营养和代谢疾病

973327原发性骨质疏松症病人降钙素储备功能的改变/詹志伟…//中华内科杂志一l”7.36(1)一11~14 观察结果表明:48例未发生骨质疏松的健康妇女血降钙素基础值、峰值、升高幅度及曲线下面积与绝经前妇女均无显著性差异;而21例原发性骨质疏松症妇女上述几项指标均明撇低十健康组,较7例骨量减少妇女的血降钙峰值和升高幅度亦有降低。未见绝经对降钙索储备功能有明显影响。骨质疏松症患者降钙索储备功能降低速度与骨量丢失的程度有关‘图1表艺参6(李国芳)973328蛙鱼降钙素治疗骨质疏松症的临床观察/工军一/中华老年医学杂志,一]”7·16fl)一46~48…     

降钙素与原发性骨质疏松症

论述降钙素（ＣＴ）对血钙水平及骨代谢的影响、ＣＴ在血中的存在形式及其测定方法的进展。并着重介绍通过钙负荷－降钙素兴奋试验判断ＣＴ储备功能，以探讨降钙素在原发性骨质疏松症发生中的作用。     

降钙素与原发性骨质疏松症

论述降钙素对血钙水平及骨代谢的影响ＣＴ在血中的存在形式及其测定方法的进展。并着重介绍通过钙负荷－降钙素兴奋试验判断ＣＴ储备功能，以探讨降钙素在原发性骨质疏松症发生中的作用。     

原发性骨质疏松症

原发性骨质疏松症包括绝经后骨质疏松和老年性骨质疏松症。骨质疏松是指单位体积骨量(bone mass)减少为特征的代谢性骨改变,其矿物质和骨基质的比例正常。50岁以上的人几乎都有骨量减少,老年人和绝经后妇女全身骨量减少加速、骨脆性增加,在轻微外伤或无外伤的情况下均容易发生骨折,尤其70岁以上的老人骨折发生率高。     

全方位地关注原发性骨质疏松症的研究

原发性骨质疏松症是绝经后妇女和老年人的常见病 ,以骨量减少、骨组织微结构破坏、骨胳脆性增加、容易发生骨折为特征。骨质疏松性骨折 (常见于椎体、髋部和腕部 )严重影响老年人的身心健康 ,并造成巨额医疗消耗。随着社会人口老龄化 ,本病已成为全世界一个严重的公众卫生问题 ,被称为无声无息的流行病。骨质疏松症的发生与遗传及环境因素均密切关联 ,主要取决于年轻时的骨量峰值及此后的骨丢失率。家系调查表明骨量峰值明显受遗传因素的影响 ,对年轻女孩的研究显示其骨量 4 6 %～ 70 %决定于父母的遗传因素 ;孪生子研究也提示同卵双生的腰…     

原发性骨质疏松症及中药治疗

原发性骨质疏松症及中药治疗高举先，张瑜晋，田柏秀（湖北中医学院，武汉４３００６１）骨质疏松症是以单位体积骨量减少，骨组织显微结构异常，易发生骨折的一种多病因的疾病。按病因分原发性和继发性两大类。原发性Ⅰ型又称绝经后骨质疏松，病因为住激素不足；原发性Ⅱ...     

趋钙激素治疗骨质疏松症的前景

骨质疏松是一种全身性骨病，骨量减少，骨质的微结构破坏，坚韧性降低，因此容易断裂。常见的主要病因是妇女绝经后雌激素缺乏、老年人退化性改变和长期服用超生理量的糖皮质激素。甲状旁腺激素（PTH）、降钙素（CT）和活性型维生素D即钙三醇是正常人体具有的趋钙激素,三者协同作用到骨、肾和肠，调整骨的生长发育和骨质的不断新旧代替，保持体内钙磷的动态平衡。旧骨吸收、新骨代替称为骨转换，两者进行速度在成人是相等的，如果骨吸收速度大于骨形成则发生骨质疏松。骨质疏松症诊断和疗效观察指标[1.2]一、骨矿物盐密度[(BMD)(g/cm2)…     

