糖尿病中某些骨代谢指标的测定

糖尿病性骨关节病发生率约0.1％,骨关节病的发病机理尚不清楚。本文就80例糖尿病病人的尺、桡骨骨矿含量(BMC),血清Ca、P、AKP,血、尿cAMP,血浆iPTH,尿羟脯氨酸(Hyp)测定的结果,进行分析如下。     

Graves病治疗前及治疗中血清游离钙与血,尿钙磷代谢异常

46例Graves病患者治疗前血清游离钙(Ca~( ))、磷(P)、碱性磷酸酶(AKP)及24小时尿钙(Ca)、P、羟脯氨酸(Hyp)排量水平都显著高于正常对照组。经治疗2—3个月甲亢病情控制后,血Ca~( )、P及24小时尿Ca、P亦随之恢复正常,但血AKP与24小时尿Hyp仍高于对照组。高钙血症比率在血Ca、校正钙与Ca~( )测定中分别为11.2％、16.3％与30.0％。前臂骨密度呈现骨量减少和腰椎相示骨质疏松者分别为29.0％和13.3％。本文对Graves病患者的钙、磷和骨代谢改变及其发生作了初步讨论。     

134例甲状腺功能亢进症血清骨钙素水平的变化

对134例甲状腺功能亢进症(简称甲亢)血清骨钙素(osteocalcin,BGP)、Ca、P、AKP、桡骨及尺骨骨矿物质含量(BMC)、骨密度(BD)进行了测定。BGP水平高于相应年龄、性别的对照组(333例,P<0.01)。4.9％低血钙、6.0％低血磷、10.8％AKP升高、56％的患者BMC及BD水平降低。BGP与甲亢病程呈正相关关系,治疗前升高最显著,随病情好转逐渐降低。血清BGP测定可作为甲亢骨病的较敏感可靠的诊断指标,而AKP测定的敏感性较差。     

长期服苯妥英钠癫痫患者的骨代谢研究

本工作测定了20例长期服苯妥英钠的癫痫患者血DPH、25OH D_3、cAMP、Ca、P、AKP、离子钙;尿cAMP、Ca、P及羟脯氨酸水平;桡、尺骨骨矿物含量和骨密度,并设立相应健康人作为对照组。测定结果为:癫痫组25OHD_3水平显著低于对照;全部患者中血钙降低者占20％;血磷降低者低占25％;尿钙、磷降低者占45％和55％;血离子钙降低者占85％;AKP和尿羟脯氨酸升高各占10％。癫痫组桡骨骨矿物含量、骨密度及尺骨的骨密度值显著低于对照组。     

氟骨症患者骨密度与血清骨钙素和生化指标的相关分析

目的　了解饮水型氟骨症患者骨密度 (BMD)与血清骨钙素 (BGP)和生化指标的改变 ,以及相互之间的变化关系。方法　选取氟中毒病区氟骨症患者 6 8例 ,采用单光子骨矿物仪测量 BMD,放射免疫法测血清BGP,生化检查血清钙 (Ca)、磷 (P)、碱性磷酸酶 (AKP)及尿 Ca、尿 P、羟脯氨酸 (Hop)、肌酐 (Cr)。结果　氟骨症组的 BMD低于对照组 (P<0 .0 1) ,血清 BGP明显高于对照组 (P<0 .0 1) ,反映骨代谢生化指标血清 AKP和尿Hop/ Cr值显著升高 (P<0 .0 1) ,血清 Ca、P降低 (P<0 .0 5 )。骨密度与血清 BGP、AKP、Hop/ Cr呈显著负相关 ,与血清 Ca呈正相关。结论　骨密度及血清骨钙素和骨代谢生化指标的联合测定 ,对氟骨症患者的早期诊断均有较高临床价值     

维尼安防治绝经后及老年妇女骨质疏松的临床观察

目的 探讨维尼安减缓不同绝经年限的妇女骨量丢失的作用机制。方法 对绝经后妇女和老年妇女分别给予维尼安用药3个月，并于给药前后分别进行桡骨骨矿含量（BMC)的测定、血清碱性磷酸酶（AKP）、雌二醇（E2）、降钙素（CT）的测定。结果 维尼安给药前后两组妇女BMC和血清E2的水平未见明显的变化，但血清CT的水平给药后较给药前有不同程度的升高，尿Ca/Cr比值和血清AKP的水平给药后较给药前显下降（P＜0.05及P＜0.01)。结论 维尼安可能通过刺激甲状腺C细胞来增加CT的分泌从而抑制骨质的吸收，维护其骨矿含量的相对稳定。     

