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Coronavirus disease 2019 and coagulopathy: other prothrombotic coagulation factors
Maria-Teresa Calderon-Lopez1, Natalia Garcia-Leon1, Sergio Gomez-Arevalillo2
1Department of Hematology and Hemotherapy.
Insights
This study reveals that patients with coronavirus disease 2019 (COVID-19) exhibit a hypercoagulable state, characterized by abnormal coagulation parameters and increased thrombotic risk. These findings help explain microvascular thrombosis in COVID-19 patients.
Area of Science:
- Hematology
- Infectious Diseases
- Critical Care Medicine
Background:
- Coagulopathy is increasingly recognized in coronavirus disease 2019 (COVID-19) patients.
- Existing research often focuses primarily on D-dimer levels.
Purpose of the Study:
- To investigate a broader range of coagulation parameters in COVID-19 patients.
- To assess for a potential hypercoagulable state.
- To evaluate platelet function, specifically closure times.
Main Methods:
- Analysis of coagulation samples from 80 hospitalized COVID-19 patients.
- Assessment of platelet function using closure times in a subset of patients.
Main Results:
- Elevated D-dimer (96.2%), fibrinogen (75.2%), and factor VIII (86%) were common.
- Decreased protein S (up to 62.5%), protein C (7.6%), factor XII (25.3%), and antithrombin activity (21%) were observed.
- Short platelet closure times occurred in 20-40% of samples, indicating heightened platelet reactivity.
- Fifteen percent of patients experienced thrombotic events, all with abnormal coagulation markers.
Conclusions:
- COVID-19 patients demonstrate a significant hypercoagulable state.
- Abnormalities in coagulation parameters and platelet function contribute to increased thrombotic risk.
- Findings support the link between COVID-19-induced inflammation and microvascular thrombosis.
Abstract:
There is an increasing evidence supporting the existence of coagulopathy in coronavirus disease 2019 (COVID-19) patients. Most of reports are mainly focused on d-dimer. Our objective is to describe coagulation parameters in these patients that could be involved in a hypercoagulate state and to test platelet function to see if there are short closure times. We analyzed coagulation samples from 80 patients admitted with COVID-19 in our hospital. We also tested platelet function by closure times in a small subgroup of patients. Most of samples had increased d-dimer (96.2%) (median of d-dimer: 1158 ng/ml FEU), increased fibrinogen (75.2%) (median: 5.23 g/l), increased factor VIII (86%) (median: 264.8 U/dl), decreased protein S (22.5% of women, 62.5% of men) (median: 62.8 and 68.5 U/dl, respectively), decreased protein C (7.6%) (median: 100 U/dl), decreased factor XII (25.3%) (median: 90.3 U/dl) and decreased antithrombin activity (21%) (median: 86 U/dl). International normalized ratio was higher than normal in 24 patients (30%) (median: 1.13). The activated partial thromboplastin time ratio was below the normal range in nine patients (11.2%) and above normal in three (3.75%) (median: 0.93). The closure times were short in the 20% and 40% of samples of collagen and ADP and collagen and epinephrine, respectively. Twelve of the 80 patients (15%) had a thrombotic event and all had several abnormal coagulation parameters related with increased thrombotic risk. The results of this study support a hypercoagulability state in COVID-19 patients and it may help to explain the microvascular thrombosis caused by the inflammatory response.
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