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《LANCET，2月6日，Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury》

  • 来源专题：COVID-19科研动态监测
  • 编译者： zhangmin
  • 发布时间：2020-02-07

  • The 2019 novel coronavirus (2019-nCoV) outbreak is a major challenge for clinicians. The clinical course of patients remains to be fully characterised, little data are available that describe the disease pathogenesis, and no pharmacological therapies of proven efficacy yet exist.

  • 原文来源：https://www.thelancet.com/lancet/article/corticosteroid-treatment
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    • 来源专题：COVID-19科研动态监测
    • 编译者：xuwenwhlib
    • 发布时间：2020-02-07
    • 2019-nCoV transmission through the ocular surface must not be ignored Cheng-wei Lu，Xiu-fen Liu，Zhi-fang Jia Published:February 06, 2020 DOI:https://doi.org/10.1016/S0140-6736(20)30313-5 Chaolin Huang and colleagues1 reported the epidemiology, symptoms, and treatment of patients infected by the 2019 novel coronavirus (2019-nCoV) in Wuhan, China. As ophthalmologists, we believe that transmission of 2019-nCoV through the eyes was ignored. On Jan 22, Guangfa Wang, a member of the national expert panel on pneumonia, reported that he was infected by 2019-nCoV during the inspection in Wuhan.2 He wore an N95 mask but did not wear anything to protect his eyes. Several days before the onset of pneumonia, Wang complained of redness of the eyes. Unprotected exposure of the eyes to 2019-nCoV in the Wuhan Fever Clinic might have allowed the virus to infect the body.2 Infectious droplets and body fluids can easily contaminate the human conjunctival epithelium.3 Respiratory viruses are capable of inducing ocular complications in infected patients, which then leads to respiratory infection.4 Severe acute respiratory syndrome coronavirus (SARS-CoV) is predominantly transmitted through direct or indirect contact with mucous membranes in the eyes, mouth, or nose.5 The fact that exposed mucous membranes and unprotected eyes increased the risk of SARS-CoV transmission4 suggests that exposure of unprotected eyes to 2019-nCoV could cause acute respiratory infection. Thus, Huang and colleagues1 should have analysed conjunctival scrapings from both confirmed and suspected 2019-nCoV cases during the onset of symptoms. The respiratory tract is probably not the only transmission route for 2019-nCoV, and all ophthalmologists examining suspected cases should wear protective eyewear.
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  • 《Virologica Sinica，2月7日，Compensation of ACE2 Function for Possible Clinical Management of 2019-nCoV-Induced Acute Lung Injury》
    • 来源专题：COVID-19科研动态监测
    • 编译者：xuwenwhlib
    • 发布时间：2020-02-08
    • Compensation of ACE2 Function for Possible Clinical Management of 2019-nCoV-Induced Acute Lung Injury Published: 07 February 2020 Yuntao Wu DOI https://xs.scihub.ltd/https://doi.org/10.1007/s12250-020-00205-6 The 2019-nCoV viral infection causes clusters of severe respiratory illness such as an acute respiratory distress syndrome (ARDS) similar to that caused by SARS-CoV (severe acute respiratory syndrome coronavirus) (Huang et al.2020). Both 2019-nCoV and SARS-CoV use the same receptor, ACE2 (angiotensin converting enzyme 2), to infect cells (Li et al.2003; Zhou et al.2020). ACE2 is one of the central enzymes in the renin–angiotensin system (RAS) (Donoghue et al.2000; Imai et al.2010; Tipnis et al.2000) that regulates blood pressure, fluid and electrolyte balance, and systemic vascular resistance (Paul et al.2006; Zimmerman and Dunham 1997). In the lungs, activation of local pulmonary RAS can affect the pathogenesis of lung injury via multiple mechanisms, such as an increase in vascular permeability and alterations of alveolar epithelial cells (Kuba et al.2006; Specks et al.1990). Activation of pulmonary RAS involves renin, the initial enzyme of the RAS activation cascade (Fig. 1). Renin cleaves angiotensinogen, a globular protein, to generate angiotensin I (Ang I, a decapeptide hormone). The angiotensin-converting enzyme (ACE) then converts Ang I to angiotensin II (Ang II, an octapeptide hormone). Ang II exerts vasoactive effects through binding to its receptors, the angiotensin II type I (AT1) and type II (AT2) receptors.
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