Thromboinflammatory response in SARS-CoV-2 sepsis

Aniello Maiese; Giovanna Passaro; Alessandra DE Matteis; Valentina Fazio; La Russa Raffaele; Marco Di Paolo

doi:10.1177/0025817220926915

Thromboinflammatory response in SARS-CoV-2 sepsis

Med Leg J. 2020 Jul;88(2):78-80. doi: 10.1177/0025817220926915. Epub 2020 Jun 3.

Authors

Aniello Maiese¹, Giovanna Passaro², Alessandra DE Matteis³, Valentina Fazio³, La Russa Raffaele³, Marco Di Paolo¹

Affiliations

¹ Department of Surgical Pathology, Medical, Molecular and Critical Area, Institute of Legal Medicine, University of Pisa, Pisa, Italy.
² Gemelli IRCCS Research Hospital, Fondazione Policlinico Universitario A. Rome, Italy.
³ Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.

PMID: 32490726
DOI: 10.1177/0025817220926915

Abstract

Viral sepsis is rare, and its real incidence is not known. SARS-CoV-2 infection causes the release of a significant amount of pro-inflammatory cytokines that aggravates interstitial pneumonia and evolves in viral sepsis with prominent hypercoagulability. We believe it is useful and advisable to establish early immunomodulator therapy and the prophylaxis anticoagulant therapy should be rethought.

Keywords: Sars-CoV-2; sepsis, COVID-19, Thrombosis, Coagulopathy.

MeSH terms

Age Factors
Anticoagulants / therapeutic use
Betacoronavirus*
Biomarkers / blood
COVID-19
Comorbidity
Coronavirus Infections / complications*
Coronavirus Infections / drug therapy
Cytokines / blood*
Fibrin Fibrinogen Degradation Products / analysis
Humans
Immunosuppressive Agents / therapeutic use
Pandemics
Pneumonia, Viral / complications*
Pneumonia, Viral / drug therapy
SARS-CoV-2
Sepsis / blood
Sepsis / virology*
Thrombosis / prevention & control
Thrombosis / virology*

Substances

Anticoagulants
Biomarkers
Cytokines
Fibrin Fibrinogen Degradation Products
Immunosuppressive Agents
fibrin fragment D