Thrombosis in COVID-19.

Thomas C Hanff, Amir M Mohareb, Jay Giri, Jordana B Cohen, Julio A Chirinos

Journal: American journal of hematology 2020;95(12):1578-1589

PMID: 32857878

Free Full Text on PubMed Central View on PubMed

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.

Address: Division of Cardiology, Department of Medicine, Perelman School of Medicine, Philadelphia, Pennsylvania, USA.; Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania, Philadelphia, Pennsylvania, USA.; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA.; Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.; Renal-Electrolyte and Hypertension Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

DOI: 10.1002/ajh.25982

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MeSH Terms: Anticoagulants, Antiphospholipid Syndrome, COVID-19, Complement Activation, Critical Illness, Cytokine Release Syndrome, Disseminated Intravascular Coagulation, Ferritins, Humans, Hyperferritinemia, Macrophage Activation, Pulmonary Embolism, Renin-Angiotensin System, SARS-CoV-2, Thrombophilia, Thrombosis, COVID-19 Drug Treatment