心得安运动激发试验对儿童生长激素缺乏症的诊断价值

目的 探讨心得安运动激发试验对儿童生长激素缺乏症(GHD)的诊断价值.方法 选择在2009年1月至2013年3月期间因身材矮小症住院,同时完善胰岛素激发和心得安运动激发两项试验的儿童,共120例,记录激发试验前后静脉血GH值.将激发试验后血GH峰值<10 ng/mL定义为激发阴性,GH峰值≥10 ng/mL定义为激发阳性.将两项激发试验后血GH峰值均<10 ng/mL者诊断为GHD.结果 120例矮小儿童中,诊断为GHD者29例(24.2%).胰岛素激发试验阳性率为48.3%.心得安运动激发试验阳性率为65.8%.两项激发试验的总符合率为62.5%,阳性符合率为79.3%.心得安运动激发后血GH峰值显著高于胰岛素激发试验的GH峰值.胰岛素激发试验血GH峰值多出现在试验后30~60 min,心得安运动激发试验GH峰值多出现在试验后的120 min.心得安运动激发试验未见不良反应发生.结论 心得安运动激发试验与胰岛素激发试验对GH的激发结果符合率较高,且比胰岛素激发试验更易刺激GH分泌,临床可考虑同时应用胰岛素激发试验、心得安运动激发试验联合诊断GHD.     

三种生长激素激发试验结果分析

对63例临床疑诊HGH分泌缺乏的儿童进行精氨酸激发试验，A组30例，行胰岛素激发试验石组33例行运动激发试验。以激发后测得HGN最高值为峰值，峰值≥10ng／ml为激发试验阳性，＜10ng／ml为阴性。结果三种激发试验HGH峰值出现时间不同。激发试验阳性率精氨酸为20．6％，胰岛素70．0％，运动试验12．1％，胰岛素激发试验阳性率与精氨酸和运动试验比较有显著性差异（P＜0．001），精氨酸与运动试验阳性率比较无显著性差异（P＞0．05）。提示胰岛素激发试验阳性率最高，最为敏感。     

生长激素激发试验及头颅CT诊断矮小症

矮小症病因繁多复杂,早期诊断、及时治疗十分重要。为此在矮小症病人中采用生长激素（GH）激发试验及头颅CT检查进行临床病因分析。对象和方法一、刘象：矮小儿童来自儿科内分泌门诊及住院病人（已排除糖尿病、甲减、软骨发育不良、佝楼病等疾病引起的矮'J．'）。105例中男78例,女27例;年龄5～18a;身高均低于同龄、同性别正常儿童万ZS,体形匀称无畸形,智力正常。二、方法：卫．详细询问病史、家族史;2、体格检查;均在SAn。～gAin专人用身长计测身高．直角规测量指距、乳距作者单位;（董俊华、张兰英、魏伟）;（王建南;（女童…     

运动激发试验与药物激发试验用于气道高反应性检测的比较及临床价值评估

目的 比较运动激发试验与药物激发试验用于气道高反应性检测的优劣,以得出更佳、更安全的用于气道高反应性的检测方法。方法 选择经哮喘正规治疗后拟停药的哮喘患儿47 例,对每名受试患儿先后进行运动和药物两种激发试验检测,并与金标准(PD20)相比较得出各自的敏感度,记录和观察两种激发试验过程中支气管痉挛症状发生情况。结果 以PD20 作为金标准,药物激发试验对中、重度气道高反应性患儿的检出敏感度(61%)明显高于运动激发试验(9%)(Pκ=0.614),而运动激发试验与金标准的一致性较差(κ=0.006);但药物激发试验中,哮喘患儿支气管痉挛症状发生率高,与咳嗽和胸闷发生率呈正相关(P结论 测定经哮喘正规治疗后拟停药的患儿气道高反应性时,药物激发试验较运动激发试验敏感度高,但副反应发生率亦较高。     

