Rao M L, Ruhrmann S, Retey B, Liappis N, Fuger J, Kraemer M, Kasper S, Möller H J
Department of Psychiatry and Policlinic of Rheinische Friedrich-Wilhelms-Universität, Bonn, Germany.
Pharmacopsychiatry. 1996 Sep;29(5):180-6. doi: 10.1055/s-2007-979568.
Decreased turnover of thyroid indices and blunting of TSH release after TRH administration has been associated with depressive disorder. A further decrease in plasma thyroid hormone; during antidepressant treatment has been reported. However, the putative association between the plasma thyroid indices' concentration and response has not been addressed. In the present study 21 depressed inpatients underwent a four-week double blind antidepressant with amitriptyline and mianserin; their plasma thyroid hormone indices (total thyroxine [TT4], free thyroxine [FT4], total triiodothyronine [TT3], free triiodothyronine [FT3], thyrotropin [TSH], and thyroglobulin [TBG]) were quantified to elucidate their involvement in depression and during antidepressant drug treatment. Depressed patients' plasma TSH, when corrected for age, was significantly lower than that of healthy subjects. During antidepressant treatment the entire patient cohort showed a significant decrease in plasma TT4 and FT4 concentrations. Responders showed a significant drop in TT4 FT4, FT3, and T4/TBG, but nonresponders only a decrease in FT4. During mianserin treatment, a decrease was observed in TT4, FT4, FT3, and T4/TBG. FT4 and FT3 baseline levels correlated positively with the improvement in the Hamilton Depression Rating Score (HDRS). These findings show that depressed inpatients' serum TSH levels are within the reference range, but significantly lower than those of healthy subjects, and those patients who turn out to be nonresponders have potentially lower availability of thyroid hormones than responders. Therefore, we hypothesize that in order to assure clinical improvement in depression, an adequate capacity of the thyroid hormone pool is necessary to compensate for the additional antidepressant-provoked decrease in serum thyroid hormone availability.
甲状腺指标周转率降低以及促甲状腺激素释放激素(TRH)给药后促甲状腺激素(TSH)释放迟钝与抑郁症有关。据报道,在抗抑郁治疗期间血浆甲状腺激素会进一步降低。然而,血浆甲状腺指标浓度与反应之间的假定关联尚未得到探讨。在本研究中,21名抑郁症住院患者接受了为期四周的阿米替林和米安色林双盲抗抑郁治疗;对他们的血浆甲状腺激素指标(总甲状腺素[TT4]、游离甲状腺素[FT4]、总三碘甲状腺原氨酸[TT3]、游离三碘甲状腺原氨酸[FT3]、促甲状腺激素[TSH]和甲状腺球蛋白[TBG])进行定量,以阐明它们在抑郁症及抗抑郁药物治疗期间的作用。抑郁症患者经年龄校正后的血浆TSH显著低于健康受试者。在抗抑郁治疗期间,整个患者队列的血浆TT4和FT4浓度显著降低。有反应者的TT4、FT4、FT3和T4/TBG显著下降,但无反应者仅FT4下降。在米安色林治疗期间,观察到TT4、FT4、FT3和T4/TBG下降。FT4和FT3基线水平与汉密尔顿抑郁评定量表(HDRS)的改善呈正相关。这些发现表明,抑郁症住院患者的血清TSH水平在参考范围内,但显著低于健康受试者,而且那些无反应的患者甲状腺激素的可利用性可能低于有反应者。因此,我们假设,为了确保抑郁症的临床改善,甲状腺激素储备有足够的能力来补偿抗抑郁药物引起的血清甲状腺激素可利用性的额外降低是必要的。