Early use of cytokine adsorption in treatment of COVID-19 associated respiratory distress syndrome

2021 ◽  
pp. 71-75
Author(s):  
A. S. Rybalko ◽  
A. V. Voronin ◽  
A. O. Vagulin ◽  
A. S. Saryglar ◽  
L. V. Zabolotskaya ◽  
...  

Introduction. It is the recommendations for treatment of sepsis and septic shock combined with rheumatologists’ recommendations for monoclonal antibodies therapy that guide severe COVID-19 management in ICU. However, those recommendations may not be fully applied to patients with acute respiratory distress-syndrome associated with SARS-CoV-2, as there exists a difference in pathogenesis between sepsis and virus-associated pneumonias. Monoclonal antibodies therapy may contribute to cytokine cascade severity and promote lung injury. Cytokine storm aggravates the course of the disease. At present, there are two groups of methods described in literature for cytokine storm control and therapy: pharmacological and extracorporeal approaches.Materials and methods. We have performed a retrospective analysis of five COVID-19 patients with acute respiratory syndrome. Cytokine adsorption start criteria were respiratory insufficiency and IL-6 levels greater than 500 pg/ml. Adsorption therapy was initiated within 24 hours of ICU admission and continued for 48–120 hours in hemoperfusion mode on Multifiltrate machine (Fresenius Medical Care). The length of a single session of CytoSorb (Cytosorbents Inc.) therapy was 24 hours.Results. All patients demonstrated SpO2/FiO2 ratio growth and IL-6 concentration decrease by the end of hemoadsorption. We noted lymphocyte count rise as well as IgM и IgG SARS-CoV-2 antibodies titer substantial increase.Conclusions. Our observations suggest that the early start of hemoadsorption associates with gas-exchange stabilization and hinders respiratory distress progression. Hemoadsorption allows for pro-inflammatory cytokines concentrations decrease and prevents secondary lung injury. According to our data, hemoadsorption is beneficial to form a coronavirus infection specific immune response. Further research is needed for a detailed study of the results we here describe.

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.


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