绝经后骨量减少患者应用Kliogest激素替代治疗时骨重建生化标志物的变动

WHO推荐骨密度(BMD)与骨峰值的均值比较减少2.5以上标准差(SD)诊断为骨质疏松症,减少1～2个SD诊断为骨量减少。绝经后妇女由于雌激素的缺乏而致骨吸收过程加强,特别是绝经后3～5年骨量丢失较多,所以绝经后骨量减少的早期诊断及治疗是很重要的。本研究旨在评价以激素替代疗法(HRT)为背景的绝经后骨量减少患者骨重建生化标志物的变动。     

老年人骨质疏松症

老年人骨质疏松症山东省千佛山医院（２５００１４）陈少华骨质疏松分为原发性和继发性两类。老年人骨质疏松主要是原发性的，包括绝经后骨质疏松和老年性骨质疏松症。老年人骨质疏松症分为两型：①Ⅰ型：称绝经后骨质疏松症，主要见于女性；年龄为５５～７０岁。骨疏松主...     

原发性骨质疏松症患者的营养和运动管理专家共识

原发性骨质疏松症是一种累及绝经后妇女和老年人的慢性疾病,对其的防治除各种抗骨质疏松药物外,其基础措施包括营养和运动。鉴于目前我国尚无针对原发性骨质疏松患者生活方式管理的专家共识,中国营养学会骨营养与健康分会和中华医学会骨质疏松和骨矿盐疾病分会的专家,根据膳食模式、膳食营养素、运动对于骨骼健康影响的最新科学证据,讨论并制定了原发性骨质疏松症患者的营养和运动管理专家共识,旨在提高骨质疏松症患者的膳食质量和营养管理水平,并通过合适的运动方式维护骨骼健康。     

合并骨质疏松的自身免疫性甲状腺炎女性患者降钙素储备功能测定

目的　探讨降钙素 (CT)在女性自身免疫性甲状腺炎 (AIT)患者骨质疏松 (OP)发病中的作用。方法　对 2 5例健康女性对照者及 3 3例女性AIT患者 ,其中无OP者 16例 ,合并OP者 17例 ,用钙负荷 CT兴奋试验分别观察各组CT基础值及其储备功能的改变。结果　 (1)AIT患者CT基础值及其储备功能均低于对照组 (P <0 .0 5 )。 (2 )合并OP的AIT患者CT基础值及其储备功能比无OP的AIT患者更低 (P <0 .0 5 )。结论　在合并OP的女性AIT患者中 ,CT缺乏可能参与OP发生机制。     

CALCITONIN AND POSTMENOPAUSAL OSTEOPOROSIS

Fasting serum calcitonin levels were measured in 54 postmenopausal women who had for 10 years been taking part in a double blind trial to assess the effect of the synthetic oestrogen, mestranol, on postmenopausal bone loss. There were no differences in calcitonin levels between mestranol treated and placebo groups. Fifteen of the women were challenged with a calcium infusion to measure the secretory reserve of calcitonin. Oestrogen treatment did not increase the calcitonin response to calcium infusion. The three patients who exhibited the greatest responses were placebo treated. Bone density was measured by gamma-ray absorptiometry over the ten year period and the annual rate of change of bone density calculated. No correlation could be found between basal calcitonin level or calcitonin reserve and change in bone density. Our results indicate that postmenopausal osteoporosis is not caused by a deficiency of calcitonin and that the action of oestrogen therapy to prevent bone loss does not involve calcitonin.     

Calcitonin release from medullary thyroid carcinoma by thyrotropin-releasing hormone: comparison with calcium injection.

The effects of thyrotropin-releasing hormone on the release of calcitonin were investigated in 15 normal subjects and 12 patients with medullary thyroid carcinoma. The present study also compared the effect of TRH stimulation with calcium infusion test on calcitonin release in patients with medullary thyroid carcinoma. In normal subjects, calcitonin increased from a basal value of 7.5 +/- 2.5 pmol/l to a peak value of 9.4 +/- 3.0 pmol/l (p less than 0.01) after iv injection of synthetic TRH (500 micrograms). Basal calcitonin values in patients with medullary thyroid carcinoma were high (1216 +/- 2230 pmol/l, p less than 0.05), and TRH induced a further increase in calcitonin to 1842 +/- 3149 pmol/l in all the patients (p less than 0.05). They had a peak value of 7891 +/- 13,528 pmol/l after the calcium infusion, which was significantly higher than the basal value of 1463 +/- 2630 pmol/l (p less than 0.05). All medullary thyroid carcinoma patients displayed a marked calcitonin increase after TRH and calcium stimulation. Although the increase in serum calcitonin after TRH injection was lower than that after calcium injection (1.6-fold vs 5.4-fold, p less than 0.05), there was no significant difference in mean peak calcitonin value following TRH and calcium injection in patients with medullary thyroid carcinoma. These results indicated that TRH could stimulate calcitonin release from the thyroid C-cells in both normal subjects and patients with medullary thyroid carcinoma.     

