COVID-19 Hematologic Complications: Difference between revisions

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**[[Anemia]] is not a common finding probably due to the compensation of [[Red blood cell|erythrocyte]] proliferation caused by [[pneumonia]]-induced [[Hypoxemia|hypoxia]] and the long life span of [[erythrocytes]].<ref name="pmid32495027" />
**[[Anemia]] is not a common finding probably due to the compensation of [[Red blood cell|erythrocyte]] proliferation caused by [[pneumonia]]-induced [[Hypoxemia|hypoxia]] and the long life span of [[erythrocytes]].<ref name="pmid32495027" />


=== Coagulopathy===
== Coagulopathy==


====Pathophysiology====
====Pathophysiology====
Line 106: Line 106:
*The scoring system of the [https://www.isth.org/ International Society on Thrombosis and Hemostasis] should be used to detect DIC ([[platelet]] count, PT, [[fibrinogen]], D‐dimer, [[antithrombin]] and [[protein C]] activity monitoring), but the diagnosis and subsequent treatment should be done clinically. <ref name="pmid19222477">{{cite journal| author=Levi M, Toh CH, Thachil J, Watson HG| title=Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. | journal=Br J Haematol | year= 2009 | volume= 145 | issue= 1 | pages= 24-33 | pmid=19222477 | doi=10.1111/j.1365-2141.2009.07600.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19222477  }} </ref>
*The scoring system of the [https://www.isth.org/ International Society on Thrombosis and Hemostasis] should be used to detect DIC ([[platelet]] count, PT, [[fibrinogen]], D‐dimer, [[antithrombin]] and [[protein C]] activity monitoring), but the diagnosis and subsequent treatment should be done clinically. <ref name="pmid19222477">{{cite journal| author=Levi M, Toh CH, Thachil J, Watson HG| title=Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. | journal=Br J Haematol | year= 2009 | volume= 145 | issue= 1 | pages= 24-33 | pmid=19222477 | doi=10.1111/j.1365-2141.2009.07600.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19222477  }} </ref>


=== Other hematological findings ===
== Other hematological findings ==


==== Leukocytosis ====
==== Leukocytosis ====

Revision as of 19:53, 22 June 2020

To go to the COVID-19 project topics list, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2], Ifrah Fatima, M.B.B.S[3],Shakiba Hassanzadeh, MD[4],Oluwabusola Fausat Adogba, MD[5]

Overview

The novel COVID-19 infection has multi-systemic complications. The most common hematologic complications of COVID-19 are lymphopenia, neutrophilia and thrombocytopenia. Some other hematological findings include: decrease in hemoglobin, coagulopathy, DIC and several other laboratory abnormalities.It is also suggested that blood group may have association to COVID infection.

Blood type and COVID-19

  • Two pre-print articles from China in early 2020 suggested the association of ABO blood group with a risk of COVID-19 infection- Blood group A was associated with a higher risk of infection and Blood Group O was associated with a lower risk. These studies were non-peer reviewed and had their own limitations. [1][2]
  • A more recent Genome-wide Association Study done in patients with severe respiratory failure (requiring mechanical ventilatory support) also found a higher risk of infection among people with blood group A, compared to non-A blood groups and a lower risk for blood group O as compared with non-O blood groups. [3]
  • However, once infected, blood group type does not seem to influence clinical outcome. [4]
  • The GWA study also identified the genetic susceptibility locus (3p21.31) that places patients at a higher risk for severe COVID-19 infection. [3]

Complications

Lymphopenia

There is an association between COVID-19 infection and lymphopenia.[5]There are four hypothetical mechanisms for this matter:[6][7]

Neutrophilia

  • The human body fights infections by recruiting neutrophils early to the sites of infection by oxidative burst and phagocytosis. [8]
  • New evidence suggests that the severe symptoms of COVID-19, including Acute Respiratory Distress Syndrome (ARDS), could be caused by Neutrophil Extracellular Traps (NETs). Acute Respiratory Distress Syndrome (ARDS), pulmonary inflammation, thick mucus secretions in the airways, extensive lung damage and blood clots are suggested to be as a result of the action of Neutrophils. When neutrophils detect pathogens, they can expel their DNA in a web laced with toxic enzymes (called a NET- Neutrophil Extracellular Trap) to attack them.
  • These NETs capture and digest the unwanted pathogen but in cases of ARDS (Covid-19 manifestation) they cause damage to the lungs and other organs. [9]
  • The neutrophil-to-lymphocyte ratio (NLR) has been identified as the independent risk factor for severe illness in patients with the 2019 novel coronavirus disease.[10] A higher NLR at hospital admission in patients has been associated with a more severe outcome. An NLR of >4 has been identified as a predictor of admission to the ICU.[11]