矮小症614次激发试验检测生长激素反应结果分析

本文分析２００例矮小症患儿经６１４次药物（精氨酸、左旋多巴、可乐宁、生长激素释放激素）及夜睡眠激发试验后生长激素反应的结果。其中１６６例系精氨酶、左旋多巴（或可乐宁）、夜睡眠三种试验进行匹配观察。结果显示生长激素反应峰值于各种试验出现时间先后不一，峰值以可乐宁及夜睡眠最高，最为敏感。     

吡啶斯的明对生长激素缺乏症儿生长激素分泌的激发作用

为评价吡啶斯的明（ＰＤ）对生长激素（ＧＨ）缺乏症的诊断价值，对１５例下丘脑和８例垂体性ＧＨ缺乏儿进行ＰＤ试验，并与１５例正常儿童比较。结果显示，ＰＤ能够激发正常儿童ＧＨ分泌，血清ＧＨ峰值３３．９±１３．４μｇ／Ｌ，显著高于下丘脑性和垂体性ＧＨ缺乏组（Ｐ＜０．０１）。５例下丘脑性和２例垂体性ＧＨ缺乏者对ＰＤ刺激有反应。     

儿童运动激发试验的临床应用

运动是儿童支气管哮喘发作的常见诱因,运动激发试验(ECT)是诊断运动诱发性支气管痉挛(EIB)的金标准,并作为哮喘的诊断性检查.ECT对诊断儿童运动性哮喘具有高度特异性,对已确诊的哮喘儿童,ECT阳性反映气道炎症存在,提示哮喘未控制.因此ECT亦可用于研究哮喘的病理生理机制及指导哮喘的治疗.该文重点介绍了ECT的原理、...     

体质量指数对精氨酸与可乐定联合激发试验中生长激素峰值的影响

目的 探讨体质量指数(BMI)对矮身材儿童精氨酸与可乐定联合激发试验中生长激素(GH)分泌峰值的影响.方法 回顾性分析81例矮小儿童身高、体质量测量数据,计算BMI;并应用单因素和多元逐步回归分析患儿精氨酸与可乐定联合激发试验中GH峰值的影响因素.结果 81例矮小儿童中男45例,女36例;年龄(7.3±2.5)岁;其中GH缺乏症(GHD) 47例,特发性矮小34例;BMI为(15.9±1.7) kg·m-2,BMI标准差积分(SDS)为-0.02±0.93.单因素分析显示GH峰值与BMI及BMI SDS呈负相关;多元逐步回归分析结果显示BMI SDS与GH峰值呈负相关、胰岛素样生长因子-1与GH峰值呈正相关;GHD发生率随BMI SDS增加而升高.结论 BMI SDS是影响激发试验中GH峰值的独立因素;在解释激发试验结果时候需考虑BMI的影响.     

Diagnostic Value of Provocative Test by Insulin Combined with Clonidine for Growth Hormone Deficiency in Children

Objective

To evaluate the diagnostic value of provocative test by insulin combined with clonidine for growth hormone deficiency (GHD) during childhood.

Methods

Eighty children underwent a provocative test with insulin(0.075U/Kg, intravenous) combined with clonidine (4μg/kg, orally). Among them, 40 children underwent clonidine provocative test, 40 children underwent insulin tolerance test (ITT) in another day.

Findings

The specificity of ITT+clonidine test (74%, 88%) was remarkably higher than that of ITT (48%) or clonidine test (65%). ITT+clonidine test had a better accuracy (75%, 85%) than that of ITT (63%) or clonidine test (73%).

Conclusion

We conclude that the combined clonidine+insulin test is a feasible, reliable, convenient, time saving, and safe tool for evaluation of the growth hormone (GH) axes than the clonidine test or ITT.     

