I have often asked myself if I ever saw a patient with cytokine storm syndrome (CSS) in the COVID-19 population. The "infamous " H-score which has been proposed as a clinical tool to assess post-test probability for CSS, has never been tested in a COVID-19 population.
Manifestations of CSS include systemic inflammation including fever, tachycardia, tachypnea and hypotension . How is this different from systemic inflammatory response syndrome (SIRS).
In the attached article we will also see that inflammatory markers, particularly IL-6 are "MUCH, MUCH" lower on average compared to patients with ARDS due to other etiologies.
Giving tocilizumab for example , directed at the single inflammatory response cytokine, reminds me of the multiple trials we ran years ago, giving patient's monoclonal antibodies directed against a single inflammatory marker and sepsis. All those trials were acute disappointments.
We have absolutely no data if tocilizumab or sarilumab , beneficially affects mortality. As a matter of fact, these mediators are needed in a complex cascade of immunomodulation. Do we know for sure that we do not increase risk for secondary infections? Immunomodulation is a complex mechanism with pleiotropic effects of various modulators.
A simpler concept to understand and we now have data on is that SARS CoV-2 with it S-proteins deregulates ( and invades actual cells) endothelial function and is associated with arterial thrombosis and venous thrombosis, both intra- pulmonary and extrapulmonary. Although we have no outcome studies yet, treating patients with anticoagulation in COVID-19, biologically makes far more sense than chasing CSS.
Please send me some comments after reading the article. I quite frankly do not worry much about CSS. Identifying the need of anticoagulation is far more important, something we totally disregarded in the treatment package early on during the COVID-19 epidemic. Yet we saw patient receiving tocilizumab all the time, based on zero data.
From HCQ/AZ, no steroids and tocilizumab........to remdesivir ( I have serious doubts on its beneficial effect, Tamiflu 2.0 ), DXM and anticoagulation....
9/5/2020. Here is more data from theUniversiteit van Nijmegen in Holland that cytokine storm probably is not part of SARSCov2 infection, as already written earlier in this post, I can't recall ever seen one clinically. As a matter a fact we maybe doing the complete wrong intervention by suppressing the immune system .Tociluzimab is even given from day one by some institutions with Remdesivir, biologically that makes no sense.
Their Conclusion :
"In this study, critically ill patients with COVID-19
with ARDS had circulating cytokine levels that were lower compared with patients with bacterial sepsis and similar to other
critically ill patients. These findings are in line with lower leukocyte counts observed in patients with COVID-19, and are possibly due to lower overall disease severity, despite the presence of severe pulmonary injury. The findings of this
preliminary analysis suggest COVID-19 may not be characterized by cytokine storm. Whether anticytokine therapies will
benefit patientswith COVID-19 remains to be determined."
