COVID-19 Hematologic Complications: Difference between revisions

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==Overview==
==Overview==

Revision as of 07:16, 15 June 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]

Overview

Complications

Lymphopenia

Neutrophilia

Thrombocytopenia

There is an association between severe COVID-19 infection and thrombocytopenia.[1] Thrombocytopenia is seen in 57.7% of patients with severe COVID-19 infection compared to 31.6 % of patients with non-severe infection.[2]

The pathogenesis of thrombocytopenia in COVID-19 infection is due to several factors:[3]

  • Decrease in primary platelet production due to infection of bone marrow cells by coronaviruses[4] and inhibition of bone marrow growth,[5] which lead to abnormal hematopoietic function.[3]
  • Increase in platelet destruction due to increase in autoantibodies and immune complexes.[6]
  • Decrease in circulating platelet due to lung injury which causes megakaryocyte fragmentation and decreases platelet production, because lung is a reservoir for megakaryocyte and hematopoieitic progenitor cells and has a role in platelet production.[3][7] In addition, decrease in platelets may be due to activation of platelets that result in platelet aggregation and formation of microthrombus which increase platelet consumption.[3][8]

Decrease in hemoglobulin

Other hematological findings

References

  1. ↑ Lippi G, Plebani M, Henry BM (2020). "Thrombocytopenia is associated with severe coronavirus disease 2019 (COVID-19) infections: A meta-analysis". Clin Chim Acta. 506: 145–148. doi:10.1016/j.cca.2020.03.022. PMC 7102663 Check |pmc= value (help). PMID 32178975 Check |pmid= value (help).
  2. ↑ Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX; et al. (2020). "Clinical Characteristics of Coronavirus Disease 2019 in China". N Engl J Med. 382 (18): 1708–1720. doi:10.1056/NEJMoa2002032. PMC 7092819 Check |pmc= value (help). PMID 32109013 Check |pmid= value (help).
  3. ↑ 3.0 3.1 3.2 3.3 Xu P, Zhou Q, Xu J (2020). "Mechanism of thrombocytopenia in COVID-19 patients". Ann Hematol. 99 (6): 1205–1208. doi:10.1007/s00277-020-04019-0. PMC 7156897 Check |pmc= value (help). PMID 32296910 Check |pmid= value (help).
  4. ↑ Yang M, Ng MH, Li CK (2005). "Thrombocytopenia in patients with severe acute respiratory syndrome (review)". Hematology. 10 (2): 101–5. doi:10.1080/10245330400026170. PMID 16019455.
  5. ↑ Yeager CL, Ashmun RA, Williams RK, Cardellichio CB, Shapiro LH, Look AT; et al. (1992). "Human aminopeptidase N is a receptor for human coronavirus 229E". Nature. 357 (6377): 420–2. doi:10.1038/357420a0. PMC 7095410 Check |pmc= value (help). PMID 1350662.
  6. ↑ Nardi M, Tomlinson S, Greco MA, Karpatkin S (2001). "Complement-independent, peroxide-induced antibody lysis of platelets in HIV-1-related immune thrombocytopenia". Cell. 106 (5): 551–61. doi:10.1016/s0092-8674(01)00477-9. PMID 11551503.
  7. ↑ Lefrançais E, Ortiz-Muñoz G, Caudrillier A, Mallavia B, Liu F, Sayah DM; et al. (2017). "The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors". Nature. 544 (7648): 105–109. doi:10.1038/nature21706. PMC 5663284. PMID 28329764.
  8. ↑ Liu X, Zhang R, He G (2020). "Hematological findings in coronavirus disease 2019: indications of progression of disease". Ann Hematol. doi:10.1007/s00277-020-04103-5. PMC 7266734 Check |pmc= value (help). PMID 32495027 Check |pmid= value (help).
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