糖尿病患者骨质改变的临床意义

我们测定了50例糖尿病患者桡骨的骨密度(BD).其中20例还测定血碱性磷酸酶(AKP),血Ca、P及24小时尿Ca、P的值.与正常对照组相比,64%糖尿病患者BD降低,AKP显著升高,血Ca、P正常,而24小时尿Ca排出明显增高.糖尿病BD降低与病程、病型无关,与血糖及AKP成负相关.BD测定是糖尿病骨病的一个重要的诊断指标.     

慢性肾功能衰竭患者的血清瘦素及其相关因素分析

测定60例慢性肾功能衰竭（CRF）患者的血压、血清瘦素（Lp）、胰岛素（INS）、全段甲状旁腺激素（iPTH）、神经肽Y（NPY）、C反应蛋白（CRP）、血糖（GLU）、钙（Ca）、磷（P）和碱性磷酸酶（AKP），并与60例健康对照组进行比较。结果CRF患者的血清Lp明显高于对照组（P〈0．01）；且Lp与血压、iNS、GLU、CRP、PTH、AKP呈正相关，与NPY、Ca呈负相关。提示CRF患者血清Lp升高，且影响其血压、骨代谢、食欲等。     

IDDM儿童和青少年甲状旁腺和甲状腺功能测定及其临床价值

测定32例胰岛素依赖性糖尿病(IDDM)儿童和青少年血Ca、P、AKP、iPTH、CT、T_3和T_4浓度,与正常对照组相比,血Ca、AKP、iPTH和CT水平均明显升高,血T_3水平则明显降低。IDDM儿童和青少年患者钙磷代谢和骨代谢发生了明显异常变化,可以认为是糖尿病性骨质疏松发病的开始。作者认为,糖尿病性骨质疏松的发病可能有一个从继发性甲旁亢到甲旁低的连续变化过程。而IDDM儿童和青少年患者亚临床甲状腺功能减低对缓解钙磷代谢紊乱可能具有重要作用。     

神经节苷脂酶联免疫吸附法检测Graves病人血清甲状腺刺激性抗体

本文报道利用从牛脑中提取的Ⅱ型神经节苷脂(Gls Ⅱ)作为结合剂,建立ELISA检测Graves病病人血清中甲状腺刺激性抗体(TSAb)的方法,并应用于临床。结果表明:在适当的反应条件下,TSAb能与Gls Ⅱ发生特异性结合反应。正常人血清与Graves病病人血清与Gls Ⅱ的结合反应有显著差异。Graves病初发组阳性检出率40％(n=25),Graves病缓解组为5％(n=20),Graves病复发组为38％(n=18),与用放射受体分析测定结果有良好的对应关系,唯阳性率较低,可能与神经节苷脂的种属来源有关。本法具有特异性强、重复性好、操作简单、不涉及放射性物质等优点,可作为Graves病诊断及疗效评价的有用指标。     

Acute actions of 1,25-dihydroxy-vitamin D3 in normal man: effect on calcium and parathyroid status.

The present study was undertaken to evaluate the acute effect of 1,25-dihydroxy-vitamin D3 (1,25 (OH)2D3) on serum Ca, P and immunoreactive parathyroid (iPTH) and urinary Ca, P. and cyclic AMP. In 8 normal subjects, samples were collected over intervals of 30 to 60 min during a control day and on a treatment day following oral ingestion of 1,25(OH)2D3, 2.7 microgram. For the entire group there were no significant changes in serum Ca. P, iPTH or urinary P. Urinary Ca increased significantly 7 h after administration of 1,25(OH)2D3, and urinary cAMP decreased at 12 h. In 4 patients (group A). showing an increase in serum Ca by 0;2 to 0.4 mg/dl, serum iPTH decreased in 3, and the decrease in urinary cAMP appeared sooner. Among 4 patients showing no change in serum Ca after 1,25(HO)2D3 (group B), 3 showed an increase in iPTH. These data document the early onset of action of 1,25(OH)2D3 following its administration to normal man; increments in urinary Ca provide the most sensitive index of its action. The data provide no support for the view that 1,25(OH)2D3 exerts any direct inhibitory effect on the secretion of parathyroid hormone.     

