Coagulopathy in patients with COVID-19: a systematic review and meta-analysis

Abstract

COVID-19 patients frequently exhibit coagulation abnormalities and thrombotic events. In this meta-analysis, we investigated the association between coagulopathy and the severity of COVID-19 illness. Using PubMed, Embase, Cochrane, WanFang Database, CNKI, and medRxiv, a systematic literature search was conducted for studies published between December 1, 2019 and May 1, 2020. We then analyzed coagulation parameters in COVID-19 patients exhibiting less severe and more severe symptoms. All statistical analyses were performed using Stata14.0 software. A total of 3,952 confirmed COVID-19 patients from 25 studies were included in the meta-analysis. Patients with severe symptoms exhibited higher levels of D-dimer, prothrombin time (PT), and fibrinogen (FIB) than patients with less severe symptoms (SMD 0.83, 95% CI: 0.70-0.97, I 2 56.9%; SMD 0.39, 95% CI: 0.14-0.64, I 2 79.4%; and SMD 0.35, 95% CI: 0.17-0.53, I 2 42.4%, respectively). However, platelet and activated partial thromboplastin times did not differ (SMD -0.26, 95% CI: -0.56-0.05, I 2 82.2%; and SMD -0.14, 95% CI: -0.45-0.18, I 2 75.7%, respectively). These findings demonstrate that hypercoagulable coagulopathy is associated with the severity of COVID-19 symptoms and that D-dimer, PT, and FIB values are the main parameters that should be considered when evaluating coagulopathy in COVID-19 patients. AUTHOR CONTRIBUTIONSStudy conception and design: Xiaolin Zhang. Data acquisition: Xiaolin Zhang, Xue Yang. Statistical analysis: Xiaolin Zhang.

Genome‐wide screening of SARS‐CoV‐2 infection‐related genes based on the blood leukocytes sequencing data set of patients with COVID‐19

“…These results showed that the model has a good predictive ability, and the predictive ability of the model was higher than that of individual genes. Previous studies have shown that C‐reactive protein, ferritin, fibrinogen, d ‐dimer, lactate, and procalcitonin are common clinical indicators associated with SARS‐CoV‐2 infection and severity, which can assist in the diagnosis and treatment of COVID‐19 22–25 . The diagnostic ability of our model is also higher than these clinical indicators in the same data set.…”

COVID-19-associated acute respiratory distress syndrome (CARDS): Current knowledge on pathophysiology and ICU treatment – A narrative review

“…Pooled mortality among patients with vs. without thromboembolic events was 23% (95% CI: 14%–32%) vs. 13% (95% CI: 6%–22%) [ 71 ]. Although the exact underlying pathophysiology that leads to COVID-19-associated coagulopathy is not fully understood, it appears that endotheliopathy, vasoocclusion/stasis, and inflammation-associated activation of coagulation contribute to the respective complications [ [72] , [73] , [74] ].…”

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“…The second form of systemic pathology is hypercoagulation, resulting in microthrombus formation and, somewhat counterintuitively, bleeding (Al-Samkari et al, 2020; Bryce et al, 2020). While sharing features with the more commonly known disseminated intravascular coagulation (DIC), COVID-induced hypercoagulability exhibits unique aspects including preserved levels of circulating fibrinogen and massively increased levels of von Willebrand factor from activated or damaged endothelial cells (Ward et al, 2020; Zhang et al, 2020). The clinical ramifications are that COVID-19 patients have a dramatically increased risk of stroke, myocardial infarction, pulmonary and deep venous thromboembolism, and major hemorrhage (Helms et al, 2020b; Castro and Frishman, 2021).…”