Thrombocytopenia

  • There is an association between severe COVID-19 infection and thrombocytopenia.[12]
  • Thrombocytopenia is seen in 57.7% of patients with severe COVID-19 infection compared to 31.6 % of patients with non-severe infection.[13]

The pathogenesis of thrombocytopenia in COVID-19 infection is due to several factors:[14]

  • Decrease in primary platelet production due to infection of bone marrow cells by coronaviruses[15] and inhibition of bone marrow growth,[16] which lead to abnormal hematopoietic function.[14]
  • Increase in platelet destruction due to increase in auto-antibodies and immune complexes.[17]
  • 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.[14][18]
  • In addition, decrease in platelets may be due to activation of platelets that result in platelet aggregation and formation of micro-thrombus which increase platelet consumption.[14][19]

Hemoglobin decrease

  • Although anemia is not a common finding in patients with COVID-19 infection, decrease in hemoglobin in patients with severe COVID-19 infection has been reported.[19][13]
  • The median hemoglobin is lower in patients with severe COVID-19 (12.8 g/dL) compared to patients with non-severe infection (13.5 g/dL).[13]
  • Pathophysiology:[19]

Coagulopathy

Pathophysiology

COVID-19 induces a hypercoagulable state in the body. An increased risk of mortality has been noted in patient’s with coagulopathy in COVID-19. [20]The factors that contribute to this state are-

Clinical Features

Thrombotic complications like: [21] [24]

Laboratory Findings

COVID-19 ARDS was found to have an association with procoagulants and acute phase reactants, unlike non-COVID ARDS. [25]

Coagulation testing: Pro-coagulant profile: [26]

TEG findings: [27]

  • Reaction time (R)- decreased
  • Clot formation time (K)- decreased
  • Maximum amplitude (MA) increased
  • Clot lysis at 30 minutes (LY30) reduced

Other findings:

COVID- 19 Coagulopathy and DIC

The main feature of COVID-19 coagulopathy is thrombosis while the acute phase of DIC presents with bleeding: [28]

Other hematological findings

Leukocytosis

  • Leukocytosis is seen in 11.4% of patients with severe COVID-19 infection compared to 4.8% of patients with non-severe infection.[13][30]
  • In patients with COVID-19 infection, leukocytosis may be an indication of bacterial infection or superinfection.[30]

Increase in C-reactive protein (CRP)  

  • Increase in CRP is seen in 81.5% of patients with severe COVID-19 infection compared to 56.4% of patients with non-severe infection.[13][30]
  • CRP is an acute phase reactant that increases in conditions with inflammation.[31]
  • In patients with COVID-19 infection, increase in CRP may be an indication of severe viral infection or sepsis and viremia.[30]

Increase in procalcitonin .

  • Increase in procalcitonin is seen in 13.7% of patients with severe COVID-19 infection compared to 3.7% of patients with non-severe infection.[13][30]
  • In sepsis, the activation and adherence of monocytes increase procalcitonin, therefore procalcitonin in a biomarker for sepsis and septic shock.[32]
  • In patients with COVID-19 infection, increase in procalcitonin may be an indication of bacterial infection or superinfection.[30]

Increase in ferritin

Increase in aspartate aminotransferase (AST)  

  • Increase in AST is seen in 39.4% of patients with severe COVID-19 infection compared to 18.2% of patients with non-severe infection.[13][30]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[30]

Increase in alanine aminotransferase (ALT)  

  • Increase in ALT is seen in 28.1% of patients with severe COVID-19 infection compared to 19.8% of patients with non-severe infection.[13][30]
  • ALT is produced by liver cells and is increased in liver conditions.[31]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[30]

Increase in lactate dehydrogenase (LDH)

  • Increase in LDH is seen in 58.1% of patients with severe COVID-19 infection compared to 37.2% of patients with non-severe infection.[13][30]
  • LDH is expressed in almost all cells and an increase in LDH could be seen in damage to any of the cell types.[31]
  • In patients with COVID-19 infection, increase in LDH may indicate injury to the lungs or multi-system damage.[30]

Increase in monocyte volume distribution width (MDW)

