Department of Pediatrics, University of Massachusetts Medical School , Worcester, MA , USA.
Department of Quantitative Health Sciences, University of Massachusetts Medical School , Worcester, MA , USA.
Front Endocrinol (Lausanne). 2014 Mar 25;5:35. doi: 10.3389/fendo.2014.00035. eCollection 2014.
The hypothesis that obese children are overdiagnosed with growth hormone deficiency (GHD) has not been adequately investigated in the context of adiposity-related differences in auxology.
To investigate the differences in auxological parameters between short, prepubertal, obese children, and normal-weight peers who underwent growth hormone stimulation testing (GHST).
Over-weight/obese children with GHD [peak growth hormone (GH) < 10 μg/L] will have higher values for growth velocity (GV) standard deviation score (SDS), bone age minus chronological age (BA - CA), and child height SDS minus mid-parental height (MPTH) SDS when compared to normal-weight GHD peers.
A retrospective review of anthropometric and provocative GHST data of 67 prepubertal, GH-naïve children of age 10.21 ± 2.56 years (male n = 45, age 10.8 ± 2.60 years; female n = 22, age 8.94 ± 2.10).
GHST using arginine and clonidine.
hypopituitarism, abnormal pituitary magnetic resonance imaging scan, syndromic obesity, or syndromic short stature. Data were expressed as mean ± SD.
The over-weight/obese children with peak GH of <10 μg/L had significantly lower value for natural log (ln) peak GH (1.45 ± 0.09 vs. 1.83 ± 0.35, p = 0.022), but similar values for GV SDS, insulin-like growth factor-I, insulin-like growth factor binding protein-3, bone age, BA - CA, MPTH, and child height SDS minus MPTH SDS compared to normal-weight peers with GHD. After adjusting for covariates, the over-weight/obese children (BMI ≥ 85th percentile) were >7 times more likely than normal-weight subjects (BMI < 85th percentile) to have a peak GH of <10 μg/L, and 23 times more likely to have a peak GH of <7 μg/L (OR = 23.3, p = 0.021). There was a significant inverse relationships between BMI SDS and the ln of peak GH (β = -0.40, r (2) = 0.26, p = 0.001), but not for BMI SDS vs. GV SDS, ln peak GH vs. BA, or ln peak GH vs. GV SDS.
Subnormal peak GH levels in obese prepubertal children are not associated with unique pre-GHST auxological characteristics.
在与肥胖相关的人体测量学差异背景下,关于肥胖儿童生长激素缺乏症(GHD)被过度诊断的假设尚未得到充分研究。
研究接受生长激素刺激试验(GHST)的矮小、青春期前、肥胖儿童与正常体重同龄人之间的人体测量学参数差异。
超重/肥胖的 GHD 患儿[峰值生长激素(GH)<10μg/L]的生长速度(GV)标准差评分(SDS)、骨龄减去实际年龄(BA-CA)和儿童身高 SDS 减去中亲身高 SDS(MPTH)的数值会更高,与正常体重的 GHD 患儿相比。
对 67 名年龄为 10.21±2.56 岁(男性 n=45,年龄 10.8±2.60 岁;女性 n=22,年龄 8.94±2.10 岁)的青春期前、GH 初治、接受过精氨酸和可乐定 GHST 的儿童进行回顾性体格测量和 GHST 数据的回顾。
使用精氨酸和可乐定进行 GHST。
垂体功能减退、垂体磁共振成像异常、综合征性肥胖或综合征性身材矮小。数据表示为均值±标准差。
峰值 GH<10μg/L 的超重/肥胖儿童的自然对数(ln)峰值 GH 显著降低(1.45±0.09 与 1.83±0.35,p=0.022),但与 GHD 正常体重的同龄人相比,GV SDS、胰岛素样生长因子-I、胰岛素样生长因子结合蛋白-3、骨龄、BA-CA、MPTH 和儿童身高 SDS 减去 MPTH SDS 的数值相似。在调整协变量后,超重/肥胖儿童(BMI≥第 85 百分位)比正常体重受试者(BMI<第 85 百分位)发生峰值 GH<10μg/L 的可能性高 7 倍以上,发生峰值 GH<7μg/L 的可能性高 23 倍(OR=23.3,p=0.021)。BMI SDS 与 ln 峰值 GH 呈显著负相关(β=-0.40,r(2)=0.26,p=0.001),但 BMI SDS 与 GV SDS、ln 峰值 GH 与 BA 或 ln 峰值 GH 与 GV SDS 之间无显著相关性。
肥胖青春期前儿童的亚正常峰值 GH 水平与 GHST 前独特的人体测量学特征无关。