Zika and Chikungunya Virus and Risk for Venous Thromboembolism

Abstract

A variety of viral infections are associated with hypercoagulable states and may be linked to the development of deep venous thrombosis and pulmonary embolism. The Zika and Chikungunya viral infections spread through the South and Central American continents, moving to North America in 2016, with severe cases of polyarthralgia, fever, and Guillain-Barré syndrome leading eventually to death. A decreased trend for both infections was reported in the first quarter of 2017. In this article, we report the possible association of venous thromboembolic events associated with Zika infection. After 2 cases of deep venous thrombosis in patients with acute Zika infections, D-dimer levels were measured in 172 consecutive patients who presented to the emergency department of a university hospital in an endemic region of Brazil with either Zika or Chikungunya infections confirmed by polymerase chain reaction tests. D-dimer levels were increased in 19.4% of 31 patients with Zika and in 63.8% of 141 patients with Chikungunya infections. The mechanisms behind this association are yet to be elucidated as well as the potential for venous thromboembolism prevention strategies for in-hospital patients affected by Zika and Chikungunya infections.

COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up

“…Nevertheless, it is yet unknown whether these hemostatic changes are a specific effect of SARS-CoV-2 or are a consequence of cytokine storm that precipitates the onset of systemic inflammatory response syndrome (SIRS), as observed in other viral disease (30)(31)(32)(33). Another consideration which has not yet been investigated is that the hemostatic changes seen with COVID-19 infection are related to liver dysfunction (34).…”

The compelling arguments for the need of microvascular investigation in COVID-19 critical patients

“…Finally, the EC regulates hemostasis via the production of the von Willebrand factor (VWF), tissue factor (TF), and plasminogen activator inhibitor type 1 (PAI-1) [36]. The VWF binds platelets to collagen components once ECs have been destroyed [9]; TF interacting with the factor VII, activates the factors IX and X; the PAI-1 regulates fibrinolysis by inhibiting tissue plasminogen activator [37][38][39]. The ECs activate also the protein C via thrombomodulin and endothelial protein C receptor, which inhibits factor V, factor VIII, and PAI-1 [40].…”

ACE2: THE DOORWAY TO SARS-CoV-2

“…The high expression of ACE2 in endothelial cells and the exposition to SARS-CoV-2 may generate an environment of constant inflammatory changes reflecting other clinical markers indicative of immune response such as leukocytosis (mainly neutrophilia), thrombocytopenia [90], endothelial damage and activation leading to thrombosis and critical illness [91] as seen in other viral infections [92,93] but at a higher frequency in COVID-19 [91,94].…”