  • MDW (Beckman Coulter, Brea, CA, USA) was found to be increased in all patients with COVID-19 infection and particularly in those with the worst conditions.[30]

Increase in total bilirubin

  • Increase in total bilirubin is seen in 13.3% of patients with severe COVID-19 infection compared to 9.9% of patients with non-severe infection.[13][30]
  • Bilirubin  is produced by liver cells and increases in liver and biliray conditions.[31]
  • In patients with COVID-19 infection, increase in total bilirubin may indicate injury to the liver.[30]

Increase in creatinine

Increase in cardiac troponins

  • In myocardial infarction and acute coronary syndrome are used for diagnosis.[31]
  • In patients with COVID-19 infection, increase in cardiac troponins may indicate cardiac injury.[30]

Decrease in albumin

Increase in interleukin-6 (IL-6)

  • Increase in IL-6 has been reported to be associated with death in COVID-19 infection.[33]

References

  1. ↑ Zietz M, Tatonetti NP (2020). "Testing the association between blood type and COVID-19 infection, intubation, and death". medRxiv. doi:10.1101/2020.04.08.20058073. PMC 7276013 Check |pmc= value (help). PMID 32511586 Check |pmid= value (help).
  2. ↑ Zhao, Jiao; Yang, Yan; Huang, Hanping; Li, Dong; Gu, Dongfeng; Lu, Xiangfeng; Zhang, Zheng; Liu, Lei; Liu, Ting; Liu, Yukun; He, Yunjiao; Sun, Bin; Wei, Meilan; Yang, Guangyu; Wang, Xinghuan; Zhang, Li; Zhou, Xiaoyang; Xing, Mingzhao; Wang, Peng George (2020). doi:10.1101/2020.03.11.20031096. Missing or empty |title= (help)
  3. ↑ 3.0 3.1 Ellinghaus, David; Degenhardt, Frauke; Bujanda, Luis; Buti, Maria; Albillos, Agustín; Invernizzi, Pietro; Fernández, Javier; Prati, Daniele; Baselli, Guido; Asselta, Rosanna; Grimsrud, Marit M.; Milani, Chiara; Aziz, Fátima; Kässens, Jan; May, Sandra; Wendorff, Mareike; Wienbrandt, Lars; Uellendahl-Werth, Florian; Zheng, Tenghao; Yi, Xiaoli; de Pablo, Raúl; Chercoles, Adolfo G.; Palom, Adriana; Garcia-Fernandez, Alba-Estela; Rodriguez-Frias, Francisco; Zanella, Alberto; Bandera, Alessandra; Protti, Alessandro; Aghemo, Alessio; Lleo, Ana; Biondi, Andrea; Caballero-Garralda, Andrea; Gori, Andrea; Tanck, Anja; Carreras Nolla, Anna; Latiano, Anna; Fracanzani, Anna Ludovica; Peschuck, Anna; Julià, Antonio; Pesenti, Antonio; Voza, Antonio; Jiménez, David; Mateos, Beatriz; Nafria Jimenez, Beatriz; Quereda, Carmen; Paccapelo, Cinzia; Gassner, Christoph; Angelini, Claudio; Cea, Cristina; Solier, Aurora; Pestaña, David; Muñiz-Diaz, Eduardo; Sandoval, Elena; Paraboschi, Elvezia M.; Navas, Enrique; García Sánchez, Félix; Ceriotti, Ferruccio; Martinelli-Boneschi, Filippo; Peyvandi, Flora; Blasi, Francesco; Téllez, Luis; Blanco-Grau, Albert; Hemmrich-Stanisak, Georg; Grasselli, Giacomo; Costantino, Giorgio; Cardamone, Giulia; Foti, Giuseppe; Aneli, Serena; Kurihara, Hayato; ElAbd, Hesham; My, Ilaria; Galván-Femenia, Iván; Martín, Javier; Erdmann, Jeanette; Ferrusquía-Acosta, Jose; Garcia-Etxebarria, Koldo; Izquierdo-Sanchez, Laura; Bettini, Laura R.; Sumoy, Lauro; Terranova, Leonardo; Moreira, Leticia; Santoro, Luigi; Scudeller, Luigia; Mesonero, Francisco; Roade, Luisa; Rühlemann, Malte C.; Schaefer, Marco; Carrabba, Maria; Riveiro-Barciela, Mar; Figuera Basso, Maria E.; Valsecchi, Maria G.; Hernandez-Tejero, María; Acosta-Herrera, Marialbert; D’Angiò, Mariella; Baldini, Marina; Cazzaniga, Marina; Schulzky, Martin; Cecconi, Maurizio; Wittig, Michael; Ciccarelli, Michele; Rodríguez-Gandía, Miguel; Bocciolone, Monica; Miozzo, Monica; Montano, Nicola; Braun, Nicole; Sacchi, Nicoletta; Martínez, Nilda; Özer, Onur; Palmieri, Orazio; Faverio, Paola; Preatoni, Paoletta; Bonfanti, Paolo; Omodei, Paolo; Tentorio, Paolo; Castro, Pedro; Rodrigues, Pedro