Division of Endocrinology, Universidade Federal de São Paulo, UNIFESP-EPM, Rua Pedro de Toledo 910, 04039-002, São Paulo, Brazil.
Pituitary. 2010 Dec;13(4):315-23. doi: 10.1007/s11102-010-0238-3.
In thyrotoxicosis GH responses to stimuli are diminished and the hypothalamic-pituitary-adrenal axis is hyperactive. There are no data on ghrelin or GHRP-6-induced GH, ACTH and cortisol release in treated hyperthyroidism. We, therefore, evaluated these responses in 10 thyrotoxic patients before treatment and in 7 of them after treatment. GHRH-induced GH release was also studied. Peak GH (μg/L; mean ± SE) values after ghrelin (22.6 ± 3.9), GHRP-6 (13.8 ± 2.3) and GHRH (4.9 ± 0.9) were lower in hyperthyroidism before treatment compared to controls (ghrelin: 67.6 ± 19.3; GHRP-6: 25.4 ± 2.7; GHRH: 12.2 ± 2.8) and did not change after 6 months of euthyroidism (ghrelin: 32.7 ± 4.7; GHRP-6: 15.6 ± 3.6; GHRH: 7.4 ± 2.3), although GH responses to all peptides increased in ~50% of the patients. In thyrotoxicosis before treatment ACTH response to ghrelin was two fold higher (107.4 ± 26.3) than those of controls (54.9 ± 10.3), although not significantly. ACTH response to GHRP-6 was similar in both groups (hyperthyroid: 44.7 ± 9.0; controls: 31.3 ± 7.9). There was a trend to a decreased ACTH response to ghrelin after 3 months of euthyroidism (35.6 ± 5.3; P = 0.052), but after 6 months this decrease was non-significant (50.7 ± 14.0). After 3 months ACTH response to GHRP-6 decreased significantly (20.4 ± 4.2), with no further changes. In hyperthyroidism before treatment, peak cortisol (μg/dL) responses to ghrelin (18.2 ± 1.2) and GHRP-6 (15.9 ± 1.4) were comparable to controls (ghrelin: 16.4 ± 1.6; GHRP-6: 13.5 ± 0.9) and no changes were seen after treatment. Our results suggest that the pathways of GH release after ghrelin/GHRP-6 and GHRH are similarly affected by thyroid hormone excess and hypothalamic mechanisms of ACTH release modulated by ghrelin/GHSs may be activated in this situation.
在甲状腺功能亢进症中，GH 对刺激的反应减弱，下丘脑-垂体-肾上腺轴活性亢进。在治疗后的甲状腺功能亢进症中，尚无关于 ghrelin 或 GHRP-6 诱导的 GH、ACTH 和皮质醇释放的数据。因此，我们在 10 例甲状腺功能亢进症患者治疗前和其中 7 例治疗后评估了这些反应。还研究了 GHRH 诱导的 GH 释放。甲状腺功能亢进症患者治疗前 ghrelin（22.6 ± 3.9）、GHRP-6（13.8 ± 2.3）和 GHRH（4.9 ± 0.9）诱导的 GH 峰值（μg/L；平均值 ± SE）低于对照组（ghrelin：67.6 ± 19.3；GHRP-6：25.4 ± 2.7；GHRH：12.2 ± 2.8），并且在 6 个月的甲状腺功能正常后没有变化（ghrelin：32.7 ± 4.7；GHRP-6：15.6 ± 3.6；GHRH：7.4 ± 2.3），尽管所有肽的 GH 反应在约 50%的患者中增加。在甲状腺功能亢进症患者治疗前，ghrelin 诱导的 ACTH 反应是对照组的两倍（107.4 ± 26.3），尽管没有显著差异。两组的 GHRP-6 诱导的 ACTH 反应相似（甲状腺功能亢进症：44.7 ± 9.0；对照组：31.3 ± 7.9）。甲状腺功能正常后 3 个月，ghrelin 诱导的 ACTH 反应呈下降趋势（35.6 ± 5.3；P = 0.052），但 6 个月后这种下降无统计学意义（50.7 ± 14.0）。GHRP-6 诱导的 ACTH 反应在甲状腺功能亢进症患者治疗后 3 个月显著下降（20.4 ± 4.2），此后无进一步变化。甲状腺功能亢进症患者治疗前，ghrelin（18.2 ± 1.2）和 GHRP-6（15.9 ± 1.4）诱导的皮质醇峰值（μg/dL）与对照组相似（ghrelin：16.4 ± 1.6；GHRP-6：13.5 ± 0.9），治疗后无变化。我们的结果表明，ghrelin/GHRP-6 和 GHRH 后 GH 释放的途径受甲状腺激素过多的相似影响，ghrelin/GHSs 调节的 ACTH 释放的下丘脑机制可能在此情况下被激活。
