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改变的甲状腺功能和神经代谢特征为了解双相II型抑郁症和强迫症综合征的共患性提供了线索
Jiali He1, Dong Huang2, Qilin Zhong2
1Department of Psychiatry, First Affiliated Hospital, Jinan University, Guangzhou, 510630, China; Department of Psychology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Journal of psychiatric research
|March 12, 2025
概括
双极性障碍 (BD) 与强迫性障碍 (OCD) 显示出明显的甲状腺功能障碍和大脑代谢变化. 这些神经生物学标志物,包括甲状腺刺激激素 (TSH) 和前额前白质 (PWM) 神经代谢物,可能有助于识别这种并发症.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 生物化学 生物化学
背景情况:
- 双极性障碍 (BD) 经常与强迫症 (OCD) 一起发生,对治疗结果产生负面影响.
- 这种BD-OCD并发症的潜在神经生物学机制尚不清楚.
研究的目的:
- 为了研究双相II型抑郁症患者与强迫症并发症的神经内分泌和神经代谢差异.
- 确定潜在的生物标志物,以区分BD-II-抑郁症-强迫症共患病.
主要方法:
- 招募了69名未经治疗的双相II型抑郁症患者 (35名患有强迫症,34名没有) 和38名健康对照.
- 用磁共振光谱学测量前额前白质 (PWM) 中的血清甲状腺激素水平和神经代谢比率 (NAA/Cr,Cho/Cr).
- 采用多变量逻辑回归和受限立方线分析.
主要成果:
- 在BD-II-抑郁症-强迫症患者中,甲状腺刺激激素 (TSH) 血清水平较低.
- 在伴并发症组中观察到左侧PWM中减少的N-乙酸/肌 (NAA/Cr),右侧PWM中增加的含胆化合物/肌 (Cho/Cr).
- TSH和右PWM Cho/Cr显示非线性关联与强迫症症状严重程度.
结论:
- 抑郁症-强迫症并发症与特定的甲状腺功能障碍和神经代谢变化有关.
- 血清TSH水平和双边PWM神经代谢障碍可能是这种并发症的基础.
- 已确定的神经内分泌和神经代谢标志物显示出诊断BD-II-抑郁症-强迫症的潜力.
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