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Cytokine Storm May Not Be the Chief Culprit for the Deterioration of COVID-19
Viral Immunology ( IF 2.2 ) Pub Date : 2021-06-14 , DOI: 10.1089/vim.2020.0243
Yang Gao 1 , Changsong Wang 1, 2 , Kai Kang 1 , Yahui Peng 1 , Yunpeng Luo 1 , Haitao Liu 2 , Wei Yang 1 , Mingyan Zhao 1 , Kaijiang Yu 1
Affiliation  

COVID-19 is spreading and ravaging all over the world, and the number of deaths is increasing day by day without downward trend. However, there is limited knowledge of pathogenesis on the deterioration of COVID-19 at present. In this study we aim to determine whether cytokine storm is really the chief culprit for the deterioration of COVID-19. The confirmed COVID-19 patients were divided into moderate group (n = 89), severe group (n = 37), and critical group (n = 41). Demographic data were collected and recorded on admission to ICU. Clinical data were obtained when moderate, severe, or critical COVID-19 was diagnosed, and then compared between groups. The proportion of enrolled COVID-19 patients was slightly higher among males (52.5%) than females (47.5%), with an average age of 64.87 years. The number of patients without comorbidities exceed one third (36.1%), and patients with 1, 2, 3, 4 kinds of comorbidities accounted for 23.0%, 23.0%, 13.1%, and 4.9%, respectively. IL-6, IL-10, TNF, and IFN-γ, including oxygenation index, sequential organ failure assessment score, white blood cell count, lymphocyte count, lymphocyte percentage, platelet, C-reaction protein, lactate dehydrogenase, creatine kinase isoenzyme, albumin, D-Dimer, and fibrinogen showed significant difference between groups. Some, but not all, cytokines and chemokines were involved in the deterioration of COVID-19, and thus cytokine storm maybe just the tip of the iceberg and should be used with caution to explain pathogenesis on the deterioration of COVID-19, which might be complex and related to inflammation, immunity, blood coagulation, and multiple organ functions. Future studies should focus on identification of specific signaling pathways and mechanisms after severe acute respiratory syndrome coronavirus 2 infections (IRB number: IRB-AF/SC-04/01.0).

中文翻译:

细胞因子风暴可能不是 COVID-19 恶化的罪魁祸首

COVID-19正在世界各地蔓延和肆虐,死亡人数每天都在增加,没有下降的趋势。然而,目前对 COVID-19 恶化的发病机制知之甚少。在这项研究中,我们旨在确定细胞因子风暴是否真的是 COVID-19 恶化的罪魁祸首。确认COVID-19患者分为中度组(Ñ  = 89),重度组(Ñ  = 37),和关键组(Ñ = 41)。在入住 ICU 时收集并记录人口统计学数据。在诊断出中度、重度或危重 COVID-19 时获得临床数据,然后进行组间比较。纳入的 COVID-19 患者比例在男性(52.5%)中略高于女性(47.5%),平均年龄为 64.87 岁。无合并症患者超过三分之一(36.1%),有1、2、3、4种合并症的患者分别占23.0%、23.0%、13.1%和4.9%。IL-6、IL-10、TNF 和 IFN- γ,包括氧合指数、序贯器官衰竭评估评分、白细胞计数、淋巴细胞计数、淋巴细胞百分比、血小板、C-反应蛋白、乳酸脱氢酶、肌酸激酶同工酶、白蛋白、D-二聚体和纤维蛋白原显示组间差异显着。一些但不是全部的细胞因子和趋化因子参与了 COVID-19 的恶化,因此细胞因子风暴可能只是冰山一角,应谨慎用于解释 COVID-19 恶化的发病机制,这可能是复杂且与炎症、免疫、凝血和多器官功能有关。未来的研究应侧重于鉴定严重急性呼吸综合征冠状病毒 2 感染后的特定信号通路和机制(IRB 编号:IRB-AF/SC-04/01.0)。
更新日期:2021-06-18
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