Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19
Coagulopathy is a frequently reported finding in the pathology of coronavirus disease 2019 (COVID-19); however, the molecular mechanism, the involved coagulation factors, and the role of regulatory proteins in homeostasis are not fully investigated. We explored the dynamic changes of nine coagulatio...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-12-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2021.762782/full |
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| author | Daniel Elieh Ali Komi Yaghoub Rahimi Rahim Asghari Reza Jafari Reza Jafari Javad Rasouli Mehdi Mohebalizadeh Ata Abbasi Rahim Nejadrahim Farzin Rezazadeh Vahid Shafiei-Irannejad |
| author_facet | Daniel Elieh Ali Komi Yaghoub Rahimi Rahim Asghari Reza Jafari Reza Jafari Javad Rasouli Mehdi Mohebalizadeh Ata Abbasi Rahim Nejadrahim Farzin Rezazadeh Vahid Shafiei-Irannejad |
| author_sort | Daniel Elieh Ali Komi |
| collection | DOAJ |
| description | Coagulopathy is a frequently reported finding in the pathology of coronavirus disease 2019 (COVID-19); however, the molecular mechanism, the involved coagulation factors, and the role of regulatory proteins in homeostasis are not fully investigated. We explored the dynamic changes of nine coagulation tests in patients and controls to propose a molecular mechanism for COVID-19-associated coagulopathy. Coagulation tests including prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen (FIB), lupus anticoagulant (LAC), proteins C and S, antithrombin III (ATIII), D-dimer, and fibrin degradation products (FDPs) were performed on plasma collected from 105 individuals (35 critical patients, 35 severe patients, and 35 healthy controls). There was a statically significant difference when the results of the critical (CRT) and/or severe (SVR) group for the following tests were compared to the control (CRL) group: PTCRT (15.014) and PTSVR (13.846) (PTCRL = 13.383, p < 0.001), PTTCRT (42.923) and PTTSVR (37.8) (PTTCRL = 36.494, p < 0.001), LACCRT (49.414) and LACSVR (47.046) (LACCRL = 40.763, p < 0.001), FIBCRT (537.66) and FIBSVR (480.29) (FIBCRL = 283.57, p < 0.001), ProCCRT (85.57%) and ProCSVR (99.34%) (ProCCRL = 94.31%, p = 0.04), ProSCRT (62.91%) and ProSSVR (65.06%) (ProSCRL = 75.03%, p < 0.001), D-dimer (p < 0.0001, χ2 = 34.812), and FDP (p < 0.002, χ2 = 15.205). No significant association was found in the ATIII results in groups (ATIIICRT = 95.71% and ATIIISVR = 99.63%; ATIIICRL = 98.74%, p = 0.321). D-dimer, FIB, PT, PTT, LAC, protein S, FDP, and protein C (ordered according to p-values) have significance in the prognosis of patients. Disruptions in homeostasis in protein C (and S), VIII/VIIIa and V/Va axes, probably play a role in COVID-19-associated coagulopathy. |
| first_indexed | 2024-12-13T21:21:04Z |
| format | Article |
| id | doaj.art-9d337e7a90eb4d0bb66a6744827d4728 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-13T21:21:04Z |
| publishDate | 2021-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-9d337e7a90eb4d0bb66a6744827d47282022-12-21T23:31:07ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-12-011210.3389/fimmu.2021.762782762782Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19Daniel Elieh Ali Komi0Yaghoub Rahimi1Rahim Asghari2Reza Jafari3Reza Jafari4Javad Rasouli5Mehdi Mohebalizadeh6Ata Abbasi7Rahim Nejadrahim8Farzin Rezazadeh9Vahid Shafiei-Irannejad10Cellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, IranCellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, IranHematology, Immune Cell Therapy, and Stem Cells Transplantation Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, IranHematology, Immune Cell Therapy, and Stem Cells Transplantation Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, IranNephrology and Kidney Transplant Research Center, Clinical Research Institute, Urmia University of Medical Sciences, Urmia, IranDepartment of Epidemiology and Biostatistics, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, IranStudent Research Committee, Urmia University of Medical Sciences, Urmia, IranDepartment of Pathology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, IranDepartment of Infectious Diseases, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, IranDepartment of Emergency Medicine, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, IranCellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, IranCoagulopathy is a frequently reported finding in the pathology of coronavirus disease 2019 (COVID-19); however, the molecular mechanism, the involved coagulation factors, and the role of regulatory proteins in homeostasis are not fully investigated. We explored the dynamic changes of nine coagulation tests in patients and controls to propose a molecular mechanism for COVID-19-associated coagulopathy. Coagulation tests including prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen (FIB), lupus anticoagulant (LAC), proteins C and S, antithrombin III (ATIII), D-dimer, and fibrin degradation products (FDPs) were performed on plasma collected from 105 individuals (35 critical patients, 35 severe patients, and 35 healthy controls). There was a statically significant difference when the results of the critical (CRT) and/or severe (SVR) group for the following tests were compared to the control (CRL) group: PTCRT (15.014) and PTSVR (13.846) (PTCRL = 13.383, p < 0.001), PTTCRT (42.923) and PTTSVR (37.8) (PTTCRL = 36.494, p < 0.001), LACCRT (49.414) and LACSVR (47.046) (LACCRL = 40.763, p < 0.001), FIBCRT (537.66) and FIBSVR (480.29) (FIBCRL = 283.57, p < 0.001), ProCCRT (85.57%) and ProCSVR (99.34%) (ProCCRL = 94.31%, p = 0.04), ProSCRT (62.91%) and ProSSVR (65.06%) (ProSCRL = 75.03%, p < 0.001), D-dimer (p < 0.0001, χ2 = 34.812), and FDP (p < 0.002, χ2 = 15.205). No significant association was found in the ATIII results in groups (ATIIICRT = 95.71% and ATIIISVR = 99.63%; ATIIICRL = 98.74%, p = 0.321). D-dimer, FIB, PT, PTT, LAC, protein S, FDP, and protein C (ordered according to p-values) have significance in the prognosis of patients. Disruptions in homeostasis in protein C (and S), VIII/VIIIa and V/Va axes, probably play a role in COVID-19-associated coagulopathy.https://www.frontiersin.org/articles/10.3389/fimmu.2021.762782/fullCOVID-19coagulopathyfibrinogenprotein C (PC)protein Santithrombin III (ATIII) |
| spellingShingle | Daniel Elieh Ali Komi Yaghoub Rahimi Rahim Asghari Reza Jafari Reza Jafari Javad Rasouli Mehdi Mohebalizadeh Ata Abbasi Rahim Nejadrahim Farzin Rezazadeh Vahid Shafiei-Irannejad Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 Frontiers in Immunology COVID-19 coagulopathy fibrinogen protein C (PC) protein S antithrombin III (ATIII) |
| title | Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 |
| title_full | Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 |
| title_fullStr | Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 |
| title_full_unstemmed | Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 |
| title_short | Investigation of the Molecular Mechanism of Coagulopathy in Severe and Critical Patients With COVID-19 |
| title_sort | investigation of the molecular mechanism of coagulopathy in severe and critical patients with covid 19 |
| topic | COVID-19 coagulopathy fibrinogen protein C (PC) protein S antithrombin III (ATIII) |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2021.762782/full |
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