Calcitonin reserve in different stages of atrophic autoimmune thyroiditis.

The objective of this study was to determine the calcitonin (CT) hormone reserve in different severity of atrophic autoimmune thyroiditis (AAT). Forty-eight female patients with AAT were divided into four groups based on basal and peak thyrotropin (TSH) values (after oral thyrotropin-releasing hormone [TRH], free triiodothyronine (FT3) and free thyroxine (FT4) ranging from normal in group 1 to overt hypothyroidism in group 4. All had thyroid antibodies. The control group comprised euthyroid females of comparable age, without thyroid antibodies. Basal CT and CT response to calcium infusion (area under the curve) were investigated as parameters of CT reserve. Basal CT was lower in groups 2 to 4 of patients with AAT (compared to controls), but the difference was not significant. Stimulated CT levels were lower (p < 0.05) in all groups of patients compared to controls, with markedly reduced CT-secretory reserve in group 4. Thyroid antibody concentrations and, basal and postinfusion calcium levels were not significantly different among the various groups. In conclusion CT deficiency (especially stimulated values) occurs in AAT and is more severe in hypothyroid patients than in earlier stages of AAT.     

Basal plasma immunoreactive calcitonin in postmenopausal osteoporosis

Calcitonin (CT) deficiency has been suggested as an etiologic factor in postmenopausal osteoporosis (PM-OP). Basal immunoreactive calcitonin (iCT) was measured with a sensitive radioimmunoassay (RIA) in 62 PM-OP women with compressin fractures (CF) and in 28 normal age-matched women. Mean iCT values in the two groups were not significantly different (43.5 and 45.1 pg/ml, p > 0.10). In the 62 PM-OP females, no significant correlation was noted between basal plasma iCT levels and (1) age; (2) severity of disease as assessed by number of CF; (3) serum calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone; and (4) total bone mass as assessed by neutron activation analysis determinations of total body calcium (TBC). In 20 PM-OP patients treated for 24 mo with 100 Medical Research Council (MRC) units daily of synthetic salmon CT, no correlation was observed between basal plasma iCT and response of bone mass (TBC) to therapy. These data suggest that basal CT is not decreased in women with PM-OP, and that the level of circulating CT does not influence therapeutic changes in bone mass during CT therapy. CT is probably not a major etiologic or pathogenetic factor in PM-OP.     

A COMPARISON OF CALCIUM PENTAGASTRIN AND TRH TESTS IN SCREENING FOR MEDULLARY CARCINOMA OF THE THYROID IN MEN IIA

Intravenous injections of calcium gluconate and pentagastrin (CPG) or TRH were compared as secretagogues for calcitonin (CT) in screening for medullary thyroid carcinoma (MTC) in multiple endocrine neoplasia type IIA (MEN IIA). Administration of CPG resulted in a prompt increase in plasma CT in all five patients with MTC studied, one of whom had a normal baseline value (peak 412-371,000 ng/l, 636-4847% above basal). TRH produced a rise in plasma CT levels only in MTC patients with elevated basal values; the magnitude of increase was less than that observed with CPG (peak 168-17,200 ng/l, 113-180% above basal). CT levels did not rise above 300 ng/l with either test in four unaffected first-degree relatives of MEN IIA patients, three subjects with sporadic unilateral phaeochromocytomas and five controls with essential hypertension. CPG remains the CT secretagogue of choice in screening for MTC in MEN II A.     

