Hartman M L, Veldhuis J D, Vance M L, Faria A C, Furlanetto R W, Thorner M O
Department of Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
J Clin Endocrinol Metab. 1990 May;70(5):1375-84. doi: 10.1210/jcem-70-5-1375.
Alterations in pulsatile GH release in 13 acromegalic patients (7 men and 6 women) were studied by measuring serum GH concentrations in blood sampled every 5 min over 24 h. Specific properties of pulsatile GH release were quantitated by Cluster analysis, and Fourier expansion time series analysis was used to resolve fixed periodicities underlying GH secretion. Compared with sex-matched controls, 24-h integrated GH concentrations (IGHC; min.mg/L) were elevated 15-fold in the acromegalic men (40 +/- 27 vs. 2.6 +/- 0.35; P = 0.02) and 10-fold in the acromegalic women (43 +/- 19 vs. 4.1 +/- 0.35; P = 0.01). The increase in integrated GH concentrations was accounted for by an increase in the nonpulsatile fraction [men, 31 +/- 20 vs. 0.65 +/- 0.10 (P = 0.001); women, 35 +/- 14 vs. 1.2 +/- 0.10 (P = 0.0008)]; the pulsatile component was not different from that in normal subjects. Acromegalics had an increased number of pulses per 24 h [men, 17 +/- 1.5 vs. 6.7 +/- 1.4 (P = 0.0001); women, 19 +/- 1.6 vs. 11 +/- 1.0 (P = 0.002)] and increased basal GH concentrations [men, interpulse valley mean, 22 +/- 14 vs. 1.4 +/- 0.30 micrograms/L (P = 0.0006); women, 27 +/- 12 vs. 1.3 +/- 0.20 micrograms/L (P = 0.0001)]. The proportion of the mean GH concentration attributable to 24-h rhythmicity was decreased in the acromegalic patients. Five patients studied during biochemical remission (4 after transsphenoidal surgery and 1 during bromocriptine therapy) had GH profiles that resembled those of normal subjects. Pulsatile GH secretion in acromegaly is characterized by augmented basal GH concentrations, increased GH pulse frequency, and an attenuation of the underlying 24-h rhythm. Such a pattern may be secondary to the intrinsic pathology of adenomatous somatotrophs and/or the effects of altered hypothalamic regulation.
通过每5分钟采集一次血液样本，测量24小时内血清生长激素（GH）浓度，研究了13例肢端肥大症患者（7例男性和6例女性）脉冲式GH分泌的变化。通过聚类分析对脉冲式GH分泌的特定特性进行定量，并使用傅里叶展开时间序列分析来解析GH分泌背后的固定周期。与性别匹配的对照组相比，肢端肥大症男性的24小时综合GH浓度（IGHC；min.mg/L）升高了15倍（40±27 vs. 2.6±0.35；P = 0.02），肢端肥大症女性升高了10倍（43±19 vs. 4.1±0.35；P = 0.01）。综合GH浓度的增加是由于非脉冲部分增加所致[男性，31±20 vs. 0.65±0.10（P = 0.001）；女性，35±14 vs. 1.2±0.10（P = 0.0008）]；脉冲成分与正常受试者无差异。肢端肥大症患者每24小时的脉冲数增加[男性，17±1.5 vs. 6.7±1.4（P = 0.0001）；女性，19±1.6 vs. 11±1.0（P = 0.002）]，基础GH浓度升高[男性，脉冲间期谷值均值，22±14 vs. 1.4±0.30微克/升（P = 0.0006）；女性，27±12 vs. 1.3±0.20微克/升（P = 0.0001）]。肢端肥大症患者中可归因于24小时节律性的平均GH浓度比例降低。在生化缓解期研究的5例患者（4例经蝶窦手术后和1例接受溴隐亭治疗期间）的GH谱与正常受试者相似。肢端肥大症中的脉冲式GH分泌的特征是基础GH浓度升高、GH脉冲频率增加以及潜在的24小时节律减弱。这种模式可能继发于腺瘤性生长激素细胞的内在病理和/或下丘脑调节改变的影响。
