难治性抑郁症患者免疫内分泌及REM睡眠结构研究

目的探讨难治性抑郁症患者的下丘脑-垂体-肾上腺轴、细胞免疫调节功能及REM睡眠结构。方法选择符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)单相抑郁发作诊断标准的难治性抑郁症患者和非难治性抑郁症患者各30例。采用汉密尔顿焦虑(HAMA)、汉密尔顿抑郁量表(HAMD-17)分别评定焦虑、抑郁症状。测定白细胞介素6(IL-6)和肿瘤坏死因子-α(TNF-α),皮质醇,采用多导睡眠记录仪监测整夜睡眠。结果1难治性抑郁症共病焦虑、重度抑郁组血清皮质醇、IL-6、TNF-α高于非难治性抑郁症组,差异有统计学意义(P0.05或0.01)。2IL-6浓度与HAMD总评分、认识障碍因子分、HAMA总评分、躯体性焦虑因子分呈正相关(r=0.395~0.635,P0.05或0.01),TNF-α浓度与HAMA总评分、躯体性焦虑因子分呈正相关(r=0.522、0.563,P0.01)。3难治性抑郁症组REM睡眠密度增加,持续时间、周期缩短(P0.05或0.01),与抑郁严重程度呈正相关(r=0.492,P0.01)。结论下丘脑-垂体-肾上腺轴功能异常和细胞免疫调节紊乱可能参与难治性抑郁症的发病机制。REM睡眠密度可能提示难治性抑郁症的严重程度和预后。

Study of the neuroendocrine immune system and REM sleep in treatment resistant depression patients

Objective The study investigated mechanisms underlying dysregulations of hypothalamic - pituitary - adrenal axis and cellular immune, and the structure of REM sleep in treatment resistant depression patients. Methods 30 treatment resistant de- pression patients, 30 treatment non - resistant depression patients and 30 normal controls were involved in the study. All the subjects completed general condition questionnaire, while HAMD and HAMA were evaluated by the researcher. Cortisol, IL - 6 and TNF - α were detected. The whole night sleep was monitored by Polysomnography. The t test, X2 test, Pearson correlation, analysis of variance and stepwise regression analysis were used to analysis with SPSS 10.0. Results①The serum levels of cortisol, IL - 6 and TNF - α in eomorbid anxiety and severity TRD groups were significantly higher than that in TNRD patients（ P 〈0.05 or 0.01 ）. ②The serum level of IL -6 was positively related to the scores of HAMD and HAMA, cognitive disturbance and somatic anxiety（ r = 0. 395 ～ 0. 635 ,P 〈 0.05 or 0.01 ）. The serum level of TNF - α was positively correlated with the scores of HAMA and somatic anxiety（ r = 0. 522,0. 563, P 〈0. 01 ）. ③TNRD patients showed significantly decline in duration and period of REM（P 〈0.05 or 0. 01 ）, increased REM density which correlated well with the severity of depression （ r = 0. 492, P 〈 0.01 ）. Conclusion The dysfunction of HPA axis and cellular immune activity may be involved in the pathophysiology of TRD. REM density may hint the severity and prognosis in TRD.