Loosen P T
Psychoneuroendocrinology. 1985;10(3):237-60. doi: 10.1016/0306-4530(85)90002-2.
The finding of a diminished TSH response to exogenously administered TRH in a significant proportion of depressed patients has now been established as one of the most reproducible findings in biological psychiatry. More than 50 reports, in which more than 1000 patients have been studied, reveal that the TSH response is blunted in approximately 25% of patients with major depression. TSH blunting is clearly not specific for depression, because it also has been observed in mania, alcoholism, and borderline personality disorder. It is doubtful that TSH blunting represents a non-specific response to mental stress: it was found only rarely in schizophrenic patients, and the TSH response to in vivo flooding therapy in phobic patients was normal. In both depression and alcoholism, TSH blunting has been reported to be sometimes a state marker and sometimes a trait marker, i.e. the fault was found to persist into remission in more than half the patients. In both conditions, TSH blunting was unrelated to the patients' age, body weight, height, body surface, thyroid status, and serum cortisol concentrations. It also is unlikely that TSH blunting was due to increased dopaminergic inhibition of thyrotroph cells: serum prolactin concentrations in TSH blunters were found to be normal, and pretreatment with haloperidol had no effect on either basal TSH levels or TSH blunting. In depression, TSH blunting was not associated with previous drug intake, dexamethasone suppression test abnormalities, or variables of biogenic amine metabolism, nor did it usefully segregate between primary and secondary depression or between unipolar and bipolar subgroups. Preliminary evidence suggests that TSH blunting in depression may be related to duration of illness, history of violent suicide attempts, and a reduced 24 h TSH secretion. In alcoholism, TSH blunting was unrelated to family or personal history of depression and duration of abstinence. With reference to clinical utility, TSH blunting may aid in assessing the response to antidepressant treatment, predicting outcome to such treatment, assessing the risk for violent suicide attempts, and describing relationships between different psychiatric populations (e.g. depression and alcoholism).
在相当一部分抑郁症患者中，发现其对外源性给予促甲状腺激素释放激素（TRH）的促甲状腺激素（TSH）反应减弱，这一发现现已成为生物精神病学中最具重复性的发现之一。超过50份报告对1000多名患者进行了研究，结果显示，在约25%的重度抑郁症患者中，TSH反应迟钝。TSH反应迟钝显然并非抑郁症所特有，因为在躁狂症、酒精中毒和边缘性人格障碍中也观察到了这一现象。TSH反应迟钝是否代表对精神压力的非特异性反应，这一点值得怀疑：在精神分裂症患者中很少发现这一现象，而且恐惧症患者对体内冲击疗法的TSH反应是正常的。在抑郁症和酒精中毒中，TSH反应迟钝有时被报道为一种状态标志物，有时被报道为一种特质标志物，也就是说，在一半以上的患者中，这种缺陷被发现会持续到病情缓解期。在这两种情况下，TSH反应迟钝都与患者的年龄、体重、身高、体表面积、甲状腺状态和血清皮质醇浓度无关。TSH反应迟钝也不太可能是由于对促甲状腺细胞的多巴胺能抑制增加所致：TSH反应迟钝者的血清催乳素浓度正常，用氟哌啶醇预处理对基础TSH水平或TSH反应迟钝均无影响。在抑郁症中，TSH反应迟钝与既往用药情况、地塞米松抑制试验异常或生物胺代谢变量无关，也无助于区分原发性抑郁症和继发性抑郁症，或区分单相抑郁症和双相抑郁症亚组。初步证据表明，抑郁症中的TSH反应迟钝可能与病程、暴力自杀未遂史以及24小时TSH分泌减少有关。在酒精中毒中，TSH反应迟钝与抑郁症的家族史或个人史以及戒酒时间无关。关于临床应用，TSH反应迟钝可能有助于评估对抗抑郁治疗的反应、预测此类治疗的结果、评估暴力自杀未遂的风险以及描述不同精神疾病群体之间的关系（如抑郁症和酒精中毒）。
