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理解抑郁癥和焦慮癥的生物應(yīng)激系統(tǒng)失調(diào)的綜合方法

 蘭墨閣 2021-03-26

背景

情感障礙涉及主要生物應(yīng)激系統(tǒng)(下丘腦-垂體-腎上腺(HPA)軸,免疫系統(tǒng),自主神經(jīng)系統(tǒng)(ANS))的調(diào)節(jié)異常。很少在不同的壓力系統(tǒng)中同時檢查這種失調(diào)。

方法

在荷蘭抑郁癥和焦慮癥研究(n = 2789)中,我們調(diào)查了當(dāng)前或緩解的抑郁癥和/或焦慮癥(基于CIDI半結(jié)構(gòu)化訪談),包括特定的癥狀特征,是否與單獨的標志物和累積指標相關(guān)聯(lián)HPA軸(皮質(zhì)醇喚醒反應(yīng),夜間皮質(zhì)醇,地塞米松抑制試驗皮質(zhì)醇),免疫系統(tǒng)(C反應(yīng)蛋白,白介素-6,腫瘤壞死因子-α)和ANS(心率,呼吸道竇性心律不齊,彈射期)。

結(jié)果

抑郁和焦慮癥與三種生物應(yīng)激系統(tǒng)的變化顯著相關(guān),包括HPA軸亢進,炎癥活動增加和ANS音調(diào)升高,尤其是與對照組相比,這些應(yīng)激系統(tǒng)的綜合指數(shù)和累積指數(shù)(pFDR <.05)。與當(dāng)前的HPA軸疾病和累積指數(shù)(β= .124,pFDR = .001),免疫系統(tǒng)(β= .057,pFDR = .032)以及整個應(yīng)激系統(tǒng)的總累積指數(shù)之間存在最強的關(guān)聯(lián)( β= .102,pFDR = .004)。與能量相關(guān)的非典型抑郁癥嚴重程度與免疫系統(tǒng)標志物(pFDR <0.001),憂郁抑郁癥嚴重程度與HPA軸標志物(pFDR = .032)相關(guān),而與焦慮相關(guān)的嚴重程度與HPA軸心和免疫系統(tǒng)標志物相關(guān)(pFDR < 0.05)。較差的生活方式,更多的慢性疾病,

局限性

橫斷面分析限制了時間關(guān)聯(lián)的檢查。

結(jié)論

抑郁癥和焦慮癥患者在整個生物應(yīng)激系統(tǒng)中表現(xiàn)出持續(xù)的失調(diào),尤其是對于當(dāng)前的發(fā)作。要了解情感性疾病中的應(yīng)激系統(tǒng)功能,一種綜合的方法應(yīng)能夠捕獲生物應(yīng)激系統(tǒng)內(nèi)部和整個生物應(yīng)激系統(tǒng)的累積壓力指標。

Background

Affective disorders involve dysregulation of major biological stress systems (hypothalamic-pituitary-adrenal (HPA)-axis, immune system, autonomic nervous system (ANS)). Suchdysregulationshave rarely beensimultaneously examined across different stress systems.

Methods

In the Netherlands Study of Depression and Anxiety (n=2789), we investigated whether current or remitted depressive and/or anxiety disorders (based on the CIDI semi-structured interview), including specific symptom profiles, were associated with separate markers and cumulative indexes of the HPA-axis (cortisol awakening response, evening cortisol, dexamethasone suppression test cortisol), immune system (C-reactive protein, interleukin-6, tumor necrosis factor-α), and ANS (heart rate, respiratory sinus arrhythmia, pre-ejection period).

Results

Depressive andanxiety disorderswere significantlyassociated with changes in three biological stress systemsincluding HPA-axis hyperactivity, increased inflammatory activity, and a higher ANS tone, particularly for integrative and cumulative indexes of these stress systems (pFDR <.05) vs. controls. The strongest associations were seen with current disorders andcumulative indexes of the HPA-axis (β=.124, pFDR=.001), the immune system (β =.057, pFDR=.032), and total cumulative index across stress systems (β=.102, pFDR=.004). Atypical, energy-related depression severity was linked to immune system markers (pFDR<0.001), melancholic depression severity to HPA-axis markers (pFDR=.032), and anxiety arousal severity to both HPA-axis and immune system markers (pFDR<0.05). Findings were partially explained by poorer lifestyle, more chronic diseases,or (especially for ANS-function) antidepressant use.

Limitations

Cross-sectional analyses limit examination of temporal associations.

Conclusion

Patients withdepressive and anxiety disorders showed consistent dysregulation across biological stress systems, particularly for current episodes.To understand stress system functionality in affective disorders, an integrated approach capturing cumulative stress indices within and across biological stress systems is important.

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