异常。     

驱铜联合活性维生素D3治疗对Wilson’s病患者骨骼及代谢的影响

目的 观察Wilson＇s病患者骨骼X线摄片表现，及驱铜治疗联合活性维生素D3补充治疗对骨代谢的影响。方法 对35例入选Wilson＇s病患者入院时进行骨骼X线摄片，并分别于治疗前及二巯基丙磺酸钠驱铜辅以活性维生素D3治疗8疗程后，放射免疫法测定骨代谢相关激素：PTH、CT、及血清BGP水平；用生化法测定血钙、血磷，尿钙、尿磷等。并用单光子吸收法（SPA）测定尺桡骨中远端1/3处平均骨密度值。结果 Wilson＇s病患者手腕部X线检测异常率达60%。治疗后，血PTH、血钙均降低，骨密度（BMD）值升高，较治疗前差异有统计学意义（P〈0.05）；血磷、尿钙、磷及血清CT、BGP水平较治疗前差异无显著性。结论 Wilson＇s病患者常并发骨质疏松或骨质软化等代谢性骨病，驱铜治疗联合活性维生素D3补充治疗可更好改善骨骼代谢，更快改善其骨密度。     

肝硬化、肝癌患者骨代谢生化指标与骨质疏松的临床研究

目的 观察肝硬化、肝癌患者骨质疏松的发生率探讨其发病机制。方法 选择病毒性肝炎肝硬化患者40例、肝癌患者20例分别作为研究组,选择40例原发性骨质疏松和骨量减少患者作为对照组,采用双能X线吸收仪(DXA)检测骨密度(BMD),并检测骨代谢相关指标,采用放射免疫分析法测定血清骨钙素(BGP)、甲状旁腺激素( PTH)、血钙(Ca) ,磷(P)。结果 肝炎肝硬化患者中骨量减少及骨质疏松发生率为65 %( 26/40),肝癌组中骨质疏松发生率为70% (14/20),均明显高于对照组22.5 %( 9/40 ),差异有统计学意义(P<0.05),在Child-Pugh C级患者更显著(90.9% )。肝硬化、肝癌组的BMD , Ca较对照组降低((1.90±0. 33vs2. 31±0. 11 mmol/L),血清PTH水平明显高于对照组,有统计学意义P< 0. 05。随着肝功能损害加重,肝硬化、肝癌患者的血Ca逐渐下降,血中PTH水平逐渐升高,BGP水平降低,骨形成减少,原发性骨质疏松不存在这种关系。肝硬化、肝癌患者的BMD与Ca呈正相关,(r =0. 483,P <0.05)。结论 肝硬化、肝癌患者骨质疏松发病率明显升高,且发病率随肝功能损害的逐渐加重而逐渐升高,其机理可能与血钙降低、维生素D,Ca,P的代谢紊乱及PTH升高有关。     

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。     

维生素D受体基因ApaⅠ多态性与终末期肝病患者骨代谢的相关性研究

目的探讨维生素D受体（VDR）基因Apal位点多态性与终末期肝病患者骨代谢的关系。方法选择72例终末期肝病患者,并以50例原发性骨质疏松和骨量减少患者作为对照组。采用聚合酶链反应和限制性片段长度多态性技术（PCR-RFLP）检测VDR基因ApaⅠ位点多态性,双能X线吸收仪（DXA）检测腰椎（L1～4）及股骨颈骨密度（BMD）,并检测骨代谢相关指标,包括甲状旁腺激素（PTH）、骨钙素（BGP）、血钙（Ca）、血磷（P）、尿钙（uCa）、尿肌酐（uCr）。结果①Apa Ⅰ多态性等位基因频率分布符合Hardy—Weinberg定律,终末期肝病组基因型分布为AA（12．5％）、Aa（34．7％）、aa（52．8％）;对照组基因型分布为AA（10．0％）、Aa（36．0％）、aa（54．0％）。基因型分布频率两组间差异无统计学意义（P〉0．05）。②终末期肝病组中,ApaⅠ基因型与L1～4及股骨颈BMD相关（P〈0．01）,AA基因型L1-4及股骨颈的BMD显著高于aa型（P〈0．05）。对照组中,ApaⅠ基因型与L1-4及股骨颈BMD均无明显相关性。③终末期肝病组中,ApaⅠ基因型与BGP水平相关,AA基因型的BGP水平高于aa型（P〈0．05）;ApaⅠ基因型与PTH、血Ca、血P及uCa／Cr水平差异无统计学意义。结论终末期肝病患者VDR基因ApaⅠ位点多态性与BMD及BGP水平均相关,ApaⅠ位点多态性与终末期肝病患者骨代谢存在相关性。     