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。     

Effect of propranolol on calcium, phosphorus, and magnesium metabolic disorders in Graves' disease.

The purpose of this study was to determine whether propranolol alone can improve mineral metabolic disorders in thyrotoxicosis. Ten Graves' disease patients and 11 normal age- and sex-matched controls participated in the study. In the untreated Graves' patients, serum levels of calcium (Ca), calcium x phosphorus product (Ca x P), urinary Ca, phosphorus (P), magnesium (Mg), and hydroxyproline (Hp) were higher than in control subjects (P less than .05), intestinal Ca absorption was lower than in control subjects (P less than .05), and Ca, P, and Mg balance were negative (P less than .05). After 40 mg propranolol four times per day (qid) for 28 days, serum triiodothyronine (T3) had decreased (P less than .05), serum reverse triiodothyronine (rT3) increased (P less than .05), serum thyroxine (T4) remained unchanged (P greater than .05), serum Ca and urine Ca and Mg decreased (P less than .05), intestinal Ca absorption increased, Ca balance was corrected, and P and Mg balance was improved (P less than .05). Our results indicate that propranolol can improve the metabolic disorders in addition to the symptomatic manifestations of Graves' disease. The mechanism responsible for the improved mineral balance is unclear, but may be related to beta-adrenergic blockade, increased membrane stability, or a decrease in the thyrotoxic state caused by the therapeutically induced decrease in serum T3.     

Effect of age on serum immunoreactive parathyroid hormone and its biological effects

Immunoreactive parathyroid hormone (iPTH) levels, nephrogenous cAMP (ncAMP), and tubular maximum phosphate reabsorption (TmP) were measured in 10 young and 12 healthy volunteers. The fasting urinary calcium to creatinine ratio (Ca:Cr) was also quantitated as an index of bone resorption. Aging was attended by increased iPTH levels (6.9 +/- 0.8 vs. 3.4 +/- 0.4 mu leq/ml; P less than 0.01) as well as increased ncAMP levels (2.48 +/- 0.28 vs. 1.12 +/- 0.21 nmol/100 ml glomerular filtrate; P less than 0.005) and decreased TmP (2.9 +/- 0.2 vs. 4.1 +/- 0.2 mg/100 ml glomerular filtrate; P less than 0.005), indicating that the increased iPTH levels reflected the biological effects of the hormone. A significant positive correlation of iPTH and ncAMP and a significant negative correlation of iPTH and TmP were observed. The Ca:Cr was increased in the older volunteers (0.10 +/- 0.02 vs. 0.05 +/- 0.01; P less than 0.05). The elderly subjects had significantly decreased daily calcium ingestion, serum phosphate and albumin, and creatinine clearance. Our findings suggest that the increased biological effects of PTH in the elderly subjects may contribute to the increases in Ca:Cr and bone loss that occur with age.     

Age-related changes in parathyroid hormone and parathyroid hormone action in normal humans

We evaluated parathyroid function in 158 normal subjects, aged 23-85 yr. Calcium, phosphorus, creatinine, and cAMP were measured in blood and urine in the fasting state and after a 1-g oral calcium challenge. Serum immunoreactive PTH (iPTH) was measured with a goat antiserum developed against human PTH, using (43Tyr) human PTH-(44-68) as tracer and standards. With age, a decrease in total serum Ca (r = -0.14; P less than 0.05) was attributable to a fall in serum albumin (r = -0.40; P less than 0.001). Creatinine clearance fell from 124 ml/min at age 20 yr to 61 ml/min at age 80 yr (r = -0.44; P less than 0.001). iPTH rose with age in men (r = 0.21; P less than 0.05) and women (r = 0.31; P less than 0.001) from 29 pg/ml at age 20 yr to 48 pg/ml at 80 yr. iPTH was also correlated with creatinine clearance (r = -0.32; P less than 0.001. When renal function was controlled in the analysis, the regression of iPTH with age was no longer significant. Other significant correlations with age include a decrease in renal phosphorus reabsorption (r = -0.17; P less than 0.05) and an increase in urinary nephrogenous cAMP excretion (r = 0.34; P less than 0.01). The rise in nephrogenous cAMP was not accompanied by a change in total urinary cAMP, since plasma, and therefore filtered, cAMP decreased with age. Basal calcium excretion was stable, but the calciuric response to oral calcium decreased (r = -0.27; P less than 0.01). We conclude that loss of renal function is the major cause of rising iPTH levels with age.     

