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1.
Critical Care Conference: 42nd International Symposium on Intensive Care and Emergency Medicine Brussels Belgium ; 27(Supplement 1), 2023.
Article in English | EMBASE | ID: covidwho-2315181

ABSTRACT

Introduction: During the COVID-19 pandemic, various virus variants evolved worldwide. COVID-19 omicron (CO) was associated with a decrease in length of hospital stay, ICU admission and death [1] as compared to COVID-19 delta (CD). To estimate impact of CO on ICUs worldwide, we investigated characteristics, disease course and outcome of critically ill CO patients. Method(s): Of 8562 critically ill COVID-19 patients included in the prospective international multicenter RISC-19-ICU registry [2,3], characteristics and outcome were compared for 1890 CD and 272 CO patients admitted to ICU between 1-2021 and 9-2022. Mixed model analysis corrected for individual center effects and adjusted for age, sex, vaccination status, use of steroids and anticoagulants was used. Result(s): There was no difference in age, sex and BMI between groups. CO patients had more comorbidities [mean difference (MD) 0.7, 95% CI (0.5-1.0), p = 0.02], especially arterial hypertension, and higher SAPS II score [MD 0.0 (0-0.1), p < 0.001], SOFA score [MD 0.1 (0.1-0.3), p < 0.0001]. CO patients presented with higher cardiovascular system SOFA subscore, but better PF-ratio at ICU admission and smaller risk for intubation and mechanical ventilation throughout their ICU stay [OR 0.5 (0.3-0.8)]. There was no difference in ECMO treatments, ICU length of stay [MD 0.6 (0-11.4), p = 0.72] or ICU survival [HR 1 (0.7-1.5), p = 0.88] between the two groups. Conclusion(s): We show that critically ill CO patients present with more comorbidities, less severe respiratory disease but more severe hemodynamic instability at ICU admission as compared to CD patients, although the ICU length of stay and mortality was similar. These differences could be explained by differences in disease characteristics caused by CO, or by the increasing prevalence of CO as co-factor to preexisting disease. Continued monitoring of critically ill CO patients in ICUs worldwide is warranted.

2.
Multiple Sclerosis Journal ; 28(3 Supplement):776, 2022.
Article in English | EMBASE | ID: covidwho-2138820

ABSTRACT

Introduction: Infection with the SARS-CoV-2 coronavirus can lead to a wide range of acute and also chronic disease manifestations. The rapidly developed vaccinations are highly effective in preventing severe disease courses and have been proven safe. Both natural infection and, to a much lower extent, the mRNAbased vaccinations can be accompanied by transient autoimmune phenomena or onset of autoimmune diseases. Objective(s): We report here two cases of multiple sclerosis (MS) with clinical and new radiological signs beginning in close temporal relation to spike (S) protein mRNA-based vaccinations. Aim(s): To establish that the onset of MS in these two cases is very likely caused by CD4+ T cell clones that cross-recognize SARSCoV- 2 S protein-derived peptides and peptides derived from myelin proteins, which have previously been implicated in MS. Method(s): Spike specific CD4+ T cells from peripheral blood and CD4+ T cells from CSF sample were isolated and expanded for autoantigen screening test. A list of well-known MS-related autoantigens including immunodominant peptides and isoforms from MBP, MOG, PLP, RASGRP2, TSTA3 peptides were included to assess T cell reactivity. CD4+ CFSElow fraction were sorted after stimulate with positive autoantigen pools or SARSCov- 2 Spike protein, followed by expansion and testing with autoantigen peptides and Spike protein. Supernatant from cell culture were further analyzed for IFN-gamma secretion. Result(s): Self-reactive T cells were detected from Spike specific T cell population in both patients. CD4+ T from CSF also showed reactivity to MBP, MOG, PLP peptide pools. Finally, we found proinflammatory T cell clones that recognize both Spike protein and immunodominant MBP peptides and MOG peptides, which have previously been implicated in MS. Conclusion(s): Detailed studies of both peripheral blood- and CSFderived CD4+ T cells show that the onset of MS in these two cases is very likely caused by CD4+ T cell clones that cross-recognize SARS-CoV-2 S protein-derived peptides and peptides derived from myelin proteins, which have previously been implicated in MS.

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