Foltyn Wanda, Nowakowska-Zajdel Ewa, Danikiewicz Aleksander, Brodziak Andrzej
Katedry i Oddziału Klinicznego Chorób Wewnetrznych Slaskiej AM w Bytomiu.
Psychiatr Pol. 2002;36(2):281-92.
Depressed patients, although viewed as chemically euthyroid, have alterations in the function of hypothalamic-pituitary-thyroid axis including slight elevation of the serum thyroxine (T4), loss of the nocturnal TSH rise, blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) stimulation and predisposition to autoimmune thyroiditis. Both hypothyroid and depressed patients share a number of clinical features in common. This is the reason that some research workers use the "brain hypothyroidism" hypothesis to explain the pathogenesis of depression. They suggest that depression is a state of local hypothyroidism in brain with normal peripheral thyroid hormone concentrations as a result of brain type II deiodinase inhibition and impaired transport T4 across the blood brain barrier. This theory seems to be compatible with the serotonin deficiency hypothesis of depression. Some studies confirm the existence of classical feedback between serotoninergic and hypothalamus-pituitary-thyroid systems. TRH remains under a constant inhibition by serotonin and reduced intracerebral serotonin concentration seen in depression will lead to increased TRH concentration in brain tissue. This mechanism is probably responsible for blunted TSH response to TRH stimulation.
抑郁症患者尽管被视为甲状腺功能正常，但下丘脑 - 垂体 - 甲状腺轴功能存在改变，包括血清甲状腺素（T4）略有升高、夜间促甲状腺激素（TSH）升高消失、促甲状腺素（TSH）对促甲状腺激素释放激素（TRH）刺激的反应迟钝以及易患自身免疫性甲状腺炎。甲状腺功能减退患者和抑郁症患者有许多共同的临床特征。这就是一些研究人员用“脑甲状腺功能减退”假说来解释抑郁症发病机制的原因。他们认为，抑郁症是由于脑II型脱碘酶受抑制以及T4穿过血脑屏障的转运受损，导致外周甲状腺激素浓度正常的情况下脑内局部甲状腺功能减退的一种状态。该理论似乎与抑郁症的血清素缺乏假说相符。一些研究证实了血清素能系统与下丘脑 - 垂体 - 甲状腺系统之间存在经典反馈。血清素持续抑制TRH，抑郁症患者脑内血清素浓度降低会导致脑组织中TRH浓度升高。这种机制可能是TSH对TRH刺激反应迟钝的原因。
