Pirazzoli P, Mandini M, Zucchini S, Gualandi S, Vignutelli L, Capelli M, Cacciari E
First Paediatric Clinic, University of Bologna, Italy.
Arch Dis Child. 1996 Sep;75(3):228-31. doi: 10.1136/adc.75.3.228.
Urinary growth hormone was measured in 54 children with short stature who had growth hormone deficiency that was initially diagnosed pharmacologically (arginine and L-dopa) and physiologically (mean growth hormone concentration during sleep evaluated twice). Based on the growth hormone response to pharmacological tests the subjects were subdivided into three groups: group A, 20 subjects with normal response (peak concentration > 8 micrograms/l); group B, 20 subjects with response between 4 and 8 micrograms/l; and group C, 14 subjects with response < 4 micrograms/l. In group A four subjects had an abnormally low nocturnal mean growth hormone concentration (< or = 3.3 micrograms/l). In group C seven subjects had multiple pituitary hormone deficiency and abnormal magnetic resonance imaging. All subjects had urine collected from 8.00 pm to 8.00 am for 4-5 consecutive nights. A positive correlation was found between serum nocturnal mean growth hormone values and urinary growth hormone in all subjects. Mean (SD) concentrations of urinary growth hormone were similar in groups A (18.0 (9.5) ng/g creatinine) and B (13.6 (5.9) ng/g creatinine), but significantly higher than that of group C (3.4 (3.7) ng/g creatinine). Considering as abnormal urinary growth hormones below the lower limit of the range in group A, specificity and sensitivity of urinary growth hormone was 100% and 35% respectively. Sensitivity for groups B and C were 5% and 78% respectively. When considering only the subjects of group C with pathological magnetic resonance findings, sensitivity increased to 100%. In the four subjects of group A with mean growth hormone concentration < or = 3.3 micrograms/l, specificity decreased to 80%. It is concluded that urinary growth hormone assay is characterised by a sensitivity too low to be regarded as improving the traditional diagnostic approach to define growth hormone deficiency, unless it is used to identify subjects with the most severe deficiencies.
对54名身材矮小的儿童进行了尿生长激素检测,这些儿童最初经药理学方法(精氨酸和左旋多巴)和生理学方法(评估睡眠期间平均生长激素浓度,检测两次)诊断为生长激素缺乏症。根据生长激素对药理学试验的反应,将受试者分为三组:A组,20名反应正常的受试者(峰值浓度>8微克/升);B组,20名反应在4至8微克/升之间的受试者;C组,14名反应<4微克/升的受试者。A组中有4名受试者夜间平均生长激素浓度异常低(≤3.3微克/升)。C组中有7名受试者存在多种垂体激素缺乏且磁共振成像异常。所有受试者连续4至5个晚上从晚上8点到早上8点收集尿液。在所有受试者中,血清夜间平均生长激素值与尿生长激素之间呈正相关。A组(18.0(9.5)纳克/克肌酐)和B组(13.6(5.9)纳克/克肌酐)的尿生长激素平均(标准差)浓度相似,但显著高于C组(3.4(3.7)纳克/克肌酐)。将低于A组范围下限的尿生长激素视为异常,尿生长激素的特异性和敏感性分别为100%和35%。B组和C组的敏感性分别为5%和78%。仅考虑C组中有病理磁共振结果的受试者时,敏感性增至100%。在A组中平均生长激素浓度≤3.3微克/升的4名受试者中,特异性降至80%。结论是,尿生长激素检测的敏感性太低,不能被视为改进定义生长激素缺乏症的传统诊断方法,除非用于识别最严重缺乏症的受试者。