Epidemiological and clinical features of 2019-nCoV acute respiratory disease cases in Chongqing municipality, China: a retrospective, descriptive, multiple-center study

Qi, Di; Yan, Xiaofeng; Tang, Xumao; Peng, Junnan; Yu, Qian; Feng, Liqun; Yuan, Guodan; Zhang, An; Chen, Yaokai; Yuan, Jing; Huang, Xia; Zhang, Xianxiang; Hu, Ping; Song, Yuyan; Qian, Chunfang; Sun, Qiangzhong; Wang, Daoxin; Jin, Tao; Xiang, Junyi

doi:10.1101/2020.03.01.20029397

Cited by 62 publications

(61 citation statements)

References 35 publications

(58 reference statements)

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“…Our results indicated that, as an infection-related factor, ESR was also significantly higher in severe patients compared to mild patients, which is consistent with previous studies [9,23] . ESR is a simple laboratory test for evaluating the inflammatory or acute response state.…”

Section: Discussionsupporting

confidence: 93%

Potential Factors for Prediction of Disease Severity of COVID-19 Patients

zhang

wang

et al. 2020

Preprint

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Objective: Coronavirus disease 2019 is an escalating global epidemic caused by SARS-CoV-2, with a high mortality in critical patients. Effective indicators for predicting disease severity in SARS-CoV-2 infected patients are urgently needed. Methods: In this study, 43 COVID-19 patients admitted in ChongqingPublic Health Medical Center were involved. Demographic data, clinical features, and laboratory examinations were obtained through electronic medical records. Peripheral blood specimens were collected from COVID-19 patients and examined for lymphocyte subsets and cytokine profiles by flow cytometry. Potential contributing factors for prediction of disease severity were further analyzed.Results: A total of 43 COVID-19 patients were included in this study, including 29 mild patients and 14 sever patients. Severe patients were significantly older (61.9±9.4 vs 44.4±15.9) and had higher incidence in co-infection with bacteria compared to mild group (85.7%vs27.6%).Significantly more severe patients had the clinical symptoms of anhelation (78.6%) and asthma (71.4%). For laboratory examination, 57.1% severe cases showed significant reduction in lymphocyte count.The levels of Interluekin-6 (IL6), IL10, erythrocyte sedimentation rate (ESR) and D-Dimer (D-D) were significantly higher in severe patients than mild patients, while the level of albumin (ALB) was remarkably : medRxiv preprint lower in severe patients. Further analysis demonstrated that ESR, D-D, age, ALB and IL6 were the major contributing factors for distinguishing severe patients from mild patients. Moreover, ESR was identified as the most powerful factor to predict disease progression of COVID-19 patients. Conclusion:Age and the levels of ESR, D-D, ALB and IL6 are closely related to the disease severity of COVID-19 patients. ESR can be used as a valuable indicator for distinguishing severe COVID-19 patients in early stage, so as to increase the survival of severe patients.

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Section: Discussionsupporting

confidence: 93%

Potential Factors for Prediction of Disease Severity of COVID-19 Patients

zhang

wang

et al. 2020

Preprint

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“…This upregulation is likely mediated at least in part by the expansion of ACE2+ mucus-secreting goblet cells triggered by chronic smoke exposure. The overabundance of ACE2 in the lungs of smokers may partially explain why smokers are significantly more likely to develop severe SARS-CoV-2 infections that require aggressive medical interventions 12,23 . Furthermore, as quitting smoking is associated with a decrease in ACE2 expression, we speculate that giving up cigarettes may reduce susceptibility to COVID-19.…”

Section: Discussionmentioning

confidence: 99%

“…Cigarette smoking is strongly associated with adverse outcomes from COVID-19 12,23 . To investigate whether smoking could affect ACE2 levels, we first assessed gene expression in mouse lungs.…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tract

Smith

Sausville

Girish

et al. 2020

Preprint

100

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The coronavirus SARS-CoV-2 has infected more than 600,000 people and has overwhelmed hospital systems around the world. However, the factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of Angiotensin Converting Enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of epithelial cells that line the respiratory tract, including goblet cells, club cells, and alveolar type 2 cells. Chronic smoke exposure triggers a protective expansion of mucus-secreting goblet cells and a concomitant increase in ACE2 expression. In contrast, quitting smoking causes a decrease in lung ACE2 levels. Taken together, these results may partially explain why smokers are particularly likely to develop severe SARS-CoV-2 infections, and they suggest that quitting smoking could lessen coronavirus susceptibility.

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“…In 6 studies, the clinical course of 1,841 patients was investigated, 21% of whom developed a severe manifestation of the disease. 7,10,12,[21][22][23] Median age ranged from 49 to 71.5 years and was up to 28.5 years older than in patients with nonsevere course. Male patients were more affected by severe manifestations from 57.8 to 78%.…”

Section: Clinical Covid-19 Manifestationsmentioning

confidence: 99%

Pathological Role of Angiotensin II in Severe COVID-19

Miesbach

2020

TH Open

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The activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

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Epidemiological and clinical features of 2019-nCoV acute respiratory disease cases in Chongqing municipality, China: a retrospective, descriptive, multiple-center study

Abstract: Background

Cited by 62 publications

References 35 publications

Potential Factors for Prediction of Disease Severity of COVID-19 Patients

Potential Factors for Prediction of Disease Severity of COVID-19 Patients

Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tract

Pathological Role of Angiotensin II in Severe COVID-19

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