格林-巴利综合征与covid -19后综合征的相关性分析

Matheus Lopes Martins, Sabrina Carvalho Melo, Amanda De Brito Silva, Luan Kelves Miranda de Souza
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摘要

目的:将格林-巴利综合征与covid -19后综合征联系起来,评估其病理生理、免疫原性和流行病学机制。方法:利用在以下数据库中发表的文章,利用二手数据进行了系统审查:拉丁美洲加勒比科学与健康文献(LILACS)、科学电子图书馆(ScIELO)和Pubmed;使用描述符:格林-巴罗综合征;脱髓鞘疾病和COVID-19,使用布尔运算符“and”,在它们之间进行交换。结果和讨论:根据Abu-Rumeileh等人(2021)的研究,即使无症状,COVID-19患者也更有可能发展为GBS,且以典型感觉运动形式和急性炎症性脱髓鞘多神经病变的男性人群为主,由于Sars-Cov-2的广泛年龄范围,也观察到儿科病例的增加。感染后免疫介导的病理生理机制观察到一些易感因素,即:Sars-Cov-2感染后出现神经系统症状、免疫调节剂改善GBS临床表现、脑脊液中病毒RNA缺失。结论:吉兰-巴罗综合征是一种免疫介导的神经肌肉疾病,通常发生在感染过程之后,感染过程触发炎症反应,随后分子模仿导致个体周围神经系统的自身免疫反应。尽管科学界对COVID-19与GBS之间的因果关系尚未达成共识,但人们认为,感染新型冠状病毒会引发免疫介导的反应,引发这种神经肌肉疾病,其特征是进行性、对称性和上升性无力,以及反射性。
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Analysis of the correlation between Guillain-Barré and post-COVID-19 syndromes
OBJECTIVE: To correlate Guillain-Barré as a consequence of the Post-COVID-19 syndrome, evaluating the pathophysiological, immunogenic and epidemiological mechanisms. METHODOLOGY: A systematic review was carried out, with secondary data, using articles published in the following databases: Latin American Caribbean Literature on Science and Health (LILACS), Scientific Electronic Library (ScIELO) and Pubmed; using the descriptors: Guillain-Barré syndrome; Demyelinating Diseases and COVID-19, using the Boolean operator “AND”, swapping between them. RESULTS AND DISCUSSION: According to Abu-Rumeileh et al. (2021), patients with COVID-19, even if asymptomatic, were more likely to develop GBS, with a predominance of the male population, in the classic sensorimotor form and in acute inflammatory demyelinating polyneuropathy, with an increase in pediatric cases also being observed, due to of the wide age range of Sars-Cov-2. The post-infection immune-mediated pathophysiological mechanism observed some predisposing factors, namely: neurological symptoms after Sars-Cov-2 infection, improvement of the clinical picture of GBS with immunomodulators and absence of viral RNA in the cerebrospinal fluid. CONCLUSION: Guillain-Barré Syndrome consists of an immune-mediated neuromuscular condition usually subsequent to an infectious process, which triggers an inflammatory response followed by a molecular mimicry that causes an autoimmune response in the individual's peripheral nervous system. Although there is no consensus in the scientific community regarding the causal relationship between COVID-19 and GBS, it is believed that infection with the new coronavirus precipitates an immune-mediated reaction that triggers this neuromuscular condition characterized by progressive, symmetrical and ascending weakness, in addition to areflexia.
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