Ilondo M M, Vanderschueren-Lodeweyckx M, De Meyts P, Eggermont E
Department of Pediatrics, University of Leuven, Brussels, Belgium.
J Clin Endocrinol Metab. 1990 May;70(5):1445-51. doi: 10.1210/jcem-70-5-1445.
Serum GH levels were measured by RIA and RRA in 133 subjects (19 healthy controls and 114 patients with various growth disturbances, aged 2.3-24.8 yr). Serum samples obtained from 147 stimulation tests representing a total of 1065 samples were analyzed by both methods, and the results compared. The data are expressed in absolute values and in RRA/RIA ratios. The area under the curve after a stimulation test (area GH) was calculated by planimetry. RIA was performed by the classical double antibody method using a polyclonal anti-serum. For the RRA, human cultured lymphocytes (IM-9 cells) were used, and 125I-labeled human GH was purified by high performance liquid chromatography. The same human GH standard was used in both assay systems. In control subjects a significant (P less than 0.0001) positive correlation was found at all ages between GH levels measured by RIA and RRA (r = 0.69 after insulin and r = 0.77 after glucagon). The RRA/RIA ratio (mean +/- SEM) for the peak GH level was 0.88 +/- 0.05, and the area under the GH curve was 0.85 +/- 0.05. The peak mean RRA/RIA ratios were significantly lower (P less than 0.05 and P = 0.03, respectively). No relationship was found with the absolute value of either peak or area GH. In patients with growth delay and Turner's syndrome, lower GH levels were found than in control subjects in both assay systems. The RRA/RIA ratios were also lower. In the other patients with some growth disorder, normal GH levels and ratios were found. In patients with renal failure, high levels of RIA-GH and RRA-GH were found, with a normal RRA/RIA ratio. In patients with documented pituitary GH deficiency, GH-releasing factor administration resulted in an increase in GH levels that was identical in both assays. The RRA/RIA ratio remained constant throughout the test. No correlation was found between the ratio and the absolute value of either RIA-GH or RRA-GH regardless of the stimulation test used. It is concluded that the presence of an abnormal GH molecule is extremely rare in patients with short stature. Thus, the presence of a bioinactive hormone is not a common cause of growth failure. During provocative testing some changes in the ratio may occur that do not appear after GH-releasing factor, further illustrating the different mechanisms involved in GH secretion.
采用放射免疫分析法（RIA）和放射受体分析法（RRA）对133名受试者（19名健康对照者和114名患有各种生长障碍的患者，年龄在2.3 - 24.8岁）的血清生长激素（GH）水平进行了测定。对来自147次刺激试验的血清样本（共1065份样本）用两种方法进行分析，并比较结果。数据以绝对值和RRA/RIA比值表示。刺激试验后的曲线下面积（GH面积）通过平面测量法计算。RIA采用经典的双抗体法，使用多克隆抗血清。对于RRA，使用人培养淋巴细胞（IM - 9细胞），并用高效液相色谱法纯化125I标记的人生长激素。两种检测系统使用相同的人生长激素标准品。在对照受试者中，各年龄段通过RIA和RRA测定的GH水平之间均存在显著的正相关（P < 0.0001）（胰岛素刺激后r = 0.69，胰高血糖素刺激后r = 0.77）。GH峰值水平的RRA/RIA比值（均值±标准误）为0.88±0.05，GH曲线下面积为0.85±0.05。峰值的平均RRA/RIA比值显著更低（分别为P < 0.05和P = 0.03）。未发现与GH峰值或面积的绝对值存在相关性。在生长迟缓患者和特纳综合征患者中，两种检测系统中测得的GH水平均低于对照受试者。RRA/RIA比值也更低。在其他患有某些生长障碍的患者中，GH水平和比值正常。在肾衰竭患者中，RIA - GH和RRA - GH水平升高，但RRA/RIA比值正常。在有记录的垂体GH缺乏患者中，给予生长激素释放因子后GH水平升高，两种检测方法的结果相同。整个试验过程中RRA/RIA比值保持恒定。无论使用何种刺激试验，该比值与RIA - GH或RRA - GH的绝对值之间均未发现相关性。结论是身材矮小患者中异常GH分子的存在极为罕见。因此，生物无活性激素的存在并非生长失败的常见原因。在激发试验期间，该比值可能会发生一些变化，而生长激素释放因子刺激后则不会出现这种变化，这进一步说明了GH分泌所涉及的不同机制。