M.; Blandino Ortiz, Aaron; de Cid, Rafael; Ferrer, Ricard; Gualtierotti, Roberta; Nieto, Rosa; Goerg, Siegfried; Badalamenti, Salvatore; Marsal, Sara; Matullo, Giuseppe; Pelusi, Serena; Juzenas, Simonas; Aliberti, Stefano; Monzani, Valter; Moreno, Victor; Wesse, Tanja; Lenz, Tobias L.; Pumarola, Tomas; Rimoldi, Valeria; Bosari, Silvano; Albrecht, Wolfgang; Peter, Wolfgang; Romero-Gómez, Manuel; D’Amato, Mauro; Duga, Stefano; Banales, Jesus M.; Hov, Johannes R; Folseraas, Trine; Valenti, Luca; Franke, Andre; Karlsen, Tom H. (2020). "Genomewide Association Study of Severe Covid-19 with Respiratory Failure". New England Journal of Medicine. doi:10.1056/NEJMoa2020283. ISSN 0028-4793.
  4. ↑ "The effects of blood group types on the risk of COVID-19 infection and its clinical outcome". TURKISH JOURNAL OF MEDICAL SCIENCES. 2020. doi:10.3906/sag-2005-395. ISSN 1303-6165.
  5. ↑ Tan, Li; Wang, Qi; Zhang, Duanyang; Ding, Jinya; Huang, Qianchuan; Tang, Yi-Quan; Wang, Qiongshu; Miao, Hongming (2020). "Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study". Signal Transduction and Targeted Therapy. 5 (1). doi:10.1038/s41392-020-0148-4. ISSN 2059-3635.
  6. ↑ Fischer, Karin; Hoffmann, Petra; Voelkl, Simon; Meidenbauer, Norbert; Ammer, Julia; Edinger, Matthias; Gottfried, Eva; Schwarz, Sabine; Rothe, Gregor; Hoves, Sabine; Renner, Kathrin; Timischl, Birgit; Mackensen, Andreas; Kunz-Schughart, Leoni; Andreesen, Reinhard; Krause, Stefan W.; Kreutz, Marina (2007). "Inhibitory effect of tumor cell–derived lactic acid on human T cells". Blood. 109 (9): 3812–3819. doi:10.1182/blood-2006-07-035972. ISSN 0006-4971.
  7. ↑ Liao, Yuan-Chun; Liang, Wei-Guang; Chen, Feng-Wei; Hsu, Ju-Hui; Yang, Jiann-Jou; Chang, Ming-Shi (2002). "IL-19 Induces Production of IL-6 and TNF-α and Results in Cell Apoptosis Through TNF-α". The Journal of Immunology. 169 (8): 4288–4297. doi:10.4049/jimmunol.169.8.4288. ISSN 0022-1767.
  8. ↑ "Targeting potential drivers of COVID-19: Neutrophil extracellular traps | Journal of Experimental Medicine | Rockefeller University Press".
  9. ↑ "Severe COVID-19 symptoms may be caused by overactive neutrophils".
  10. ↑ "Neutrophil-to-Lymphocyte Ratio Predicts Severe Illness Patients with 2019 Novel Coronavirus in the Early Stage | medRxiv".
  11. ↑ Akagi Y, Itoi M, Sano Y, Andonian MR, Barrett AS, Vinogradov SN, Moroi K, Sato T, Gheorghescu B, Baghurst PA, Nichol LW, Rainsford KD, Akagi Y, Itoi M, Sano Y (August 1980). "[Monoaminergic neurons of monkey retina (author's transl)]". Nippon Ganka Gakkai Zasshi (in Japanese). 84 (8): 771–80. doi:10.1016/0005-2795(75)90035-5. PMID 7211594.
  12. ↑ 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).
  13. ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 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).
  14. ↑ 14.0 14.1 14.2 14.3 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).
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 19.0 19.1 19.2 19.3 19.4 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).
  20. ↑ Tang N, Li D, Wang X, Sun Z (2020). "Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia". J Thromb Haemost. 18 (4): 844–847. doi:10.1111/jth.14768. PMC 7166509 Check |pmc= value (help). PMID 32073213 Check |pmid= value (help).
