Butenandt O
Kinderklinik, Dr. von Haunersches Kinderspital, Universität München.
Monatsschr Kinderheilkd. 1990 Apr;138(4):198-201.
We investigated the spontaneous secretion of GH during sleep (20.00 to 8.00) in 76 children with short statute. No difference could be found between a group of 12 children with familiar short stature or a group of 28 children with familial delay of growth and development: mean GH level 5.88:5.71 maxima 26.9:25.4 ng/ml, and integrated concentration of GH 2360:2617 ng x min/ml. 14 children with severe growth hormone deficiency proven by 2 stimulation tests, secreted significantly lower amounts of GH (mean 0.83 ng/ml, maximum 2.9 ng/ml, integrated concentration 371 ng x min/ml). 22 children with nonfamilial delay of growth and development presented values being lower than the first two groups, but higher than the group of GH deficiency patients (mean 3.07 ng/ml, maximum 13.8 ng/ml, integrated concentration 1429 ng x min/ml). Since in these children the anamnesis revealed events like breech delivery, shock or commotio cerebri as the history of patients with GH deficiency does, these events apparently cause the defective GH secretion in nonfamilial delay of growth and development.
我们对76名身材矮小儿童在睡眠期间(20:00至8:00)的生长激素(GH)自发分泌情况进行了研究。在12名家族性身材矮小儿童组和28名家族性生长发育迟缓儿童组之间未发现差异:平均GH水平分别为5.88和5.71,最大值分别为26.9和25.4 ng/ml,GH的积分浓度分别为2360和2617 ng·min/ml。经两次刺激试验证实为严重生长激素缺乏的14名儿童,分泌的GH量显著更低(平均0.83 ng/ml,最大值2.9 ng/ml,积分浓度371 ng·min/ml)。22名非家族性生长发育迟缓儿童的数值低于前两组,但高于生长激素缺乏患者组(平均3.07 ng/ml,最大值13.8 ng/ml,积分浓度1429 ng·min/ml)。由于在这些儿童的既往史中发现了臀位分娩、休克或脑震荡等情况,与生长激素缺乏患者的病史一样,这些事件显然导致了非家族性生长发育迟缓中生长激素分泌缺陷。