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。     

rhGH替代治疗对生长激素缺乏儿童糖代谢的影响

目的探讨重组人生长激素(rhGH)替代治疗对生长激素缺乏症(GHD)儿童糖和胰岛素代谢的影响以及 GH 与糖代谢平衡之间的关系。方法对44例(男28例,女16例)4.5～16.5(10.4±2.6)岁 GHD 患儿在接受 rhGH 治疗前及治疗后每3个月检测体重指数、胰岛素样生长因子-1(IGF-1)、行口服葡萄糖耐量试验,计算稳态模型胰岛素抵抗指数。结果 (1)空腹血糖和 IGF-1在治疗3个月时即显著提高,一直持续较高水平,每个随访时间点与治疗前比较,差异均有统计学意义(F=6.81,7.31,P 均<0.01);稳态模型胰岛素抵抗指数和空腹胰岛素分别在治疗3和9个月时提高(P<0.01和 P<0.05),1年后下降,治疗1年半时与治疗前比较,差异已无统计学意义(均 P>0.05)。(2)相关分析发现,稳态模型胰岛素抵抗指数与体重指数、IGF-1和治疗持续时间显著相关(r=0.251,0.437,0.281,P 均<0.001)。二次方程曲线回归分析发现,稳态模型胰岛素抵抗指数与治疗持续时间呈近似抛物线量变关系。(3)发现2例暂时性高血糖,分别在停用 rhGH 治疗后1个月和5d 血糖恢复正常,再注射 rh GH 后,行口服葡萄糖耐量试验正常。结论 GHD 儿童接受 rhGH 治疗(尤第1年内)可增加胰岛素抵抗,极少数引起短暂糖代谢紊乱。循环 IGF-1可能参与控制胰岛素的敏感性,在 GH 与胰岛素平衡间起重要作用。有必要对所有接受 rhGH 治疗者定期监测糖代谢指标和 IGF-1水平。     

生长激素神经分泌功能不全患儿夜12小时生长激素分泌相和治疗的…

对生长激素神经分泌功能不全（ＧＨＮＤ）患儿进夜间连续１２小时生长激素（ＧＨ）测定，并与生长激素缺乏症（ＧＨＤ）和正常儿童比较，观察三组儿童ＧＨ均值，峰数和峰值。结果表明：三组ＣＨ平均浓度分别为２．９±１．１，２．５±１．６和５．７±２．０μｇ／Ｌ；峰数分别为１．４±０．５，１．０±１．５和３．３±１．６；最高峰值分别为１６．５±１２．４，１４．３±１６．５和３６．４±１３．７μｇ／Ｌ。ＧＨＮＤ和Ｇ     

重组人生长激素对生长激素缺乏儿童脂代谢和脂联素水平的影响

目的研究重组人生长激素(rhGH)对生长激素缺乏症(GHD)患儿脂代谢和脂联素水平的影响。方法对53例GHD患儿及33例年龄、性别相匹配的正常对照儿童,及接受rhGH治疗时间达1年以上的23例GHD患儿检测血三酰甘油(TG)、总胆固醇(TC)、胰岛素样生长因子-1(IGF-1)和脂联素水平,比较GHD组与正常对照组及rhGH治疗前后血脂和脂联素水平变化。结果GHD患儿53例中高脂血症22例(41.5%),GHD与对照组血TG、TC分别为(1.6±1.6)vs(1.1±0.4)mmol/L、(4.5±0.8)vs(4.1±0.6)mmol/L,两组比较有显著差异(P均<0.05);经rhGH治疗后,GHD患儿TG、TC均明显下降,而IGF-1明显升高,治疗前后比较均有显著差异(P<0.01,0.05);治疗后脂联素水平略上升,但治疗前后比较无显著差异。多元回归分析显示,IGF-1与年龄呈正相关,与其他因素无关;脂联素与TG呈负相关。结论GH可能直接参与GHD患儿血脂的调节,脂联素可能部分参与TG的代谢。     

基因重组人生长激素治疗儿童生长激素缺乏症26例

目的　探讨基因重组人生长激素 (rhGH)对生长激素缺乏症 (GHD)患儿的疗效。方法　对 2 6例GHD给rhGH治疗 ,0 .1IU/ (kg·d) ,每晚皮下注射 ,疗程 0 .5年。结果　 2 6例身高平均增加 8.2± 0 .8cm/ 6个月 ,生长速率由治疗前 1.5± 0 .4cm/ 6个月增加至 6.5± 1.7cm/ 6个月 ,身高标准差由治疗前 4.5± 1.2减少至3 .2± 1.1,骨龄无明显增加 ,体重也略有增加。治疗期间第 1～ 3个月 75 %左右患儿出现甲状腺功能低下症状 ,但未影响体格线性增长。结论　rhGH是治疗GHD的一种有效、安全的促生长药物     

