Graves病中某些骨代谢指标的测定

本文测定了31例Graves病病人的血清Ca、P、AKP,iPTH,血浆cAMP,尿Hyp以及骨矿含量(BMC)。结果示约有66.67％的病人BMC降低,而血清Ca、P、iPTH,血浆cAMP均在正常范围内,提示约有54.6％的病人血清AKP升高,但若无肝病AKP一般不超过25金氏单位;血清T_3与尿Hyp,尿Hyp与血清AKP间有正相关关系,而尿Hyp与BMC间呈负相关关系,所以血清AKP和尿Hyp可作为Graves病骨代谢负平衡的指标。这些骨质改变可能直接由甲状腺激素过多所引起。     

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。     

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.     

甲状腺功能亢进症患者的骨密度改变

对24例甲状腺功能亢进症的血钙(Ca)、磷(P)、碱性磷酸酶(AKP)、25(OH)D、1-25(OH)_2D,24小时尿Ca、P及骨密度进行了测定。结果显示骨密度降低占58.3％(±2s)。骨密度降低组T_3浓度高于骨密度正常组(P<0.05),病程长、病情重者骨密度降低更显著。两组血Ca、P、AKP、25(OH)D、1-25(OH)_2D及尿Ca、P等差异均无显著性,但1-25(OH)_2D比正常人低。     

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     

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。     

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。     

糖尿病患者血中降钙素和甲状旁腺激素水平的变化及其临床意义

本文共观测了51例糖尿病患者血中钙(Ca)、磷(P)、碱性磷酸酶(AKP)、甲状旁腺激素(PTH)、降钙素(CT)及血糖水平的变化。与正常对照组相比,在糖尿病各组中血Ca、P水平正常;AKP活性及PTH水平明显升高;在病情较重的糖尿病中血CT水平下降。糖尿病患者血PTH水平升高和CT水平的下降是机体的一种代偿调节,以使血Ca、P水平维持正常,但这种变化可以引起糖尿病性骨质疏松。     

Graves病患者血清磷水平与甲状腺功能的相关分析

目的 探讨Graves病患者血清磷水平与甲状腺功能的相关性。方法 纳入初次发病或复发但未使用药物治疗的Graves病患者348例,收集电解质、肝肾功能、甲状腺功能、促甲状腺素受体抗体（TRAb）、摄碘率等临床资料。以血清磷正常参考值范围上限1.45mmol/L为切点数值将其分为高磷组和正常磷组,采用非参数检验比较两组间各参数的差异,logistic回归分析评估可能影响血清磷水平的相关因素。结果 348例患者中,144例(41.38％)出现高磷血症。高磷组患者年龄和BMI均明显低于正常磷组（P<0.05）,而三碘甲状腺原氨酸（T₃）、游离三碘甲状腺原氨酸（FT₃）、TRAb、3小时摄碘率（3h RAIU）、24小时摄碘率（24h RAIU）和血清钙（Ca）均明显高于正常磷组（P<0.05）。Graves病患者的年龄（r=-0.158）和BMI（r=-0.146）与血清磷水平呈负相关,T₃（r=0.188）、FT₃（r=0.134）、3h RAIU（r=0.159）、24h RAIU（r=0.186）与血清磷水平呈正相关(P<0.05)。Logistic回归分析结果示,年龄（OR=0.982,95%CI 0.966～0.998,P=0.032）、性别（OR=0.555,95%CI 0.346～0.891,P=0.015）、FT₃（OR=1.030,95%CI1.007～1.053,P=0.011）是Graves病患者血清磷水平的影响因素。结论 Graves病患者存在磷代谢异常,年龄偏低、女性、FT₃水平升高患者更易出现高磷血症。     

甲状腺机能亢进症患者血钙、磷水平及心得安的影响

我们测定了20例甲亢进患者及20名正常人血钙、磷、钙磷乘积、碱性磷酸酶（AKP）、灭活AKP及尿羟（HP）的水平，其中11例患者以心得安160mg／日连续治疗28天后进行了复查。甲亢患者血钙增高，高血钙发生率为10％，血磷及钙磷乘积增加，AKP、来活AKP和尿HP水平亦增高。心得安治后T3及血钙降低，尿HP减少。甲亢患者血钙增高的主要机制是骨吸收增加；心得安降低血钙主要通过T3减少，β受体阻滞作用和对骨的直接作用。     

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。     

COPD患者骨密度与肿瘤坏死因子-α的关系

目的观察慢性阻塞性肺疾病患者骨密度的变化与血清肿瘤坏死因子-α（TNF-α）的相互关系。方法选取稳定期COPD患者32例,另选30例健康正常男性作为对照组,测定腰椎（L2-L4）、右髋骨（股骨颈、大转子、Word′s三角）的骨密度（BMD）,并测定骨代谢生化指标血钙（Ca）、磷（P）、碱性磷酸酶（AKP）、尿羟脯氨酸/尿肌酐（HOP/Cr）及TNF-α,分析骨密度与TNF-α的关系。结果 COPD患者与对照组相比,骨形成指标血钙（Ca）、磷（P）、血清碱性磷酸酶（AKP）无明显差异（P〉0.05）,而骨吸收指标尿羟脯氨酸/尿肌酐（HOP/Cr）明显增高,差异有显著性（P〈0.05）。COPD患者的腰椎与右髋骨（股骨颈、大转子、Word′s三角）的骨密度值较健康对照组均明显减低（P〈0.05）。COPD患者的TNF-α水平明显增高（P〈0.01）,TNF-α的水平与腰椎（L2-L4）及右髋骨（股骨颈、大转子、Word′s三角）的骨密度值均呈显著负相关（P〈0.01）。结论 COPD患者骨吸收增加,骨密度减低,继发于COPD的骨质疏松可能与慢性炎症和缺氧有关。     

