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Introduction We report an Intervention/outcome study of 33 severe COVID-19 subjects who received Seraph100 Microbind Affinity Blood Filter (Seraph 100) hemoperfusion therapy (15 survivors, 18 non-survivors) under emergency authorization from the FDA. Our objective was to determine if Seraph 100 hemoperfusion reduces SARS-CoV-2 RNA titers and/or markers of inflammation and/or epi/endothelial damage.a Methods Viral RNA and 78 protein analytes related to endothelial/epithelial damage and/or inflammation were quantified in systemic blood samples from 33 severe COVID-19 subjects collected upon ICU admission and then immediately before and after blood passed through the heparin-based Seraph 100 filter at two time points on the first day of hemoperfusion. Viral RNA titers were quantified using droplet-digital PCR. Protein analytes were quantified using multiplex/multi-analyte panels on MesoScale Discovery and ProteinSimple-Ella platforms. Results A total of 15/33 subjects had detectable viral RNA in baseline samples (shortly after ICU admission). These initial viremia levels were low, and they did not change uniformly post-perfusion. Five of 55 protein analytes that were up-regulated 1.4-120X at ICU admission relative to healthy controls showed significant decreases across the filter during the indicated time points on the first day of hemoperfusion: IP-10/CXCL10, fms-like tyrosine kinase (Flt-1), MIG/CXCL9, Hepatocyte Growth Factor (HGF) and receptor for advanced glycosylation end-products (RAGE). Paired t-tests identified 25 additional analytes that showed significant decreases (p<0.05) only without Bonferroni correction. Conclusion Initial freely circulating SARS-CoV-2 RNA levels of ICU-admitted subjects were low or undetectable. The Seraph 100 filter did not significantly reduce viral RNA titers in their plasma. However, multiple circulating proteins with roles in inflammation, endothelial/epithelial damage and/or angiogenesis decreased significantly across the filter. Larger prospective trials will be required to determine if such transient reductions translate into improved patient outcomes. However, this study did not demonstrate a direct reduction of free SARS-CoV-2 viral RNA by the Seraph 100., (S. Karger AG, Basel.)

Background and Objectives: Prediction of patient outcomes after severe traumatic brain injury (sTBI) is limited with current clinical tools. This study aimed to improve such prognostication by combining clinical data and serum inflammatory and neuronal proteins in patients with sTBI to develop predictive models for post-traumatic vasospasm (PTV) and mortality., Methods: Fifty-three adult civilian patients were prospectively enrolled in the sTBI arm of the Surgical Critical Care Initiative (SC2i). Clinical, serum inflammatory, and neuronal protein data were combined using the parsimonious machine learning methods of least absolute shrinkage and selection operator (LASSO) and classification and regression trees (CART) to construct parsimonious models for predicting development of PTV and mortality., Results: Thirty-six (67.9%) patients developed vasospasm and 10 (18.9%) died. The mean age was 39.2 years; 22.6% were women. CART identified lower IL9, lower presentation pulse rate, and higher eotaxin as predictors of vasospasm development (full data area under curve (AUC) = 0.89, mean cross-validated AUC = 0.47). LASSO identified higher Rotterdam computed tomography score and lower age as risk factors for vasospasm development (full data AUC 0.94, sensitivity 0.86, and specificity 0.94; cross-validation AUC 0.87, sensitivity 0.79, and specificity 0.93). CART identified high levels of eotaxin as most predictive of mortality (AUC 0.74, cross-validation AUC 0.57). LASSO identified higher serum IL6, lower IL12, and higher glucose as predictive of mortality (full data AUC 0.9, sensitivity 1.0, and specificity 0.72; cross-validation AUC 0.8, sensitivity 0.85, and specificity 0.79)., Conclusion: Inflammatory cytokine levels after sTBI may have predictive value that exceeds conventional clinical variables for certain outcomes. IL-9, pulse rate, and eotaxin as well as Rotterdam score and age predict development of PTV. Eotaxin, IL-6, IL-12, and glucose were predictive of mortality. These results warrant validation in a prospective cohort., (Copyright © 2024 Written work prepared by employees of the Federal Government as part of their official duties is, under the U.S. Copyright Act, a “work of the United States Government” for which copyright protection under Title 17 of the United States Code is not available. As such, copyright does not extend to the contributions of employees of the Federal Government.)