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。     

慢性乙肝性肝硬化症男性患者血清性激素、钙调节激素和骨转换指标的变化

目的　慢性严重肝脏损害常合并肝性骨病。为了探讨终末期肝病患者的钙调节激素变化和骨转换率状态 ,我们回顾性分析了 17例乙肝后肝硬化失代偿的男性患者 ,并和年龄、身高、体重相匹配的健康男性进行对照研究。方法　肝硬化组和对照组均检测其血清性激素 [雄激素 (T)、雌激素 (E2 ) ],钙调节激素 [甲状旁腺素 (PTH)、降钙素 (CT)和 2 5羟维生素D3(2 5 -OHVD3) ]和骨转换指标 [血清骨钙素 (BGP)和尿脱氧吡啶啉 肌酐比值 (Dpd Cr) ]以及钙 (Ca2 + )、磷 (PO3- )和碱性磷酸酶 (ALP)。结果　显示与对照组相比 ,肝硬化组血清T明显降低、E2 水平和E2 T比值显著升高 ;血清PTH显著升高、2 5 -OHVD3明显降低 ,而CT差异不大。其中E2 升高和 2 5 -OHVD3降低有极显著意义。肝硬化组血清BGP和Ca2 + 水平明显降低、尿Dpd Cr比值和尿Ca2 + Cr比值明显升高。而血清CT和PO3- 差异不大。结论　我们认为慢性严重肝硬化患者骨量减低 ,呈现出骨形成降低、骨吸收增强之特征 ,与维生素D和性激素代谢异常有关 ,而PTH升高乃继发性改变     

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。     

Effect of immobilization upon renal synthesis of 1,25-dihydroxyvitamin D in disabled elderly stroke patients

A 1,25-dihydroxyvitamin D [1,25-(OH)2D] deficiency and immobilization-related increased serum calcium concentration have been observed in hemiplegic stroke patients. To elucidate the influence of increased serum calcium concentration on bone metabolism, we measured serum biochemical indices and bone mineral density (BMD) in the second metacarpals of 170 elderly subjects with hemiplegic stroke and 72 age-matched healthy controls. Serum concentrations of 25-hydroxyvitamin D [25-(OH)D], 1,25-(OH)2D, ionized calcium, intact parathyroid hormone (PTH), intact bone Gla protein (BGP), and pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) were measured. An increased serum calcium concentration (mean 2.543 mEq/L) was observed in this population and correlated negatively with the Barthel index (mean 66), indicating immobilization-induced bone resorption with consequent increased serum calcium. Decreased serum concentrations of 1,25-(OH)2D (mean 25.0 pg/mL) and serum 25-OHD concentration (mean 11.6 ng/mL) were noted. Serum PTH was not increased (mean 34.8 pmol/L). Serum levels of BGP were decreased significantly, whereas serum ICTP concentrations were elevated (mean 15.2 ng/mL). A strong negative correlation was seen between the serum calcium concentration and 1,25-(OH)2D (p < 0.0001). BMD of the second metacarpal in patients was decreased significantly compared with control subjects and highly correlated with 25-(OH)D and 1,25-(OH)2D concentrations. Immobilization-related increased serum calcium levels may inhibit PTH secretion, and thus 1,25-(OH)2D production. In addition, 25-(OH)D insufficiency also may contribute to decreased concentration of 1,25-(OH)2D.     

Absence of hyperparathyroidism in severe liver disease

Summary Elevated serum levels of intact parathyroid hormone (PTH) have been reported in severe versus mild biliary cirrhosis. The aim of this study was to determine whether hyperparathyroidism was present in severe liver disease on the basis of the inability of the liver to catabolize the hormone. Because biologic activity resides in the amino terminal, and amino terminal PTH determinations have not been routinely made in liver disease, it is possible that hyperparathyroidism was previously missed in these patients. Accordingly, we obtained fasting blood from 11 patients with severe liver disease and 8 age-matched controls. We measured intact, amino terminal, and mid-region PTH, vitamin D metabolites, bone gamma carboxyglutamic acid protein (BGP), ionized calcium, phosphorus, magnesium, and liver function tests. Serum levels of PTH were normal with all assays and 1,25(OH)₂D levels were not elevated. These findings argue against the possibility that hyperparathyroidism plays a role in the pathogenesis of hepatic osteodystrophy.     

