Intersections between pneumonia, lowered oxygen saturation percentage and immune activation mediate depression, anxiety, and chronic fatigue syndrome-like symptoms due to COVID-19: A nomothetic network approach.

Intersections between pneumonia, lowered oxygen saturation percentage and immune activation mediate depression, anxiety, and chronic fatigue syndrome-like symptoms due to COVID-19: A nomothetic network approach.
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肺炎,降低氧饱和百分比和免疫激活之间的相互作用介导了抑郁症,焦虑和慢性疲劳综合征,因为COVID-19引起的类似于-19的症状:一种名义上的网络方法。

DOI:
10.1016/j.jad.2021.10.039
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发表时间:
2022-01-15
影响因子:
6.6
通讯作者:
Maes M
Maes M
中科院分区:
医学2区
文献类型:
--
作者:
Al-Jassas HK;Al-Hakeim HK;Maes M

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新冠肺炎与神经精神症状有关,包括抑郁、焦虑和慢性疲劳综合征样症状和生理症状。目的:探讨新冠肺炎情感性症状和CFS样症状与胸部CT扫描异常(CCTA)、血氧饱和度(SpO2)、白细胞介素6(IL)-6、IL-10、C反应蛋白(CRP)、白蛋白、钙、镁、可溶性血管紧张素转换酶(ACE2)和可溶性晚期糖基化产物(SRAGE)的关系。上述生物标志物在60名新冠肺炎患者和30名健康对照组中进行了评估,他们接受了汉密尔顿抑郁(HDRS)和焦虑(HAM-A)以及纤维肌痛和慢性疲劳(FF)评定量表的测量。偏最小二乘扫描电子显微镜分析表明,可靠的潜在载体可以从a)关键的抑郁、焦虑和生理躯体症状(生理情感或PA核心),b)IL-6、IL-10、CRP、白蛋白、钙和sRAGEs(免疫反应核心);c)不同的CCTA(包括磨玻璃样阴影、实变和疯狂铺设)和降低的SpO2%(肺部病变)。偏最小二乘回归分析显示,PA-core变异的70.0%可以用免疫应答和肺病变潜伏向量的回归来解释。一个常见的“感染-免疫-炎症(III)核心”支持肺炎相关的CCTA,降低SpO2和免疫激活,这个III核心解释了PA核心70%的差异,以及忧郁症、失眠和神经认知症状的相关部分差异。SARS-CoV-2急性感染伴有肺部病变和血氧饱和度降低,可能导致免疫-炎症通路的激活,介导前者对SARS-CoV-2感染所致的PA核心和其他神经精神症状的影响。
COVID-19 is associated with neuropsychiatric symptoms including increased depressive, anxiety and chronic fatigue-syndrome (CFS)-like and physiosomatic symptoms. To delineate the associations between affective and CFS-like symptoms in COVID-19 and chest computed tomography scan anomalies (CCTAs), oxygen saturation (SpO2), interleukin (IL)-6, IL-10, C-Reactive Protein (CRP), albumin, calcium, magnesium, soluble angiotensin converting enzyme (ACE2) and soluble advanced glycation products (sRAGEs). The above biomarkers were assessed in 60 COVID-19 patients and 30 healthy controls who had measurements of the Hamilton Depression (HDRS) and Anxiety (HAM-A) and the Fibromyalgia and Chronic Fatigue (FF) Rating Scales. Partial Least Squares-SEM analysis showed that reliable latent vectors could be extracted from a) key depressive and anxiety and physiosomatic symptoms (the physio-affective or PA-core), b) IL-6, IL-10, CRP, albumin, calcium, and sRAGEs (the immune response core); and c) different CCTAs (including ground glass opacities, consolidation, and crazy paving) and lowered SpO2% (lung lesions). PLS showed that 70.0% of the variance in the PA-core was explained by the regression on the immune response and lung lesions latent vectors. One common “infection-immune-inflammatory (III) core” underpins pneumonia-associated CCTAs, lowered SpO2 and immune activation, and this III core explains 70% of the variance in the PA core, and a relevant part of the variance in melancholia, insomnia, and neurocognitive symptoms. Acute SARS-CoV-2 infection is accompanied by lung lesions and lowered SpO2 which may cause activated immune-inflammatory pathways, which mediate the effects of the former on the PA-core and other neuropsychiatric symptoms due to SARS-CoV-2 infection.
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