tetano
Editor, Senior Moderator
Blood Rev
. 2020 Aug 24;100745.
doi: 10.1016/j.blre.2020.100745. Online ahead of print.
Coagulation dysfunction in COVID-19: The interplay between inflammation, viral infection and the coagulation system
Maria Grazia Lazzaroni[SUP] 1 [/SUP], Silvia Piantoni[SUP] 2 [/SUP], Stefania Masneri[SUP] 3 [/SUP], Emirena Garrafa[SUP] 4 [/SUP], Giuliana Martini[SUP] 5 [/SUP], Angela Tincani[SUP] 6 [/SUP], Laura Andreoli[SUP] 7 [/SUP], Franco Franceschini[SUP] 8 [/SUP]
Affiliations
Abstract
COVID-19 is a new pandemic, caused by Severe Acute Respiratory Syndrome-CoronaVirus-2 (SARS-Cov2) infection and characterized by a broad spectrum of clinical manifestations. Inflammation and the innate immune system have been recently recognized as pivotal players in the most severe forms, characterized by significantly elevated levels of pro-inflammatory cytokines. In this setting, several studies have also reported the presence of abnormalities in coagulation parameters and platelets count, possibly identifying a subgroup of patients with poor prognosis. Some reports of full-blown thromboembolic events are emerging. Among the possible mechanisms underlying coagulation dysfunction, the so-called "cytokine storm" seems to play a pivotal role. Other candidate factors include virus-specific mechanisms, related to the virus interaction with renin angiotensin system (RAS) and the fibrinolytic pathway, but also comorbidities affecting these patients. Coagulation dysfunction is therefore a candidate risk factor for adverse outcomes in COVID-19 and should be carefully addressed in clinical practice.
Keywords: COVID-19; Coagulation; Inflammation; SARS-CoV2; Thrombosis.
. 2020 Aug 24;100745.
doi: 10.1016/j.blre.2020.100745. Online ahead of print.
Coagulation dysfunction in COVID-19: The interplay between inflammation, viral infection and the coagulation system
Maria Grazia Lazzaroni[SUP] 1 [/SUP], Silvia Piantoni[SUP] 2 [/SUP], Stefania Masneri[SUP] 3 [/SUP], Emirena Garrafa[SUP] 4 [/SUP], Giuliana Martini[SUP] 5 [/SUP], Angela Tincani[SUP] 6 [/SUP], Laura Andreoli[SUP] 7 [/SUP], Franco Franceschini[SUP] 8 [/SUP]
Affiliations
- PMID: 32868115
- DOI: 10.1016/j.blre.2020.100745
Abstract
COVID-19 is a new pandemic, caused by Severe Acute Respiratory Syndrome-CoronaVirus-2 (SARS-Cov2) infection and characterized by a broad spectrum of clinical manifestations. Inflammation and the innate immune system have been recently recognized as pivotal players in the most severe forms, characterized by significantly elevated levels of pro-inflammatory cytokines. In this setting, several studies have also reported the presence of abnormalities in coagulation parameters and platelets count, possibly identifying a subgroup of patients with poor prognosis. Some reports of full-blown thromboembolic events are emerging. Among the possible mechanisms underlying coagulation dysfunction, the so-called "cytokine storm" seems to play a pivotal role. Other candidate factors include virus-specific mechanisms, related to the virus interaction with renin angiotensin system (RAS) and the fibrinolytic pathway, but also comorbidities affecting these patients. Coagulation dysfunction is therefore a candidate risk factor for adverse outcomes in COVID-19 and should be carefully addressed in clinical practice.
Keywords: COVID-19; Coagulation; Inflammation; SARS-CoV2; Thrombosis.