Journal of Medical Cases, ISSN 1923-4155 print, 1923-4163 online, Open Access
Article copyright, the authors; Journal compilation copyright, J Med Cases and Elmer Press Inc
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Case Report

Volume 13, Number 4, April 2022, pages 168-171

COVID-19 Presenting With a Challenging Combination of Thrombocytopenia and Thrombosis

Tables

Table 1. Proposed Mechanisms of COVID-19-Associated Thrombocytopenia
 
Proposed mechanisms of thrombocytopeniaReferences
COVID-19: coronavirus disease 2019; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.
Direct inhibition of hematopoiesis through binding to angiotensin-converting enzyme-2 on hematopoietic tissues and organsXu et al [3], Zhang et al [4], Mei et al [7]
The inflammatory cytokine-mediated destruction of hematopoietic progenitor cellsXu et al [3]
The inflammatory cytokine-mediated inhibition of hematopoiesis or megakaryocytopoiesisZhang et al [4], Mei et al [7]
Decreased production of thrombopoietin either by damaged liver cells or inflammationZhang et al [4]
Block release of platelets from megakaryocytes in capillary beds of consolidated lungXu et al [3], Zhang et al [4]
Damaged endothelium triggers platelet aggregation and microthrombi formation and thereby increasing platelet consumptionXu et al [3], Zhang et al [4], Mei et al [7]
Viral-mediated platelet-leukocyte aggregationWool et al [1]
SARS-CoV-2-induced autoimmune destruction of plateletsXu et al [3], Zhang et al [4], Mei et al [7]
Hyperactivated platelets swallowed by hepatic/splenic macrophageMei et al [7]

 

Table 2. Proposed Mechanisms of COVID-19-Associated Coagulopathy
 
Proposed mechanisms of thrombocytopeniaReferences
COVID-19: coronavirus disease 2019; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.
SARS-CoV-2 binds to ACE2 on host cell membrane by using its spike protein. Both SARS-CoV-2 and its spike protein can directly activate platelets leading to platelet aggregation and leukocyte-platelet aggregation subsequently leading to thrombus formation.Zhang et al [13]
Immature platelets are elevated in COVID-19, which are functional and increase the risk of coagulopathy.Wool et al [1]
COVID-19 triggers significant inflammatory reaction leading to endothelial damage and clot formation.Wool et al [1]