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In bivariate Cox regression analysis, risk factors associated with the development of acute respiratory distress syndrome and progression from acute respiratory distress syndrome to death included older age, neutrophilia, and organ and coagulation dysfunction
Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China.
JAMA INTERNAL MEDICINE, no. 7 (2020): 934-943
Question What clinical characteristics are associated with the development of acute respiratory distress syndrome (ARDS) and progression from ARDS to death among patients with coronavirus disease 2019 (COVID-19) pneumonia? Findings In this cohort study involving 201 patients with confirmed COVID-19 pneumonia, risk factors associated with ...More
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- We report the clinical characteristics and factors associated with developing ARDS after hospital admission and progression from ARDS to death in patients with COVID-19 pneumonia from a single hospital in Wuhan, China.
- Findings In this cohort study involving 201 patients with confirmed COVID-19 pneumonia, risk factors associated with the development of ARDS and progression from ARDS to death included older age, neutrophilia, and organ and coagulation dysfunction.
- In bivariate Cox regression analysis, risk factors associated with the development of acute respiratory distress syndrome and progression from acute respiratory distress syndrome to death included older age, neutrophilia (HR, 1.14; 95% CI, 1.09-1.19; and hazard ratio, 1.08; 95% CI, 1.01-1.17, respectively), and organ and coagulation dysfunction
- Among patients with acute respiratory distress syndrome, treatment with methylprednisolone decreased the risk of death (HR, 0.38; 95% CI, 0.20-0.72)
- Older age was associated with greater risk of development of acute respiratory distress syndrome and death likely owing to less rigorous immune response
- High fever was associated with the development of acute respiratory distress syndrome, it was associated with better outcomes among patients with acute respiratory distress syndrome
- We reported the clinical characteristics and risk factors associated with clinical outcomes in patients with COVID-19 pneumonia who developed acute respiratory distress syndrome after admission, as well as those who progressed from acute respiratory distress syndrome to death
- We reported the clinical characteristics and risk factors associated with clinical outcomes in patients with COVID-19 pneumonia who developed ARDS after admission, as well as those who progressed from ARDS to death.
- High fever was positively associated with development of ARDS, it was negatively related to death, which is consistent with results noted in a study by Schell-Chaple et al. the differences in patient temperature between the groups were very small and self-reported before hospital admission, the data regarding high fever should be cautiously interpreted.
- The generation of cytokine storm can lead to ARDS, which is a leading cause of death in patients with severe acute respiratory syndrome and Middle East respiratory syndrome. In this study, patients with COVID-19 pneumonia who had developed ARDS had significantly higher neutrophil counts than did those without ARDS, perhaps leading to the activation of neutrophils to execute an immune response against the virus, but contributing to cytokine storm.
- The results of this study show that higher CD3 and CD4 T-cell counts might protect patients from developing ARDS, but similar results were not observed when examined for death, possibly because of limited sample size.
- Earlier studies have revealed that SARS-CoV, which was reported to share the same cell entry receptors with SARS-CoV-2,17,18 could infect immune cells, including T lymphocytes, monocytes, and macrophages. The CD3, CD4, and CD8 T-cell counts decreased at the onset of illness; this decrease persisted until the recovery period of SARS-CoV pneumonia. In addition, CD4 and CD8 T-cell counts decreased in the peripheral blood specimen of patients with fatal SARS-CoV pneumonia[10,20,21], which was consistent with these results that patients with COVID-19 pneumonia and ARDS presented with lymphocytopenia (CD3, CD4, and CD8 T cells).
- A larger cohort study of patients with COVID-19 pneumonia from Wuhan, China, other cities in China, and other countries would help to further define the clinical characteristics and risk factors of the disease.
- Double-blinded randomized clinical trials to determine the most effective treatments for COVID-19 are still needed.
- Table1: Demographic Characteristics of Patients With Coronavirus Disease 2019 Pneumonia. Demographic Characteristics of Patients With Coronavirus Disease 2019 Pneumonia (continued)
- Table2: Initial Laboratory Indices of Patients With Coronavirus Disease 2019 Pneumonia
- Table3: Clinical Characteristics and Initial Laboratory Indices Among Patients With and Without ARDS. Clinical Characteristics and Initial Laboratory Indices Among Patients With and Without ARDS (continued)
- Table4: Bivariate Cox Regression of Factors Associated With ARDS Development or Progression From ARDS to Death
- Funding/Support: This study was supported by a grant from Prevention and Treatment of Infection in Novel Coronavirus Pneumonia Patients from the Shanghai Science and Technology Committee (to Dr Yuanlin Song), the Special Fund of Shanghai Jiaotong University for Coronavirus Disease 2019 Control and Prevention (2020RK47 to Dr Junhua Zheng), and Academic Leader of Shanghai Qingpu District Healthcare Commission (WD2019-36 to Dr Chaomin Wu)
- World Health Organization. Coronavirus disease 2019 (COVID-19): situation report—37. February 25, 2020. Accessed February 26, 2020. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200226-sitrep37-covid-19.pdf?sfvrsn=6126c0a4_2.