The 24-h urinary cyclic adenosine 3', 5' monophosphate/creatinine ratio: an useful approach to the diagnosis of parathyroid disorders and function

24-h urinary cyclic adenosine 3', 5'-monophosphate/creatinine (cAMP/Cr) ratio was assessed in 10 patients with hypoparathyroidism, 6 with primary hyperparathyroidism, 7 with normocalcemic hypercalciuria and recurrent nephrolithiasis, 14 with osteomalacia, 25 with Paget's disease and 53 with symptomatic postmenopausal osteoporosis. In hypoparathyroid subjects the mean values of 24 h cAMP/Cr ratio were significantly lower than the control values, whereas in patients with parathyroid adenoma the mean values were higher and fell after parathyroid surgery. Patients with nephrolithiasis due to absorptive hypercalciuria showed low or normal cAMP/Cr ratio, whereas in those with osteomalacia and mean values of cAMP/Cr ratio were significantly higher than the control values and decreased after vitamin D treatment. The mean value of the 24 h urine cAMP/Cr ratio was normal in patients with Paget's disease or postmenopausal osteoporosis and increased significantly after long term treatment with calcitonin or diphosphonate. This increase paralleled a significant decrease of calcium plasma level. A significant improvement of fractional calcium absorption was observed in women with postmenopausal osteoporosis at the end of treatment with calcitonin or diphosphonate.     

Comparison of prevalence of atherosclerotic vascular disease in postmenopausal women with osteoporosis or osteopenia versus without osteoporosis or osteopenia

Atherosclerotic vascular disease (AVD) and osteoporosis or osteopenia are common conditions among postmenopausal women and appear to be linked in a manner that is not fully understood. In a retrospective study that was conducted among 1,000 postmenopausal women who were seen in a general medicine clinic, AVD was more commonly seen among women with osteoporosis (92 of 154, 60%) than among those with osteopenia (63 of 179, 35%, p <0.001) or no osteoporosis or osteopenia (148 of 667, 22%, p <0.001). AVD was also more prevalent in women with osteopenia than in those with no osteoporosis or osteopenia (p <0.001). Modifiable risk factors for AVD were present to the same extent in women with osteoporosis, osteopenia, or no osteoporosis or osteopenia.     

Calcitonin and estrogens

Estrogen deficiency is thought to be the main factor leading to postmenopausal osteoporosis (PMO). A role for calcitonin (CT) has been proposed as mediator of estrogen action on bone, and therefore, as pathogenetic factor of PMO. However, this hypothesis is still controversial. To further analyze the relationships between estrogens and CT in PMO, we studied the effects of one-year estro/progesterone therapy on CT secretory reserve, evaluated by a calcium infusion test in 12 postmenopausal women, as compared to 12 placebo treated subjects. In the hormone treated group, blood levels of CT showed a progressive increase during the study and a plateau was reached at 9 months, indicating that CT production achieved a new steady state. Hormonal therapy also significantly improved the CT response to calcium stimulation test. A concomitant increase of vertebral bone mass was observed in the hormone treated women, who also maintained initial bone density of femoral dyaphyses. On the contrary, the placebo treated group continued to lose bone mineral at both sites. Our study demonstrates that estrogens regulate CT secretion in postmenopausal women; thus, CT may be considered a mediator of estrogen action on bone.     

Decreased plasma calcitonin response to a calcium clamp in primary hyperparathyroidism

In order preoperatively to evaluate the calcium induced plasma calcitonin (CT) response in patients with mild primary hyperparathyroidism (PHPT), 7 postmenopausal (PM) females with PHPT and 14 PM healthy subjects underwent a 2 h calcium infusion. The infusions were performed by means of the 'calcium clamp' technique previously described by us in order to obtain an identical calcium stimulus in all subjects. Immunoreactive calcitonin (iCT) was determined by means of a sensitive RIA utilizing rabbit antibodies directed against the carboxy-terminal amino acid sequence of the CT molecule. All patients with PHPT had normal basal plasma iCT levels: 10 +/- 5 pg-eq/ml (mean +/- SD) as a group and not different from the control group: 13 +/- 5 pg-eq/ml. In the control group significantly increased plasma iCT was seen at 30, 60, 90 and 120 min in contrast to that of the PHPT group where a blunted response was observed. The results indicate a diminished CT reserve in these patients which may imply an impaired defence against the PTH mediated bone resorption seen in patients with PHPT.