Ramos-Dias J C, Yateman M, Camacho-Hübner C, Grossman A, Lengyel A M
Division of Endocrinology, Escola Paulista de Medicina, São Paulo, Brazil.
Clin Endocrinol (Oxf). 1995 Nov;43(5):583-9. doi: 10.1111/j.1365-2265.1995.tb02923.x.
Several abnormalities in the GH response to pharmacological stimuli have been described in hyperthyroidism. Both normal and high serum IGF-I levels have been reported, as well as a decrease in IGF-I bioactivity. We have evaluated the GH response to GH-releasing hormone (GHRH) in hyperthyroid patients and the effects of hyperthyroidism on serum IGF-I levels. The possible relations between nutritional status, thyroid hormones and IGF-I levels were also investigated. We also studied the influence of long-term beta-adrenoceptor blockade on the GH response to GHRH in these patients.
In 18 hyperthyroid patients and in 12 control subjects, GHRH (100 micrograms) was administered as an i.v. bolus injection. Eight hyperthyroid patients and 8 control subjects received 50 micrograms GHRH i.v. Seven hyperthyroid patients were reevaluated after beta-adrenoceptor blockade. IGF-I and albumin levels were measured initially in all hyperthyroid patients and control subjects. Body composition was determined in 11 hyperthyroid patients and in a group of 33 matched normal controls.
Hyperthyroid patients were compared to control subjects.
GH, TSH and free T4 were measured by immunofluorometric assay. IGF-I, total T3 and total T4 were measured by radioimmunoassay. Body composition was determined using a dual-energy X-ray absorptiometer.
The GH response to 100 micrograms GHRH in hyperthyroid patients was blunted compared to control subjects. The mean peak GH levels and the area under the curve were significantly lower in hyperthyroid patients compared to control subjects (11 +/- 1 vs 27 +/- 5 micrograms/l and 820 +/- 113 vs 1879 +/- 355 micrograms/l 120 min, respectively; P < 0.01). IGF-I levels were significantly reduced in hyperthyroid patients compared to controls (131 +/- 10 vs 201 +/- 16 micrograms/l, respectively; P < 0.01). Ideal body weight, serum albumin levels and the lean body mass were also reduced in hyperthyroid patients. After beta-adrenoceptor blockade there were no changes in the blunted GH response to GHRH in hyperthyroid patients.
Our data suggest that the blunted GH response to GHRH in hyperthyroidism is apparently not related to circulating IGF-I levels. It is possible that nutritional factors could play a role in the reduced circulating IGF-I levels found in these patients.
甲亢患者中已描述了生长激素（GH）对药物刺激反应的几种异常情况。既有血清胰岛素样生长因子-Ⅰ（IGF-Ⅰ）水平正常和升高的报道，也有IGF-Ⅰ生物活性降低的报道。我们评估了甲亢患者对生长激素释放激素（GHRH）的GH反应以及甲亢对血清IGF-Ⅰ水平的影响。还研究了营养状况、甲状腺激素与IGF-Ⅰ水平之间的可能关系。我们也研究了长期β-肾上腺素能受体阻滞剂对这些患者GH对GHRH反应的影响。
对18例甲亢患者和12例对照者静脉推注100微克GHRH。8例甲亢患者和8例对照者静脉注射50微克GHRH。7例甲亢患者在β-肾上腺素能受体阻滞剂治疗后重新评估。所有甲亢患者和对照者最初均测定了IGF-Ⅰ和白蛋白水平。对11例甲亢患者和一组33例匹配的正常对照者测定了身体成分。
将甲亢患者与对照者进行比较。
采用免疫荧光分析法测定GH、促甲状腺激素（TSH）和游离甲状腺素（free T4）。采用放射免疫分析法测定IGF-Ⅰ、总三碘甲状腺原氨酸（total T3）和总甲状腺素（total T4）。使用双能X线吸收仪测定身体成分。
与对照者相比，甲亢患者对100微克GHRH的GH反应减弱。甲亢患者的平均GH峰值水平和曲线下面积显著低于对照者（分别为11±1与27±5微克/升以及820±113与1879±355微克/升·120分钟；P<0.01）。与对照者相比，甲亢患者的IGF-Ⅰ水平显著降低（分别为131±10与201±16微克/升；P<0.01）。甲亢患者的理想体重、血清白蛋白水平和去脂体重也降低。β-肾上腺素能受体阻滞剂治疗后，甲亢患者对GHRH的GH反应减弱无变化。
我们的数据表明，甲亢患者对GHRH的GH反应减弱显然与循环IGF-Ⅰ水平无关。营养因素可能在这些患者循环IGF-Ⅰ水平降低中起作用。