- Zhu N, Zhang D, Wang W, et al; China Novel Coronavirus Investigating and Research Team. A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med. 2020;382(8):727-733. doi:10.1056/NEJMoa2001017
- Huang C, Wang Y, Li X, et al Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506. doi:10.1016/S0140-6736(20)30183-5
- Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507513. doi:10.1016/S0140-6736(20)30211-7
- Wang D, Hu B, Hu C, et al Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. Published online February 7, 2020. doi:10. 1001/jama.2020.1585
- World Health Organization. Clinical management of severe acute respiratory infection when novel coronavirus (nCoV) infection is suspected: interim guidance. January 28, 2020. Accessed March 5, 2020. https://www.who.int/publications-detail/clinical-management-of-severeacute-respiratory-infection-when-novelcoronavirus-(ncov)-infection-is-suspected.
- Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med. 1997;336(4):243-250. doi:10.1056/ NEJM199701233360402
- Schell-Chaple HM, Puntillo KA, Matthay MA, Liu KD; National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Network. Body temperature and mortality in patients with acute respiratory distress syndrome. Am J Crit Care. 2015; 24(1):15-23. doi:10.4037/ajcc2015320
- Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Semin Immunopathol. 2017;39 (5):529-539. doi:10.1007/s00281-017-0629-x
- Wang YH, Lin AS, Chao TY, et al. A cluster of patients with severe acute respiratory syndrome in a chest ward in southern Taiwan. Intensive Care Med. 2004;30(6):1228-1231. doi:10.1007/s00134-0042311-8
- Nicholls JM, Poon LLM, Lee KC, et al. Lung pathology of fatal severe acute respiratory syndrome. Lancet. 2003;361(9371):1773-1778. doi:10.1016/S0140-6736(03)13413-7
- Ng DL, Al Hosani F, Keating MK, et al. Clinicopathologic, immunohistochemical, and ultrastructural findings of a fatal case of Middle East respiratory syndrome coronavirus infection in the United Arab Emirates, April 2014. Am J Pathol. 2016;186(3):652-658. doi:10.1016/j.ajpath.2015.10. 024
- Min CK, Cheon S, Ha NY, et al. Comparative and kinetic analysis of viral shedding and immunological responses in MERS patients representing a broad spectrum of disease severity. Sci Rep. 2016;6:25359. doi:10.1038/srep25359
- Kim ES, Choe PG, Park WB, et al. Clinical progression and cytokine profiles of Middle East respiratory syndrome coronavirus infection. J Korean Med Sci. 2016;31(11):1717-1725. doi:10.3346/jkms.2016.31.11.1717
- Lew TW, Kwek TK, Tai D, et al. Acute respiratory distress syndrome in critically ill patients with severe acute respiratory syndrome. JAMA. 2003; 290(3):374-380. doi:10.1001/jama.290.3.374
- Goronzy JJ, Fang F, Cavanagh MM, Qi Q, Weyand CM. Naive T cell maintenance and function in human aging. J Immunol. 2015;194(9):4073-4080. doi:10.4049/jimmunol.1500046
- Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. Published online February 3, 2020. doi:10.1038/s41586-020-2012-7
- Hoffmann M, Kleine-Weber H, Krüger N, Müller M, Drosten C, Pöhlmann S. The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor 2 ACE2 and the cellular protease TMPRSS2 for entry into target cells. Preprint. Posted online January 31, 2020. bioRxiv. doi:10.1101/2020.01.31. 929042
- Gu J, Gong E, Zhang B, et al. Multiple organ infection and the pathogenesis of SARS. J Exp Med. 2005;202(3):415-424. doi:10.1084/jem.20050828
- Li T, Qiu Z, Zhang L, et al. Significant changes of peripheral T lymphocyte subsets in patients with severe acute respiratory syndrome. J Infect Dis. 2004;189(4):648-651. doi:10.1086/381535
- Cui W, Fan Y, Wu W, Zhang F, Wang JY, Ni AP. Expression of lymphocytes and lymphocyte subsets in patients with severe acute respiratory syndrome. Clin Infect Dis. 2003;37(6):857-859. doi: 10.1086/378587
- Kim KD, Zhao J, Auh S, et al. Adaptive immune cells temper initial innate responses. Nat Med. 2007;13(10):1248-1252. doi:10.1038/nm1633
- Zhao J, Zhao J, Perlman S. T cell responses are required for protection from clinical disease and for virus clearance in severe acute respiratory syndrome coronavirus-infected mice. J Virol. 2010; 84(18):9318-9325. doi:10.1128/JVI.01049-10