The mechanism of postoperative tetany in Graves' disease

The levels of serum calcium (Ca), inorganic phosphate (P) and mid-molecular parathyroid hormone (PTH) were measured in 37 patients with Graves' disease (12 in hyperthyroid state, 25 in euthyroid state followed by subtotal thyroidectomy), 6 with papillary carcinoma of the thyroid, 8 with benign nodular goiter and 19 healthy control subjects in order to investigate the change in these levels before and after thyroidectomy. The levels of serum Ca and P of the hyperthyroid patients with Graves' disease were 9.73 +/- 0.30 mg/dl and 4.47 +/- 0.44 mg/dl, respectively, which were significantly higher than those of healthy control subjects. No significant difference in the levels of serum PTH was observed between hyperthyroid patients with Graves' disease and healthy control subjects. The levels of serum Ca, P and PTH of euthyroid patients with Graves' disease were not significantly different from those of healthy control subjects. In the patients with Graves' disease who had undergone subtotal thyroidectomy followed by postoperative tetany, serum Ca and serum PTH decreased significantly from 9.39 +/- 0.45 mg/dl to 7.90 +/- 0.33 mg/dl and from 406.6 +/- 164.4 pg/ml to 229.9 +/- 136.0 pg/ml, respectively, after surgery, but there was no change in serum P. In the patients without postoperative tetany, serum Ca and serum P decreased significantly after surgery from 9.65 +/- 0.36 mg/dl to 9.15 +/- 0.33 mg/dl and from 4.03 +/- 0.46 mg/dl to 3.47 +/- 0.54 mg/dl, respectively, without any change in the levels of serum PTH. In the patients with papillary carcinoma or benign nodular goiter without postoperative tetany, the levels of serum Ca, P and PTH did not change after surgery. In the patients with papillary carcinoma followed by postoperative tetany, serum Ca decreased significantly after surgery with concomitant decrease of serum PTH. It was concluded that excessive thyroid hormones influenced Ca metabolism, and the transient tetany following subtotal thyroidectomy for Graves' disease seemed to be due to both the absorption of Ca by hungry bone and parathyroid hypofunction.     

SERUM CALCIUM CONCENTRATION IN HYPERTHYROIDISM AT DIAGNOSIS AND AFTER TREATMENT

In a large, mainly outpatient, series of hyperthyroid patients who attended a district general hospital the serum concentrations of calcium and albumin were measured before and in many cases after treatment. The calcium level (mean +/- SD) before treatment (2.41 +/- 0.21 mmol/l, n = 437) was significantly higher (P less than 0.01) than afterwards (2.36 +/- 0.15 mmol/l, n = 232) and the albumin level rose when the patients became euthyroid (from 40.5 +/- 3.1 g/l to 44.0 +/- 2.4 g/l; P less than 0.01). After treatment neither value differed from those of an unselected group of out-patients. The usual relation between the serum concentrations of calcium and albumin did not hold in the hyperthyroid subjects but reverted to normal on treatment; the variation, probably due to an increase in ionized calcium, leads to an overestimate of the 'corrected calcium' when conventional methods are used to calculate this figure. Thus, using a conventional formula 8.5% of our hyperthyroid patients would appear to have a calcium greater than 2.65 mmol/l (normal mean plus 2 standard deviations) whereas using a correction factor specific for the hyperthyroid situation the figure is reduced to 5.7% which is only twice the expected proportion. The calcium level was significantly greater (P less than 0.001) in those patients in whom initial T3 concentration was high (greater than 7.2 nmol/l). There was no effect of T4 upon serum calcium which could not be accounted for by the action of T3. In this series of 437 patients there was no case of symptomatic hypercalcaemia. The maximum value was 2.80 mmol/l in a patient with coincident primary hyperparathyroidism. Significant hypercalcaemia is rare in hyperthyroidism.     

2型糖尿病患者治疗前后部分骨和矿物质代谢指标的变化及意义

目的　观察 2型糖尿病 (T2DM)患者血糖水平与钙尔奇D对T2DM患者骨和矿物质代谢的影响。方法　以饮食控制和口服降糖药物的T2DM患者为对象 ,根据血糖水平和治疗设立血糖正常组、钙尔奇D组和高血糖组。连续治疗 3个月 ,测定所有受试者治疗前后血清总钙、磷、碱性磷酸酶 (AKP)、骨钙素 (BGP)、Ⅰ型胶原羟基肽 (ICTP)和L2L4骨密度 (BMD)。结果　钙尔奇D治疗组血清BGP较治疗前明显上升 (P <0 0 5) ;两组患者的BMD在治疗后似呈上升趋势。结论　良好控制血糖是延缓或防止T2DM患者骨矿物质异常代谢或骨质疏松的关键 ,联合使用钙剂和VitD3可更加有效地纠正上述异常     

Graves病患者一次静脉注射葡萄糖酸钙及EDTA后血浆PTH、钙、磷的动态变化

作者观察了正常人及Graves病患者静脉注射葡萄糖酸钙、EDTA后血浆PTH、钙、磷的变化。静注葡萄糖酸钙、EDTA后,正常人组血清钙迅速上升或下降,血浆PTH亦随之下降或升高;Graves病组血钙亦迅速上升或下降,而血PTH无明显动态变化。血钙与PTH无明显相关性。提示Graves病患者在血钙的平衡调节中,PTH以外的因素起主要作用,并认为甲状旁腺功能有缺陷。     

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.