Title

Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID-19

UMMS Affiliation

Department of Medicine, Hematology and Oncology

Publication Date

2020-10-15

Document Type

Article

Disciplines

Cardiovascular Diseases | Fluids and Secretions | Hematology | Hemic and Immune Systems | Hemic and Lymphatic Diseases | Immunity | Infectious Disease | Respiratory Tract Diseases | Virus Diseases

Abstract

Coronavirus disease-2019 (COVID-19) is a rapidly evolving health crisis caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a novel disease entity and we are in a learning phase with regards to the pathogenesis, disease manifestations, and therapeutics. In addition to the primary lung injury, many patients especially the ones with moderate to severe COVID-19 display evidence of endothelial damage, complement activation, which leads to a pro-coagulable state. While there are still missing links in our understanding, the interplay of endothelium, complement system activation, and immune response to the SARS-CoV-2 virus is a surprisingly major factor in COVID-19 pathogenesis. One could envision COVID-19 becoming a novel hematological syndrome. This review is to discuss the available literature with regards to the involvement of the complement system, and coagulation cascade and their interaction with endothelium.

Keywords

COVID-19, Coronavirus, Immunity, Pandemic

DOI of Published Version

10.1007/s11239-020-02297-z

Source

Wang X, Sahu KK, Cerny J. Coagulopathy, endothelial dysfunction, thrombotic microangiopathy and complement activation: potential role of complement system inhibition in COVID-19. J Thromb Thrombolysis. 2020 Oct 15:1–6. doi: 10.1007/s11239-020-02297-z. Epub ahead of print. PMID: 33063256; PMCID: PMC7561230. Link to article on publisher's site

Journal/Book/Conference Title

Journal of thrombosis and thrombolysis

Related Resources

Link to Article in PubMed

PubMed ID

33063256

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