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1.
J Med Virol ; 93(3): 1276-1287, 2021 03.
Article in English | MEDLINE | ID: mdl-32856728

ABSTRACT

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has rapidly spread throughout the world since December 2019 to become a global public health emergency for the elevated deaths and hospitalizations in Intensive Care Units. The severity spectrum of SARS-CoV-2 pneumonia ranges from mild to severe clinical conditions. The clinical course of SARS-CoV-2 disease is correlated with multiple factors including host characteristics (genetics, immune status, age, and general health), viral load and, above all, the host distribution of the airways and lungs of the viral receptor cells. In this review, we will briefly summarize the current knowledge of the characteristics and management of coronavirus disease 2019-pneumonia. However, other studies are needed to better understand the pathogenetic mechanisms induced by SARS-Cov-2 infection, and to evaluate the long-term consequences of the virus on the lungs.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Antiviral Agents/therapeutic use , COVID-19 Drug Treatment , Pneumonia, Viral/drug therapy , Acute Lung Injury/drug therapy , Acute Lung Injury/pathology , Acute Lung Injury/physiopathology , COVID-19/pathology , COVID-19/physiopathology , Disease Management , Humans , Lung/diagnostic imaging , Lung/pathology , Pneumonia, Viral/pathology , Pneumonia, Viral/physiopathology
2.
Monaldi Arch Chest Dis ; 90(2)2020 May 19.
Article in English | MEDLINE | ID: mdl-32425013

ABSTRACT

Latest evidences from literature suggest that SARS-CoV-2 disease 2019 (COVID-19) is commonly complicated with coagulopathy and that disseminated intravascular coagulation is present in the majority of deceased patients. Particularly, conventional coagulation parameters appear to be significantly altered in patients with poor prognosis. A wide-ranging cross- talk between coagulative haemostasis and inflammation, as well as the activation of coagulation cascade during viral infections, are well established. Another important evidence which may explain coagulation disorders in COVID-19 is the increase of thrombus formation under conditions of hypoxia. Despite the exact pathophysiological mechanism of coronavirus-induced thromboembolism needs to be further investigated, this finding suggests that it is good practice to assess the risk of thrombosis in COVID-19 patients to improvethe clinical management in terms of anticoagulation therapy. Anticoagulants, mainly low-molecular-weight heparin (LMWH), should be tailored in patients meeting sepsis induced coagulopathy (SIC) criteria or with markedly elevated D-dimer. In this context, further studies are needed to optimise the decision making in therapeutic approach.


Subject(s)
Blood Coagulation Disorders/virology , Coronavirus Infections/blood , Pneumonia, Viral/blood , Betacoronavirus/isolation & purification , Blood Coagulation/physiology , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/epidemiology , COVID-19 , Coronavirus Infections/epidemiology , Humans , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2
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