Thrombosis in COVID-19

Am J Hematol. 2020 Dec;95(12):1578-1589. doi: 10.1002/ajh.25982. Epub 2020 Sep 16.

Abstract

Thrombotic complications are frequent in COVID-19 and contribute significantly to mortality and morbidity. We review several mechanisms of hypercoagulability in sepsis that may be upregulated in COVID-19. These include immune-mediated thrombotic mechanisms, complement activation, macrophage activation syndrome, antiphospholipid antibody syndrome, hyperferritinemia, and renin-angiotensin system dysregulation. We highlight biomarkers within each pathway with potential prognostic value in COVID-19. Lastly, recent observational studies have evaluated a role for the expanded use of therapeutic anticoagulation in COVID-19. We review strengths and weaknesses of these studies, and we also discuss the hypothetical benefit and anticipated challenges of fibrinolytic therapy in COVID-19.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Anticoagulants / therapeutic use
  • Antiphospholipid Syndrome
  • COVID-19 / complications*
  • COVID-19 / immunology
  • COVID-19 / therapy
  • COVID-19 Drug Treatment
  • Complement Activation
  • Critical Illness / epidemiology
  • Cytokine Release Syndrome / epidemiology
  • Disseminated Intravascular Coagulation
  • Ferritins / blood
  • Humans
  • Hyperferritinemia / epidemiology
  • Macrophage Activation
  • Pulmonary Embolism / epidemiology
  • Renin-Angiotensin System / physiology
  • SARS-CoV-2*
  • Thrombophilia / blood
  • Thrombophilia / epidemiology
  • Thrombophilia / immunology
  • Thrombosis / blood
  • Thrombosis / epidemiology*
  • Thrombosis / immunology

Substances

  • Anticoagulants
  • Ferritins