Foley T P, Jacobs L S, Hoffman W, Daughaday W H, Blizzard R M
J Clin Invest. 1972 Aug;51(8):2143-50. doi: 10.1172/JCI107021.
Synthetic thyrotropin-releasing hormone (TRH) was administered to normal children and hypopituitary patients in a dose of 7 mug/kg i.v. over 30-60 sec. Serum thyrotropin (TSH) and prolactin (HPr) concentrations were measured by radioimmunoassay before and at 15-min intervals for 2 hr after TRH. In 20 normal children HPr rose from a mean baseline value of 7.0+/-1.2 (SEM) ng/ml to a mean peak value of 39.5+/-5 ng/ml. In 11 patients with growth hormone (GH) deficiency without TSH deficiency. HPr values rose from a mean baseline of 3.6+/-0.8 ng/ml to a mean peak value of 13.9+/-2.8, a significantly less peak response as compared with normal children (P < 0.005). The TSH responses to TRH, however, were statistically indistinguishable from those of normal children. In 10 patients with GH and TSH deficiency both the mean baseline HPr levels (25.0+/-5 ng/ml) and the mean peak HPr levels after TRH (68.5+/-10 ng/ml) were significantly higher (P < 0.005 and < 0.025) than those of normal children. Similar comparisons were also true for the peak TSH responses (P < 0.05). Two panhypopituitary patients released no TSH and only small amounts of HPr after TRH. After thyroid replacement therapy in eight of the patients with GH and TSH deficiency, the mean HPr baseline levels (7.6+/-1.0 ng/ml) and peak levels (23.3+/-4.6 ng/ml) after the same dose of TRH were significantly less than their pretreatment levels (P < 0.001 and < 0.01) and were within the range for normal children. Synthetic TRH stimulates the simultaneous release of TSH and HPr in normal children and most hypopituitary patients. When the concentrations of thyroxine (T4) and triiodothyronine (T3) are low, the levels of HPr before and after TRH are elevated. After thyroid replacement therapy, HPr levels decrease to normal. T4 and/or T3 may condition the production or effects of prolactin-inhibiting factor (PIF) activity. The TSH and HPr responses after TRH in hypopituitary patients will determine whether the primary defect resides in the pituitary or hypothalamus, but cannot delineate the hypothalamic defect as a deficiency of hypothalamic hormone production or neurohumoral transmission.
以7微克/千克的剂量静脉注射合成促甲状腺激素释放激素（TRH），在30 - 60秒内给予正常儿童和垂体功能减退患者。通过放射免疫分析法在注射TRH前及注射后2小时内每隔15分钟测量血清促甲状腺激素（TSH）和催乳素（HPr）浓度。在20名正常儿童中，HPr从平均基线值7.0±1.2（标准误）纳克/毫升升至平均峰值39.5±5纳克/毫升。在11名生长激素（GH）缺乏但无TSH缺乏的患者中，HPr值从平均基线值3.6±0.8纳克/毫升升至平均峰值13.9±2.8纳克/毫升，与正常儿童相比，峰值反应明显较小（P < 0.005）。然而，这些患者对TRH的TSH反应在统计学上与正常儿童无差异。在10名GH和TSH均缺乏的患者中，TRH前的平均基线HPr水平（25.0±5纳克/毫升）和TRH后的平均峰值HPr水平（68.5±10纳克/毫升）均显著高于正常儿童（P < 0.005和< 0.025）。TSH峰值反应的类似比较也得出相同结果（P < 0.05）。两名全垂体功能减退患者在注射TRH后未释放TSH，仅释放少量HPr。在8名GH和TSH缺乏患者接受甲状腺替代治疗后，相同剂量TRH后的平均HPr基线水平（7.6±1.0纳克/毫升）和峰值水平（23.3±4.6纳克/毫升）显著低于治疗前水平（P < 0.001和< 0.01），且在正常儿童范围内。合成TRH可刺激正常儿童和大多数垂体功能减退患者同时释放TSH和HPr。当甲状腺素（T4）和三碘甲状腺原氨酸（T3）浓度较低时，TRH前后的HPr水平会升高。甲状腺替代治疗后，HPr水平降至正常。T4和/或T3可能影响催乳素抑制因子（PIF）活性的产生或作用。垂体功能减退患者注射TRH后的TSH和HPr反应将确定原发性缺陷是位于垂体还是下丘脑，但无法区分下丘脑缺陷是下丘脑激素产生不足还是神经体液传递障碍。