The relationship of vitamin D status to bone mineral density in an Italian population of postmenopausal women

Several authors have found a relationship between vitamin D status and bone mineral density (BMD). To our knowledge, no previous studies on this topic have been carried out on the Italian postmenopausal population. We studied this relationship retrospectively in 156 Italian postmenopausal women. We also investigated the relationship between parathyroid hormone (PTH) and BMD. Measurements of BMD were taken at the lumbar spine and upper femur by dual X-ray absorptiometry. Serum 25(OH)D (calcidiol), 1,25(OH)2D (calcitriol), PTH, calcium, phosphorus, creatinine, osteocalcin and urinary calcium and phosphorus were measured according to the current laboratory methods of analysis. We found a positive statistically significant correlation between BMD, both at the spine and hip, and 25(OH)D, and a negative statistically significant correlation between BMD and PTH. No statistically significant correlation was found between BMD and 1,25(OH)2D. Crude logistic regression showed age, 25(OH)D and PTH were significant predictors of low BMD, while 1,25(OH)2D was not. Backward logistic regression showed 25(OH)D was the best predictive model for spine osteoporosis together with age, and on its own it was the best predictive model for femoral neck osteoporosis.No funding sources supported this publication.     

Vitamin D in Paget's disease of bone

The role of vitamin D metabolism in Paget's disease of bone has not been well defined. Serum levels of the main, circulating vitamin D metabolites were measured in 23 patients with Paget's disease. Values of 25(OH)D3 and 24,25(OH)2D3 were within the normal range in most (more than 90%) of the subjects. 1,25(OH)2D3 was increased in 11 (48%) patients. Markedly elevated levels (93-298 pg/ml) were found in five patients. In a subgroup of patients with high 1,25(OH)2D3, the mean serum alkaline phosphatase activity was insignificantly higher, while serum calcium, phosphorous, and kidney function were the same as in a subgroup with normal 1,25(OH)2D3. 1,25(OH)2D3 levels were not affected by treatment with either calcitonin or etidronate disodium. Serum 1,25(OH)2D3 levels may be increased in a subset of patients with Paget's disease of bone.     

Calciotropic hormones in elderly people with and without hip fracture

The effects of age on calciotropic hormones are not completely understood. The presence of secondary hyperparathyroidism has previously been demonstrated, particularly in patients with hip fracture. The role of a disturbance of vitamin D metabolism, especially a defect in l-hydroxylation, is debated. The aim of this study was to compare serum parathyroid hormone (PTH), osteocalcin and vitamin D metabolites (25(OH)D and 1,25(OH)2D) in osteoporotic elderly patients with hip fracture (HF) and in elderly controls. We studied 57 HF patients aged 83.9±5.9 years (mean±SD) and 68 controls aged 82.5±5 years recruited during two periods: 1 January and 30 April 1988 and 1989. Patients with chronic renal failure (serum creatinine above 150, µmol/l), cancer, or other metabolic bone disease were excluded. Thirty healthy young adults were studied in 1989 only for measurement of 1,25(OH)2D. (1,25(OH)2D was measured by different laboratories in 1988 and 1989 for technical reasons.) We also measured serum PTH, osteocalcin, total calcium and ionized calcium. 1,25(OH)2D levels were not statistically different between HF patients and controls for the two years, nor between HF patients and young healthy adults in 1989. 25(OH)D was decreased in HF patients (p<0.003), as was ionized calcium. Serum PTH levels were higher in HF patients than in controls (p<0.01). A positive correlation has been found between PTH and age in HF patients (r=0.29;p<0.03) and in the whole group of HF patients and controls. There was a significant decrease in osteocalcin in HF patients versus elderly controls (p<0.04). Our results confirm the high levels of intact PTH in elderly HF patients, this elevation of PTH being known to increase bone resporption. Low serum osteocalcin in HF patients seems to reflect decreased bone formation. Thus, this association contributes to the accelerated bone loss in hip fracture. This study also suggests that 1,25(OH)2D is not significantly lowered in case of hip fracture, and l-hydroxylase is not deficient, in spite of a lack of the substrate of this enzyme (25(OH)D). Therefore, a defect of 1,25(OH)2D does not appear to be a pathogenetic factor in bone aging.     

