The study of growth disorder in basic of abnormality of GH secretion

近年来，很明显，除了完全的生长激素(GHD)缺乏(GHD)，GH分泌的部分或一过性异常也可能发生。在生长激素水平正常的矮小儿童中，已经有记录表明24小时内生长激素浓度很低，并且有几个报告表明人类生长激素(HGH)治疗在这些儿童中有效。为了证实这些发现，我们对CH水平正常的矮个儿进行了24小时自发GH分泌和hGH治疗效果的评估，并对62名7-16岁无典型GH缺乏症(GHD)的儿童进行了24小时内源性GH分泌的评估。24小时生长激素平均浓度在24小时内每隔20分钟测定一次，变化范围为1.28到11.39微克/L，平均值为4.95和2.55微克/L。24小时平均生长激素浓度与血浆胰岛素样生长因子…呈正相关。血清胰岛素样生长因子I(IGF-I)值升高(r=0.54；p&lt；0.01)。其中30例给予重组人生长激素0.1IU/kg/d，疗程6个月，观察6个月。此后，16名儿童继续服用相同剂量的生长激素6个月。第一个疗程前、中、后的平均身高速度分别为4.3&lt；正负0.9、7.3&lt；正负1.9和4.9&lt；正负2.0 cm/年(均值正负SD)。治疗期间的高度速度大于治疗前和治疗后的值(p&lt；0.001)。在第二个治疗期间，身高速度再次增加，平均为8.52.0cm年(p&lt；0.001)。另外9名儿童以类似的方式连续治疗1年，他们的身高速度从4.1&lt；+-1.4显著增加到6.0&lt；+-1.9 cm/年(P&lt；0.001)。根据我们的标准，在接受治疗6-12个月的39名儿童中，有29名(74.4%)在治疗期间出现了生长激素依赖性的身高增加。对GH治疗有反应的儿童与未接受GH治疗的儿童在年龄、骨龄、血浆IGF-I水平、胰岛素诱导低血糖的最大GH水平或平均24小时血浆GH浓度方面没有差异。这些数据表明，一些没有生长激素缺乏的矮小儿童对生长激素治疗的反应是身高速度增加。还需要进一步的研究来确定G减量的效果

In recent years it has become evident that in addition to complete growth hormone (GH) deficiency (GHD), partial or transient abnormalities in GH secretion can occur. Low 24-hour GH concentrations have been documented in groups of short children with normal stimulated GH levels and there have been several reports of the effectiveness of human GH (hGH) treatment in these children. In order to confirm these findings, 24-hour spontaneous GH secretion and the effect of hGH treatment was evaluated in short children with normal stimulated CH levels.Evaluation of 24-hour endogenous growth hormone secretion was carried out in 62 children, aged 7-16 years, who did not have classic GH deficiency (GHD). The mean 24-hour GH concentration, determined at 20-minute intervals over 24 hours, was variable, ranging from 1.28 to 11.39 mug/l with a mean of 4.95 <plus-minus> 2.55 mug/l (<plus-minus> SD). There was a positive correlation between mean 24-hour GH concentration and plasma insulin-like growth fa … More ctor I (IGF-I) values (r=0.54; p<0.01). Recombinant human GH, 0.1 IU/kg/day was administered to 30 of the 62 children for 6 months followed by 6 months' observation without treatment. Thereafter, GH was administered at the same dose for a further 6 months to 16 children. The mean height velocities before, during, and after the first treatment period were 4.3 <plus-minus> 0.9, 7.3 <plus-minus> 1.9 and 4.9 <plus-minus> 2.0 cm/year (mean <plus-minus> SD), respectively. The height velocity during treatment was greater than pre- and post-treatment values (p<0.001). The height velocity increased again during the second treatment period to a mean of 8.5 <plus-minus> 2.0 cm/year (p<0.001). Nine other children were treated continuously in a similar manner for 1 year and their height velocity increased significantly from 4.1 <plus-minus> 1.4 to 6.0 <plus-minus> 1.9 cm/year (P<0.001). According to our criteria, 29 of the 39 children (74.4 %) who were treated for 6-12 months showed a GH-dependent height increase during therapy. There were no differences between the children who responded to GH treatment and those who did not in terms of chronological age, bone age, plasma IGF-I level, maximal GH level to insulin-induced hypoglycemia, or mean 24-hour plasma GH concentration. These data indicate that some short children without GHD respond to GH treatment with an increased height velocity. Further investigations are required to determine the effect of G Less