Abstract
Coronavirus disease 2019 (COVID-19) is a highly contagious disease that appeared in China in December 2019 and spread rapidly around the world. Several patients with severe COVID-19 infection can develop a coagulopathy according to the ISTH criteria for disseminated intravascular coagulopathy (DIC) with fulminant activation of coagulation, resulting in widespread microvascular thrombosis and consumption of coagulation factors. We conducted a meta-analysis in order to explore differences in coagulopathy indices in patients with severe and non-severe COVID-19. An electronic search was performed within PubMed, Google Scholar and Scopus electronic databases between December 2019 (first confirmed Covid-19 case) up to April 6th, 2020. The primary endpoint was the difference of D-dimer values between Non-Severe vs Severe disease and Survivors vs Non-Survivors. Furthermore, results on additional coagulation parameters (platelet count, prothrombin time, activated partial thromboplastin time) were also analyzed. The primary analysis showed that mean d-dimer was significantly lower in COVID-19 patients with non-severe disease than in those with severe (SMD − 2.15 [− 2.73 to − 1.56], I2 98%, P < 0.0001). Similarly, we found a lower mean d-dimer in Survivors compared to Non-Survivors (SMD − 2.91 [− 3.87 to − 1.96], I2 98%, P < 0.0001). Additional analysis of platelet count showed higher levels of mean PLT in Non-Severe patients than those observed in the Severe group (SMD 0.77 [0.32 to 1.22], I2 96%, P < 0.001). Of note, a similar result was observed even when Survivors were compared to Non-Survivors (SMD 1.84 [1.16 to 2.53], I2 97%, P < 0.0001). Interestingly, shorter mean PT was found in both Non-Severe (SMD − 1.34 [− 2.06 to − 0.62], I2 98%, P < 0.0002) and Survivors groups (SMD − 1.61 [− 2.69 to − 0.54], I2 98%, P < 0.003) compared to Severe and Non-Survivor patients. In conclusion, the results of the present meta-analysis demonstrate that Severe COVID-19 infection is associated with higher D-dimer values, lower platelet count and prolonged PT. This data suggests a possible role of disseminated intravascular coagulation in the pathogenesis of COVID-19 disease complications.
Highlights
Coronavirus Disease 2019 (COVID-19), caused by a novel coronavirus (SARS-CoV-2), is a highly contagious disease that appeared in Wuhan, Hubei province of China in December 2019 and spread rapidly in China and even around the world[1]
Several patients with severe COVID-19 infection can develop a coagulopathy according to the International Society on Thrombosis and Haemostasis (ISTH) criteria for disseminated intravascular coagulopathy (DIC) with fulminant activation of coagulation[4], resulting in widespread microvascular thrombosis and consumption of coagulation factors (Fig. 1)
This study aims to summarize all available data on coagulation parameters in COVID-19 patients, platelet count, Prothrombin Time (PT), D-dimer, and fibrinogen as suggested from the ISTH Interim Guidance on recognition and management of coagulopathy in COVID‐1912, and to perform a meta-analysis to assess differences in coagulopathy indices in different stages of COVID-19 disease
Summary
Coronavirus Disease 2019 (COVID-19), caused by a novel coronavirus (SARS-CoV-2), is a highly contagious disease that appeared in Wuhan, Hubei province of China in December 2019 and spread rapidly in China and even around the world[1]. Several patients with severe COVID-19 infection can develop a coagulopathy according to the International Society on Thrombosis and Haemostasis (ISTH) criteria for disseminated intravascular coagulopathy (DIC) with fulminant activation of coagulation[4], resulting in widespread microvascular thrombosis and consumption of coagulation factors (Fig. 1). The resulting hyper thrombotic state carries unique hallmarks, in a certain grade overlapping with DIC, that need to be fully discovered yet. The attention on this aspect is so high that it has been postulated that the COVID19, previously considered mainly as a respiratory disease, could be instead defined in his most severe form an endothelial disease[7]
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