Growth Response in the First Year of Growth Hormone Treatment in Prepubertal Children with Organic Growth Hormone Deficiency: a Comparison with Idiopathic Growth Hormone Deficiency

ABSTRACT. Patients in the Kabi International Growth Study (KIGS) up to 1st January 1990 who had organic growth hormone deficiency (OGHD) were identified. They accounted for 21% of all patients with growth hormone deficiency (GHD). Diagnostic categories within the OGHD group included septo-optic dysplasia, postnatal trauma, craniopharyngioma, other cranial tumours, and following acute leukaemia. Features at presentation and during the first year of hGH treatment were compared with those of children with idiopathic growth hormone deficiency (IGHD). Ninety prepubertal children with OGHD were selected for comparison of observed first-year height velocity (HV) with predicted values based on those observed in 257 children with IGHD. Those with septo-optic dysplasia, postnatal trauma and craniopharyngioma responded as predicted, whereas those with other cranial tumours appeared to grow less well than predicted. Glucocorticoid treatment did not affect response, but previous cranial or craniospinal irradiation was found to be associated with an observed HV which was significantly less than predicted.     

Diagnostic Value of Growth Hormone-Releasing Hormone Tests in Short Children

Butenandt O. (Department of Paediatric Endocrinology, Children's Hospital, University of Munich, Munich, West Germany). Diagnostic value of growth hormone-releasing hormone tests in short children. Acta Paediatr Scand [Suppl] 349 93, 1989.
The growth hormone-releasing hormone (GHRH) test was applied to more than 230 children. Twenty-five out of 61 patients with proven growth hormone (GH) deficiency responded to GHRH with a GH increase of greater than 10 ng/ml. In most of the patients with idiopathic GH deficiency, a priming procedure using daily injections of GHRH improved the secretory response to GHRH. Nearly all children with familial shortness of stature showed a prompt increase in GH levels, with a mean peak level of 34.9 ng/ml (range 0.5–144 ng/ml). A second test was performed in five children with familial short stature because of failure to respond to the first test. Children with constitutional delay of growth and development did not differ in their GH response from patients with familial shortness of stature. Ten girls with Ullrich-Turner's syndrome responded with a mean increase of 22 ng/ml GH (range 10.1–34.0 nglml). Therapy with glucocorticoids, as well as endogenous hypersecretion of cortisol, suppressed the responsiveness of the pituitary gland to GHRH. Suppression was also observed following a single dose of dexamethasone during the steroid-suppression test in eight obese children. Low responsiveness of the pituitary gland was also seen in patients with thalassaemia and transfusion-induced haemosiderosis. It is concluded that it is not possible to detect GH deficiency with a single GHRH test. A full endo-crinological evaluation is necessary to prove the diagnosis.     

Growth Hormone Releasing Hormone in the Assessment and Long-term Treatment of Growth Hormone Deficiency

The secretion of hGH after the administration of the analogue of growth hormone releasing hormone, GHRH (1–29)NH₂, to 8 normal adults and 41 short children has been studied. The children were classified on the basis of their hGH response to insulin-induced hypoglycaemia; 28 had severe hGH deficiency (peak serum hGH less than 7 mIU/litre) and 13 had simple short stature (peak serum hGH greater than 15 mIU/litre). The hGH response to GHRH was similar in normal adults and short stature children, but significantly lower in the hGH deficient children. In 23 (82%) of the hGH deficient children the peak serum hGH in response to GHRH was greater than 7 mIU/litre (the maximum value seen during hypoglycaemia), and in 14 (50%) the peak serum hGH in response to GHRH was greater than 15 mIU/litre. This suggests that in the majority of hGH deficient children the defect in hGH secretion results from hypothalamic GHRH deficiency. The hGH responses of the short stature children to insulin-induced hypoglycaemia were mainly in the low range of normal, and the majority showed normal hGH responses to GHRH. Eighteen prepubertal children with definite hGH deficiency have been treated for 3–18 months with twice daily, subcutaneous injections of GHRH. This has promoted linear growth in 12 children, of whom 8 showed an increment in height velocity of 2–11 cm/year. GHRH provides a valuable method for the assessment of hGH secretion, but by itself it cannot be used to establish deficient hGH secretion; this requires a stimulation test that promotes hypothalamic GHRH secretion, such as insulin-induced hypoglycaemia. GHRH is a practical alternative therapy to hGH for some hGH-deficient children.