  21. ↑ 21.0 21.1 Becker RC (2020). "COVID-19 update: Covid-19-associated coagulopathy". J Thromb Thrombolysis. doi:10.1007/s11239-020-02134-3. PMC 7225095 Check |pmc= value (help). PMID 32415579 Check |pmid= value (help).
  22. ↑ Maier CL, Truong AD, Auld SC, Polly DM, Tanksley CL, Duncan A (2020). "COVID-19-associated hyperviscosity: a link between inflammation and thrombophilia?". Lancet. 395 (10239): 1758–1759. doi:10.1016/S0140-6736(20)31209-5. PMC 7247793 Check |pmc= value (help). PMID 32464112 Check |pmid= value (help).
  23. ↑ 23.0 23.1 Bowles L, Platton S, Yartey N, Dave M, Lee K, Hart DP; et al. (2020). "Lupus Anticoagulant and Abnormal Coagulation Tests in Patients with Covid-19". N Engl J Med. doi:10.1056/NEJMc2013656. PMC 7217555 Check |pmc= value (help). PMID 32369280 Check |pmid= value (help).
  24. ↑ Barrett CD, Moore HB, Yaffe MB, Moore EE (2020). "ISTH interim guidance on recognition and management of coagulopathy in COVID-19: A comment". J Thromb Haemost. doi:10.1111/jth.14860. PMID 32302462 Check |pmid= value (help).
  25. ↑ 25.0 25.1 "Correction". Circulation. 131 (24): e535. 2015. doi:10.1161/CIR.0000000000000219. PMID 26078378.
  26. ↑ Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M; et al. (2020). "The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome". J Thromb Haemost. doi:10.1111/jth.14854. PMID 32302448 Check |pmid= value (help).
  27. ↑ Panigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V; et al. (2020). "Hypercoagulability of COVID-19 patients in Intensive Care Unit. A Report of Thromboelastography Findings and other Parameters of Hemostasis". J Thromb Haemost. doi:10.1111/jth.14850. PMID 32302438 Check |pmid= value (help).
  28. ↑ Levi M, Thachil J, Iba T, Levy JH (2020). "Coagulation abnormalities and thrombosis in patients with COVID-19". Lancet Haematol. 7 (6): e438–e440. doi:10.1016/S2352-3026(20)30145-9. PMC 7213964 Check |pmc= value (help). PMID 32407672 Check |pmid= value (help).
  29. ↑ Levi M, Toh CH, Thachil J, Watson HG (2009). "Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology". Br J Haematol. 145 (1): 24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.
  30. ↑ 30.00 30.01 30.02 30.03 30.04 30.05 30.06 30.07 30.08 30.09 30.10 30.11 30.12 30.13 30.14 30.15 30.16 30.17 30.18 Lippi G, Plebani M (2020). "The critical role of laboratory medicine during coronavirus disease 2019 (COVID-19) and other viral outbreaks". Clin Chem Lab Med. 58 (7): 1063–1069. doi:10.1515/cclm-2020-0240. PMID 32191623 Check |pmid= value (help).
  31. ↑ 31.0 31.1 31.2 31.3 31.4 31.5 31.6 Frater JL, Zini G, d'Onofrio G, Rogers HJ (2020). "COVID-19 and the clinical hematology laboratory". Int J Lab Hematol. 42 Suppl 1: 11–18. doi:10.1111/ijlh.13229. PMC 7264622 Check |pmc= value (help). PMID 32311826 Check |pmid= value (help).
  32. ↑ Meisner M (2014). "Update on procalcitonin measurements". Ann Lab Med. 34 (4): 263–73. doi:10.3343/alm.2014.34.4.263. PMC 4071182. PMID 24982830.
  33. ↑ 33.0 33.1 Wu C, Chen X, Cai Y, Xia J, Zhou X, Xu S; et al. (2020). "Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China". JAMA Intern Med. doi:10.1001/jamainternmed.2020.0994. PMC 7070509 Check |pmc= value (help). PMID 32167524 Check |pmid= value (help).
  34. ↑ Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z; et al. (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. PMC 7270627 Check |pmc= value (help). PMID 32171076 Check |pmid= value (help).
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