重组人生长激素替代治疗对生长激素缺乏症患儿糖代谢的影响

目的观察国产重组人生长激素(r-hGH)替代治疗对生长激素缺乏症(GHD)患儿糖代谢的影响。方法用国产r-hGH对GHD 15例患儿治疗3个月。治疗前后行口服葡萄糖耐量试验(OGTT)及胰岛素(INS)释放试验(IRT)。分别于0、30 mun,1、2 h采静脉血行血浆葡萄糖(PG)及胰岛素(INS)测定。结果治疗前患儿糖耐量均正常,治疗3个月后OGTT空腹PG 无明显增加,但PG 30min(P<0.01)、1 h(P<0.05)、2 h(P<0.05)、血糖曲线下面积(AUCglu)(P<0.01)均明显增加;虽葡萄糖耐量曲线上移,但均未出现糖耐量损伤(IGT)或糖尿病(DM)。IRT空腹INS(P<0.05)、30 min(P<0.05)、1 h(P<0.01)、2 h(P<0.01)、INS曲线下面积(AUCins)(P<0.01)均显著增加,稳态模型胰岛素抵抗指数(Homa IR)明显上升(P<0.05)。结论GHD患儿r-hGH替代治疗3个月后INS敏感性下降,糖耐量降低,提示应用r-hGH替代治疗患儿应监测PG、INS水平     

长期吸入糖皮质激素对支气管哮喘儿童血清生长激素与身高的影响

目的探讨长期吸入糖皮质激素对支气管哮喘儿童生长激素（GH）及身高的影响。方法支气管哮喘患儿22例于治疗前、治疗后6、12、24个月抽取空腹静脉血约5ml，离心10min，留取血清，用放射免疫分析法（RIA）测定GH值。同时测定用药前及用药24个月患儿的身高，应用标准法测避并记录.结果支气管哮喘儿童用药前及用药6、12、24个月后其血清GH水平差异无显著性（F=0．6625 P〉0.05）。观察组身高治疗前、用药24个月与正常年龄相匹配儿童身高比较无显著差异（t=1．022,0．612P均〉0．05）。结论长期吸入糖皮质激素对哮喘儿童的GH及身高发育无明显影响。     

儿童矮小症应用生长激素的长期安全性

生长激素(GH)于1956年首先从人垂体中分离出,其生物化学结构直到1972年才阐明.重组DNA技术和基因工程方法,实现了人生长激素(hGH)的大规模生产,使hGH普遍利用成为可能.文章综述生长激素在儿童生长激素缺乏症、慢性肾功能不全、Turner综合征、Prader-Willi综合征、小于胎龄儿持续矮小、特发性矮小、矮小同源异型盒基因(SHOX)缺陷疾病中的应用方法和安全性.提示重组hGH用于儿童的安全性令人满意,但也需注意有潜在风险的特殊群体.     

Normal growth of nephrotic children during long-term alternate-day prednisone therapy

Statural growth has been evaluated in 20 prepubertal nephrotic children who received alternate-day prednisone therapy for a year at least. Bone age was assessed in 16 of these children after 1-4 years of therapy. During the follow-up 12 children showed variations in height standard deviation score (SDs) below 0.5, 7 gained more than 0.5 SDs and 1 lost 0.5 SDs. Bone age fell within the normal range for chronological age in all the children studied. On the while alternate-day prednisone therapy does not affect statural growth and bone maturation of children with lipoid nephrosis.     

Growth hormone secretion in growth retarded asthmatic children

Summary Fifteen asthmatic children were studied for serum growth hormone response to Bovril, who were growth retarded with severe asthma, and the growth hormone was found to be normal. Ten subjects, who were receiving corticosteroids, have been small for their age before starting corticosteroid therapy. It is concluded that there is no case for treating growth retarted asthmatic children with growth hormone. From the Departments of Medicine, Paediatrics, Tuberculosis and Chest Diseases, and Physiology, M.L.B. Medical College, Jhansi-284001, U.P. Paper read in the Interasma Congress VIII, Vlissingen, The Netherlands, October 6–10, 1975.     

Effect of adrenergic blockade on glucagon and growth hormone secretion in normal and diabetic children.

