Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA.
J Clin Endocrinol Metab. 2013 Jun;98(6):2187-97. doi: 10.1210/jc.2012-4012. Epub 2013 Mar 28.
GH secretion is controlled by hypothalamic as well as intrapituitary and peripheral signals, all of which converge upon the somatotroph, resulting in integrated GH synthesis and secretion. Enabling an accurate diagnosis of idiopathic adult GH deficiency (IAGHD) is challenged by the pulsatility of GH secretion, provocative test result variability, and suboptimal GH assay standardization. The spectrum between attenuated GH secretion associated with the normal aging process and with obesity and truly well-defined IAGHD is not distinct and may mislead the diagnosis. Adult-onset GHD is mainly caused by an acquired pituitary deficiency, commonly including prior head/neck irradiation, or an expanding pituitary mass causing functional somatotroph compression. To what extent rare cryptic causes account for those patients seemingly classified as IAGHD is unclear. About 15% of patients with adult GHD and receiving GH replacement in open-label surveillance studies are reported as being due to an idiopathic cause. These patients may also reflect a pool of subjects with an as yet to be determined occult defect, or those with unclear or incomplete medical histories (including forgotten past sports head injury or motor vehicle accident). Therefore, submaximal diagnostic evaluation likely leads to an inadvertent diagnosis of IAGHD. In these latter cases, adherence to rigorous biochemical diagnostic criteria and etiology exclusion may result in reclassification of a subset of these patients to a distinct known acquired etiology, or as GH-replete. Accordingly, rigorously verified IAGHD likely comprises less than 10% of adult GHD patients, an already rare disorder. Regardless of etiology, patients with adult GHD, including those with IAGHD, exhibit a well-defined clinical phenotype including increased fat mass, loss of lean muscle mass, decreased bone mass, and enhanced cardiac morbidity. Definition of unique efficacy and dosing parameters for GH replacement and resultant therapeutic efficacy markers in true IAGHD requires prospective study.
生长激素(GH)的分泌受下丘脑以及垂体内部和外周信号的控制,所有这些信号都集中在生长激素细胞上,从而导致 GH 的合成和分泌得到整合。由于 GH 分泌的脉冲性、激发试验结果的可变性以及 GH 检测方法的标准化不完善,使得特发性成人 GH 缺乏症(IAGHD)的准确诊断受到挑战。与正常衰老过程以及肥胖相关的 GH 分泌减弱与真正定义明确的 IAGHD 之间的范围并不明确,可能会导致诊断错误。成人 GH 缺乏症主要由获得性垂体功能减退引起,常见原因包括头颈部放疗史或导致功能性生长激素细胞受压的垂体增大。由于罕见的隐匿性病因导致这些患者被归类为 IAGHD 的程度尚不清楚。在接受 GH 替代治疗的开放性监测研究中,约 15%的成人 GH 缺乏症患者被报告为特发性病因。这些患者可能也反映了一类尚未确定隐匿性缺陷的患者,或者是那些病史不明确或不完整的患者(包括遗忘的过去运动性头部损伤或机动车事故)。因此,亚最大诊断评估可能会导致无意中诊断为 IAGHD。在这些后者的情况下,严格遵循生化诊断标准和病因排除可能会导致其中一部分患者重新分类为明确的获得性病因,或者 GH 充足。因此,经过严格验证的 IAGHD 可能不到成人 GH 缺乏症患者的 10%,这已经是一种罕见疾病。无论病因如何,成人 GH 缺乏症患者,包括 IAGHD 患者,都表现出明确的临床表型,包括脂肪量增加、瘦肌肉量减少、骨量减少和心脏发病率增加。需要前瞻性研究来定义真正的 IAGHD 中 GH 替代的独特疗效和剂量参数以及相应的治疗效果标志物。