透析液钙离子浓度对维持性血液透析患者血全段甲状旁腺激素的影响

目的评价不同钙离子浓度的透析液对维持性血液透析(MHD)患者血全段甲状旁腺激素(iPTH)的影响,分析血钙、磷和钙磷乘积与iPTH之间的相关性。方法对2006年1月至3月,上海交通大学医学院附属新华医院肾内科门诊35例长期使用钙离子浓度为1·75mmol/L的透析液进行维持性血液透析的患者,于透析前留取血标本进行血Ca2 、P3-、iPTH测定,并计算钙磷乘积后,改为钙离子浓度为1·25mmol/L或1·50mmol/L的透析液进行维持性血液透析,3个月后于透析前再次留取血标本进行血Ca2 、P3-、iPTH测定,并计算钙磷乘积。结果与使用钙离子浓度为1·75mmol/L透析液比较,使用钙离子浓度为1·25mmol/L或1·50mmol/L透析液3个月后,MHD患者血Ca2 、P3-、钙磷乘积差异无显著性意义,P>0·05,血iPTH明显升高,P<0·01。血iPTH与Ca2 呈显著性负相关,r=-0·45,P<0·01;与P3-及钙磷乘积无相关性,r分别为0·13和-0·03,均P>0·05。结论1·25mmol/L或1·50mmol/L的低钙透析液可以升高MHD患者血清iPTH水平。     

肾性甲状旁腺功能亢进症甲状旁腺全切加前臂移植31例临床分析

目的总结31例尿毒症继发性甲状旁腺功能亢进症(以下简称甲旁亢)行甲状旁腺全切加前臂移植的临床经验。方法回顾性分析1996-2005年我院肾科行甲状旁腺全切加前臂移植者31例的临床特点、相关内科处理及疗效。结果 31例患者为长期血液透析者(平均透析9.2年),26例有骨痛,11例有骨折,25例有皮肤瘙痒,14例有转移性钙化。(2)31例患者血甲状旁腺激素(iPTH)平均为(1811±879)ng/L;颈部 B 超及发射型计算机体层摄影术均证实有增生肿大的甲状旁腺2～4枚,内科治疗均失败。(3)31例患者均做甲状旁腺全切加前臂移植术,术后症状明显改善。iPTH 快速下降至200 ng/L 以下。高钙、高磷恢复至正常水平,碱性磷酸酶逐步下降。随访最长时间9年,目前 iPTH、钙、磷正常。结论严重肾性甲旁亢对内科治疗失败者应及时行甲状旁腺全切加前臂移植治疗,疗效可靠。     

Cimetidine treatment of azotemic secondary hyperparathyroidism

Cimetidine, an antagonist to histamine H2-receptors, reportedly lowers serum calcium and/or serum immunoreactive parathyroid hormone (iPTH) concentrations in some patients with primary and secondary (azotemic) hyperparathyroidism. We administered the drug orally (300 mg every 6 h) to five normal volunteers and four azotemic patients with secondary hyperparathyroidism who were not undergoing chronic hemodialysis. The normal persons and one azotemic patient took the drug for 5 weeks, and the remaining azotemic patients took it for 1 week. Before treatment, all patients had elevated levels of serum iPTH (two different assay systems), with or without elevated serum calcium concentrations, and increased urinary excretion of cAMP (per 100 ml glomerular filtrate). Cimetidine treatment caused no changes in serum calcium, phosphorus, or iPTH or in urinary cAMP (expressed as nanomoles per g creatinine). Serum creatinine, however, increased significantly in patients (P less than 0.02) and control subjects (P less than 0.025), which yielded statistically significant but spurious increases of urinary cAMP when expressed per 100 ml glomerular filtrate. We conclude that short term cimetidine administration has no effect on parathyroid function in normal persons or those with azotemic hyperparathyroidism. Because of its confusing effect on serum creatinine and a possible (albeit rare) adverse effect on renal function, the drug should be used with caution in azotemic patients not yet requiring chronic dialysis.