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新冠后状况:我们目前的进展如何?

Post-COVID-19 Condition: Where Are We Now?

作者信息

Boaventura Paula, Macedo Sofia, Ribeiro Filipa, Jaconiano Sónia, Soares Paula

机构信息

Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Rua Júlio Amaral de Carvalho 45, 4200-135 Porto, Portugal.

Instituto de Investigação e Inovação em Saúde (i3S), University of Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal.

出版信息

Life (Basel). 2022 Mar 31;12(4):517. doi: 10.3390/life12040517.

DOI:10.3390/life12040517
PMID:35455008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9029703/
Abstract

COVID-19 is currently considered a systemic infection involving multiple systems and causing chronic complications. Compared to other post-viral fatigue syndromes, these complications are wider and more intense. The most frequent symptoms are profound fatigue, dyspnea, sleep difficulties, anxiety or depression, reduced lung capacity, memory/cognitive impairment, and hyposmia/anosmia. Risk factors for this condition are severity of illness, more than five symptoms in the first week of the disease, female sex, older age, the presence of comorbidities, and a weak anti-SARS-CoV-2 antibody response. Different lines of research have attempted to explain these protracted symptoms; chronic persistent inflammation, autonomic nervous system disruption, hypometabolism, and autoimmunity may play a role. Due to thyroid high ACE expression, the key molecular complex SARS-CoV-2 uses to infect the host cells, thyroid may be a target for the coronavirus infection. Thyroid dysfunction after SARS-CoV-2 infection may be a combination of numerous mechanisms, and its role in long-COVID manifestations is not yet established. The proposed mechanisms are a direct effect of SARS-CoV-2 on target cells, an indirect effect of systemic inflammatory immune response, and a dysfunction of the hypothalamic-pituitary-thyroid (HPT) axis leading to decreased serum TSH. Only a few studies have reported the thyroid gland status in the post-COVID-19 condition. The presence of post-COVID symptoms deserves recognition of COVID-19 as a cause of post-viral fatigue syndrome. It is important to recognize the affected individuals at an early stage so we can offer them the most adequate treatments, helping them thrive through the uncertainty of their condition.

摘要

目前,新冠病毒病(COVID-19)被认为是一种累及多个系统并导致慢性并发症的全身性感染。与其他病毒感染后疲劳综合征相比,这些并发症范围更广、程度更严重。最常见的症状是极度疲劳、呼吸困难、睡眠困难、焦虑或抑郁、肺功能下降、记忆/认知障碍以及嗅觉减退/嗅觉丧失。该病症的危险因素包括疾病严重程度、发病第一周出现五种以上症状、女性、老年、存在合并症以及抗SARS-CoV-2抗体反应较弱。不同的研究方向试图解释这些迁延不愈的症状;慢性持续性炎症、自主神经系统紊乱、代谢减退和自身免疫可能起了作用。由于甲状腺高表达新冠病毒用来感染宿主细胞的关键分子复合物,甲状腺可能是冠状病毒感染的一个靶点。SARS-CoV-2感染后的甲状腺功能障碍可能是多种机制共同作用的结果,其在新冠长期症状表现中的作用尚未明确。提出的机制包括SARS-CoV-2对靶细胞的直接作用、全身性炎症免疫反应的间接作用以及下丘脑-垂体-甲状腺(HPT)轴功能障碍导致血清促甲状腺激素降低。只有少数研究报道了COVID-19康复后的甲状腺状态。新冠后症状的存在值得将COVID-19视为病毒感染后疲劳综合征的一个病因。早期识别受影响的个体很重要,这样我们就能为他们提供最适当的治疗,帮助他们在病情的不确定性中茁壮成长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9029703/c888d91a874a/life-12-00517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9029703/c888d91a874a/life-12-00517-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9029703/c888d91a874a/life-12-00517-g001.jpg

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