Studies were conducted in four normal and six diabetic children to assess the role of adrenergic blockade on basal and arginine-stimulated growth hormone and glucagon secreation. Each subject had, on three separate occasions, infusion of arginine alone or in conjunction with alpha (phentolamine) or beta (propranolol) adrenergic blockade. Clinically, there was evidence of adequate blockade by each agent. Basal hormone growth levels were not significantly different in the two groups (1.3 +/- 0.2 to 2.1 +/- 1.0 ng/ml in normal subjects; 3.0 +/- 1.1 to 6.0 +/- 3.1 ng/ml in diabetics (mean +/- 1 SEM)) but the peak growth hormone after arginine was significantly greater in the diabetic children than control subjects (34.3 +/- 7.2 versus 12.3 +/- 3.1); in both groups alpha-blockade suppressed the growth hormone response, whereas beta-blockade had no significant effect. Basal glucagon concentrations were similar in both groups (147 +/- 31 to 214 +/- 21 pg/ml in normal subjects; 100 +/- 20 to 124 +/- 17 pg/ml in diabetics on three different occasions) despite the coexistent hyperglycemia of the diabetics. Neither basal nor maximally stimulated glucagon secretion was significantly affected by alpha or beta blockade in the juvenile diabetic or control children. The results suggest that sympathetic overactivity via alpha receptors may contribute to the hypersecretion of growth hormone in juvenile diabetes and that the alpha or beta adrenergic receptor alone does not appear to modulate basal or arginine stimulated glucagon secretion.     

Defective growth hormone secretion in children with pycnodysostosis and improved linear growth after growth hormone treatment

Short stature is a characteristic feature of pycnodysostosis. We report defective growth hormone secretion in response to provocation and low insulin-like growth factor-I (IGF-I) concentration in five out of six patients with pycnodysostosis. Physiological replacement with growth hormone increased IGF-I concentration and improved linear growth in these children.     

Results of early reevaluation of growth hormone secretion in short children with apparent growth hormone deficiency

OBJECTIVE: To test the hypothesis that normalization of the growth hormone (GH) response to stimulation in patients with GH deficiency (GHD) and normal magnetic resonance imaging (MRI) of the hypothalamic-pituitary area might occur earlier than at attainment of final height. STUDY DESIGN: Prepubertal children with short stature (21 boys and 12 girls; age, 5.2-10 years), in whom a diagnosis of GHD was based on a GH response <10 microg/L after 2 pharmacologic tests (clonidine, arginine, or insulin hypoglycemia), and normal MRI of the hypothalamic-pituitary area were studied. After 1 to 6 months, all children underwent reevaluation of GH secretion by means of one of the provocative tests previously used. During that time, none of the children received GH therapy or entered puberty. RESULTS: A GH response > or =10 microg/L after retesting was found in 28 patients, and a GH response <10 microg/L was found in 5. In 9 patients, the peak GH response at diagnosis was <7 microg/L to both tests used. In 8, the GH response at retesting was > or =10 microg/L and was 9.0 microg/L in the remaining child. CONCLUSIONS: We suggest that patients with pathologic GH responses to provocative tests but normal MRI should be reevaluated and followed up before a diagnosis of GHD is firmly established.     

Effect of growth hormone therapy on bone metabolism of growth hormone deficient children

The effects of human growth hormone (hGH) therapy on biochemical markers of bone metabolism were studied in 17 children (10 boys and 7girls, aged 3.7–13.1 years old) with idiopathic GH deficiency, before and 1 and 6 months after GH therapy (0.5–0.7 IU/kg weekly, SC). Serum levels of calcium, phosphate, alkaline phosphatase, osteocalcin, parathyroid hormone, 1,25 dihydroxyvitamin D, insulin-like growth factor I (IGF-I) and renal phosphate per 100 ml glomerular filtrate (TPO₄/GFR) were assessed. During therapy with hGH, a significant decrease of serum calcium levels and increases of phosphate, osteocalcin, parathyroid hormone 1,25 dihydroxyvitamin D and IGF-I were observed. TPO₄/GFR was also significantly increased. Growth response (increment in HV) was positively related with changes in alkaline phosphatase and IGF-I levels after 6 months of hGH therapy. There was also a significant positive correlation between increment in HV and increment in TPO₄/GFR after 1 month of GH therapy, whereas no correlation between HV and changes in osteocalcin levels was found. Conclusion GH treatment significantly influences mineral metabolism and the measurement of TPO₄/GFR after 1 month of GH therapy may serve as a useful predictor of growth response to hGH therapy in GH-deficient children. Received: 16 August 1996 / Accepted: 5 February 1997