Can fibrinolytic therapy be clinically useful in severe pneumonia caused by COVID-19?

The clinical course of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) meets the criteria for Acute Respiratory Distress Syndrome (ARDS) in many patients, the unfavorable course of which ultimately leads rapidly to death.

In cases with fatal outcome, the pathophysiology of ARDS has been related to a hyperimmune reaction that increases the progressive worsening of lung function [1]. SARS-CoV-2 enters into alveolar epithelial cells through ACE2 surface receptors (also present in enterocytes, endothelial cells, and smooth muscle arteries) [2].

During the hyperimmune inflammatory reaction, activation of complement leads to the formation of C3a and C5a that elicit recruitment of lymphocytes, macrophages, monocytes, and neutrophils, responsible in turn for the massive local release of proinflammatory cytokines IL-1, IL-6, IL-8 and interferon-γ [3].

In addition, leukocytes mobilized at the injury site exert a potent proinflammatory effect, causing extensive vascular-endothelial damage, alveolar epithelial cell damage, and microvascular thrombosis [4].

CITA DEL ARTÍCULO  J Thromb Thrombolysis. 2020 Aug 12.  doi: 10.1007/s11239-020-02247-9