尿毒症患者桡动脉钙化与骨密度及血清骨代谢指标的关系

目的 观察尿毒症患者桡动脉钙化情况并分析其与骨密度及血清骨代谢指标改变的关系.方法 以67例尿毒症患者为对象,取内瘘手术切除的桡动脉段,von Kossa染色及透射电镜检测血管钙化情况;检测Scr、血钙、磷、甲状旁腺素(iPTH);测定腰椎、股骨颈骨密度(BMD);放射免疫法测定血清25羟维生素D3 (25OHD)、1,25羟维生素D3[1,25(OH) 2D];ELISA法测定成纤维生长因子(FGF) 23、骨特异性碱性磷酸酶(BAP)、骨钙素(BGP)与Ⅰ型胶原吡啶交联物(ICTP).以23例健康体检者为对照,仅接受血清及骨密度检查.结果 von Kossa染色见24例(35.8％)尿毒症患者桡动脉中膜明显钙沉积;电镜发现中膜平滑肌细胞由 收缩型向分泌型转化,胞内有较多含钙囊泡,基质胶原明显增加伴钙磷结晶附着,程度与钙化评分一致.与对照组比较,尿毒症患者血磷、iPTH、FGF23、BGP、ICTP显著增加(均P＜0.05),血钙、25OHD、1,25(OH)2D显著降低(均P＜0.01),腰椎、股骨颈BMD也显著降低(均P＜0.01).相关分析显示,桡动脉钙化与糖尿病、股骨颈及腰椎骨密度Z值、ICTP、FGF23相关(r=0.62、-0.43、-0.25、0.34、0.86,P=0.000、0.012、0.001、0.018、0.000),与iPTH无相关(r=-0.08,P=0.306).按iPTH水平分层后,低iPTH(＜150 ng/L)组、高iPTH(＞300 ng/L)组患者iPTH与钙化相关(r=-0.41、0.31,P=0.044、0.023).多元回归分析显示,股骨颈骨密度Z值、ICTP、FGF23是桡动脉钙化的独立危险因素(β=-0.221、0.181、0.260,P=0.021、0.024、0.036).结论 尿毒症桡动脉钙化与平滑肌细胞合成和分泌较多的含钙基质有关,骨密度降低、骨转化率异常、骨吸收增加、血清FGF23水平增加是其危险因素.     

Vitamin D depletion following burn injury in children: a possible factor in post-burn osteopenia

BACKGROUND: Children burned > 40% total body surface area (TBSA) have chronically low bone mineral density (BMD) and increased risk for fractures and adult-onset osteoporosis. Because they are advised to avoid sunlight to prevent burn scar hyperpigmentation, we hypothesized that they develop vitamin D depletion, which could contribute to post-burn osteopenia. METHODS: We studied 24 children, ages 5-20 years, burned > or = 40% TBSA 7.1 +/- 3.8 (SD) years, range 1.9-13.3 years, previously (n = 12) and 2.0 +/- 0.2, range 1.4-2.1 years, previously (n = 12), of which half received recombinant human growth hormone during the first post-burn year. We measured lumbar spine BMD, serum 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), intact PTH (iPTH), and osteocalcin. RESULTS: Serum 25(OH)D was low in 10/11 patients and 1,25(OH)2D was low in 5/11 at 7 years post-burn. Serum 25(OH)D was low in 10/12, while 1,25(OH)2D was low in 0/12 at 2 years; osteocalcin was low in 9/12 in the 7-year group; iPTH levels were in the lowest quartile in 5/12 patients at 7 years and 10/12 patients at 2 years. Serum 25(OH)D levels correlated with BMD z-scores, r = 0.53, p < 0.05, and inversely with iPTH levels, r = -0.66, p < 0.05, in the 7-year group. CONCLUSION: Burned children have low circulating levels of 25(OH)D which correlated with BMD z-scores, suggesting that post-burn vitamin D depletion may play a role in the chronically low bone density observed in these children.     

Amelioration of osteoporosis by menatetrenone in elderly female Parkinson's disease patients with vitamin D deficiency

Significant reduction in bone mineral density (BMD) occurs in patients with Parkinson's disease (PD), correlating with immobilization and with vitamin D deficiency, and increasing the risk of hip fracture, especially in elderly women. As a biological indicator of compromised vitamin K status, an increased serum concentration of undercarboxylated osteocalcin (Oc) has been associated with reduced BMD in the hip and an increased risk of fracture in otherwise healthy elderly women. We evaluated treatment with vitamin K(2) (menatetrenone; MK-4) in maintaining BMD and reducing the incidence of nonvertebral fractures in elderly female patients with PD. In a random and prospective study of PD patients, 60 received 45 mg of MK-4 daily for 12 months, and the remaining 60 (untreated group) did not. At baseline, patients of both groups showed vitamin D and K(1) deficiencies, high serum levels of ionized calcium, and glutaminic residue (Glu) Oc, and low levels of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25-(OH)(2)D], indicating that immobilization-induced hypercalcemia inhibits renal synthesis of 1,25-(OH)(2)D and compensatory PTH secretion. BMD in the second metacarpals increased by 0.9% in the treated group and decreased by 4.3% in the untreated group (p < 0.0001). Vitamin K(2) level increased by 259.8% in the treated group. Correspondingly, significant decreases in Glu Oc and calcium were observed in the treated group, in association with an increase in both PTH and 1,25-(OH)(2)D. Ten patients sustained fractures (eight at the hip and two at other sites) in the untreated group, and one hip fracture occurred among treated patients (p = 0.0082; odds ratio = 11.5). The treatment with MK-4 can increase the BMD of vitamin D- and K-deficient bone by increasing vitamin K concentration, and it can also decrease calcium levels through inhibition of bone resorption, resulting in an increase in 1,25-(OH)(2)D concentration.