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秋水仙碱、干扰素β、静脉注射免疫球蛋白、托珠单抗和皮质类固醇对COVID-19患者生存的影响:基于所有现有已发表临床试验的叙述性综述。

Effects of colchicine, interferon β, IVIG, tocilizumab and corticosteroids on COVID-19 patient survival from all presently available published clinical trials: A narrative review.

作者信息

Bahrampour Juybari Kobra, Shamsi Meymandi Manzume, Bashiri Hamideh

机构信息

Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran.

Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.

出版信息

Caspian J Intern Med. 2025 Mar 11;16(2):198-214. doi: 10.22088/cjim.16.2.198. eCollection 2025.

Abstract

One of the deadliest diseases in the world, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the ongoing global pandemic known as COVID-19. COVID-19 symptoms range from undetectable to deadly, hyper-inflammatory response and the overproduction of pro-inflammatory cytokines or hypercytokinemia are key factors in the pathophysiology of severe COVID-19. However, no specific and effective treatment was available, anti-inflammatory drugs have been vastly used for treating patients. The goal of this narrative literature review (2020-2022) was to elucidate the connection between anti-inflammatory medications and COVID-19 outcomes, such as safety and survival rate. Overall, these studies are consistent in presenting that anti-inflammatory drug can be advised to target the host immune response in patients and have been beneficial in reducing the mortality rate. This is revealed in current recommendations from prominent global public health authorities, which support anti-inflammatory drug use for a decrease of cytokine storm during COVID-19.

摘要

严重急性呼吸综合征冠状病毒2(SARS-CoV-2)是世界上最致命的疾病之一,是当前被称为COVID-19的全球大流行的病因。COVID-19的症状从难以察觉到致命不等,过度炎症反应和促炎细胞因子的过度产生或高细胞因子血症是重症COVID-19病理生理学的关键因素。然而,由于没有可用的特异性有效治疗方法,抗炎药物已被广泛用于治疗患者。这篇叙述性文献综述(2020 - 2022年)的目的是阐明抗炎药物与COVID-19结局之间的联系,如安全性和生存率。总体而言,这些研究一致表明,抗炎药物可用于针对患者的宿主免疫反应,并有助于降低死亡率。这在全球主要公共卫生当局的当前建议中得到了体现,这些建议支持在COVID-19期间使用抗炎药物来减少细胞因子风暴。

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