Birkhäuser M H, Staub J J, Gräni R, Girard J, Good E
Schweiz Med Wochenschr. 1980 Dec 6;110(49):1877-9.
The TSH response to exogenous TRH may be diminished or absent not only on overt hyperthyroidism but also in other situations, e.g. obesity, old age, multinodular goiter and depression. To elucidate the possible role of dopaminergic control of the TSH response to TRH in such patients, the oral TRH test (40 mg) was performed with and without simultaneous administration of metoclopramide (10 mg i.v.) in 20 patients known to have diminished or absent response to oral TRH (delta TSH < 1.0 mU/l). All patients had euthyroid basal levels of FT4-index and T3, and may thus be assumed to have "preclinical hyperthyroidism" (TSH suppression syndrome). In 11 patients the history suggested they were free of symptoms of mental depression, while 9 patients were considered by two independent examiners to have various degrees of depression. The TSH response to TRH in depressive patients was significantly increased when the dopamine-receptor-blocker metoclopramide (MCL) wad added. The delta TSH rose from 0.6 +/- 0.3 mU/l (SEM) without MCL to 8.8 +/- 1.8 mU/l with MCL (p < 0.002). In contrast, MCL failed to enhance the TSH response in non-depressive patients: the delta TSH was 0.7 +/- 0.3 mU/l without MCL, and with MCL 2.1 +/- 0.9 mU/l (n.s.). Thus the dopaminergic system appears to play a major role in modulating the sensitivity of the pituitary to TRH stimulation. In clinically doubtful situations, the combined metoclopramide-TRH test may be used to distinguish patients with a diminished or absent TSH response as a consequence of depression (central dopaminergic suppression) from patients with "preclinical hyperthyroidism" where the TSH response is suppressed by feedback control of TSH by thyroid hormones (thyroid autonomy).
促甲状腺激素(TSH)对外源性促甲状腺激素释放激素(TRH)的反应不仅在显性甲状腺功能亢进时会减弱或消失,在其他情况下,如肥胖、老年、多结节性甲状腺肿和抑郁症时也会如此。为了阐明多巴胺能对这类患者TSH对TRH反应的控制可能发挥的作用,对20名已知口服TRH反应减弱或消失(TSH变化量<1.0 mU/L)的患者进行了口服TRH试验(40 mg),试验时同时或不同时静脉注射甲氧氯普胺(10 mg)。所有患者的游离甲状腺素指数(FT4-index)和T3的基础水平均正常,因此可认为患有“亚临床甲状腺功能亢进”(TSH抑制综合征)。11名患者的病史表明他们没有精神抑郁症状,而9名患者经两名独立检查者评估有不同程度的抑郁。当添加多巴胺受体阻滞剂甲氧氯普胺(MCL)时,抑郁患者对TRH的TSH反应显著增强。TSH变化量从无MCL时的0.6±0.3 mU/L(标准误)升至有MCL时的8.8±1.8 mU/L(p<0.002)。相反地,MCL未能增强非抑郁患者的TSH反应:无MCL时TSH变化量为0.7±0.3 mU/L,有MCL时为2.1±0.9 mU/L(无统计学意义)。因此,多巴胺能系统似乎在调节垂体对TRH刺激的敏感性方面起主要作用。在临床诊断存疑的情况下,联合甲氧氯普胺-TRH试验可用于区分因抑郁症(中枢多巴胺能抑制)导致TSH反应减弱或消失的患者与“亚临床甲状腺功能亢进”患者,后者的TSH反应是通过甲状腺激素对TSH的反馈控制(甲状腺自主性)而受到抑制。