The values of coagulation function in COVID-19 patients

Abstract

Objective To investigate the blood coagulation function in COVID-19 patients, and the correlation between coagulopathy and disease severity. Methods We retrospectively collected 147 clinically diagnosed COVID-19 patients at Wuhan Leishenshan Hospital of Hubei, China. We analyzed the coagulation function in COVID-19 patients through the data including thrombin-antithrombin complex (TAT), α2-plasmininhibitor-plasmin Complex (PIC), thrombomodulin (TM), t-PA/PAI-1 Complex (t-PAIC), prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (APTT), fibrinogen (FIB), thrombin time (TT), D-Dimer (DD), and platelet (PLT). Result The levels of TAT, PIC, TM, t-PAIC, PT, INR, FIB, and DD in COVID-19 patients were higher than health controls (p<0.05), and also higher in the patients with thrombotic disease than without thrombotic disease (p<0.05). What’s more, the patients with thrombotic disease had a higher case-fatality (p<0.05). TAT, PIC, TM, t-PAIC, PT, INR, APTT, FIB, DD, and PLT were also found correlated with disease severity. Meanwhile, we found that there were significant difference in TAT, TM, t-PAIC, PT, INR, APTT, DD, and PLT in the death and survival group. Further using univariate and multivariate logistic regression analysis also found that t-PAIC and DD were independent risk factors for death in patients and are excellent predicting the mortality risk of COVID-19. Conclusion Most COVID-19 patients with inordinate coagulation systems, dynamic monitoring of coagulation parameters might be a key in the control of COVID-19 death.

High levels of plasminogen activator inhibitor-1, tissue plasminogen activator and fibrinogen in patients with severe COVID-19

“…Nevertheless, the group of severe COVID- 19 patients studied here can be considered as a representative sample from the peak of the first wave of COVID-19. The reproducible nature of these findings in a variety of different medical centers (Jin et al ., 2020; Nougier et al ., 2020; Zuo et al ., 2020) supports the idea that changes in PAI-1 and fibrinogen, in particular, represent robust and universal biomarkers for COVID-19 that can be assessed in the ICU setting. Given the small size of our study, it remains unclear whether the changes in these biomarkers, and in the abnormal coagulation measured by ROTEM (Roh et al ., 2020) is related to the incidence of thrombosis, myocardial infarction, stroke, renal failure and a variety of long-term complications in these patients.…”

COVID-19 patient plasma demonstrates resistance to tPA-induced fibrinolysis as measured by thromboelastography

“…One plausible explanation is that there are increased levels of fibrinolytic inhibitors present. Plasminogen activator inhibitor-1 (PAI-1), for example, has been shown to be elevated in these patients [ 17 ]. The mechanism is thought to be due to the downregulation of angiotensin converting enzyme by the coronavirus (SARS-CoV-2), leading to increased levels of angiotensin II, an inducer of PAI-1 in endothelial cells [ 18 ].…”

Understanding the andromeda strain – The role of cytokine release, coagulopathy and antithrombin III in SARS-CoV2 critical illness

“…More specific markers of thrombin formation and antithrombin consumption include Thrombin-antithrombin complexes (TAT) [ 80 ]; TAT may also be a signal to the immunothrombosis of the sepsis syndrome and correspond to severity of sepsis and tissue hypoxia [ 80 ]. and recent work by Jin et al have shown that TAT correlates with disease severity in COVID-19 and differs significantly from levels reported in non-survivors (p< .5) [ 81 ]. D-dimer, however, appears to be a widely-accepted predictor of poor survival in SARS-CoV2 and more studies are needed to understand how AT levels on admission and serial measurements influence COVID-19 related coagulopathy and death.…”