Steroid use in elderly critically ill COVID-19 patients.
Ontology highlight
ABSTRACT:
SUBMITTER: Jung C
PROVIDER: S-EPMC8246007 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Infections caused by SARS-CoV-2 may cause a severe disease, termed COVID-19, with significant mortality. Host responses to this infection, mainly in terms of systemic inflammation, have emerged as key pathogenetic mechanisms, and their modulation is the only therapeutic strategy that has shown a mortality benefit. Herein, we used peripheral blood transcriptomes of critically-ill COVID-19 patients obtained at admission in an Intensive Care Unit, to identify two clusters that, in spite of no major clinical differences, have different gene expression profiles that reveal different underlying pathogenetic mechanisms and ultimately have different ICU outcome. A transcriptomic signature was used to identify these clusters in an external validation cohort, yielding a similar result. These results illustrate the potential of transcriptomic profiles to identify patient endotypes and point to relevant pathogenetic mechanisms in COVID-19.
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Project description:Infections caused by SARS-CoV-2 may cause a severe disease, termed COVID-19, with significant mortality. Host responses to this infection, mainly in terms of systemic inflammation, have emerged as key pathogenetic mechanisms, and their modulation is the only therapeutic strategy that has shown a mortality benefit. Herein, we used peripheral blood transcriptomes of critically-ill COVID-19 patients obtained at admission in an Intensive Care Unit, to identify two clusters that, in spite of no major clinical differences, have different gene expression profiles that reveal different underlying pathogenetic mechanisms and ultimately have different ICU outcome. A transcriptomic signature was used to identify these clusters in an external validation cohort, yielding a similar result. These results illustrate the potential of transcriptomic profiles to identify patient endotypes and point to relevant pathogenetic mechanisms in COVID-19.
2022-02-28 | GSE197258 | GEO
Project description:Infections caused by SARS-CoV-2 may cause a severe disease, termed COVID-19, with significant mortality. Host responses to this infection, mainly in terms of systemic inflammation, have emerged as key pathogenetic mechanisms, and their modulation is the only therapeutic strategy that has shown a mortality benefit. Herein, we used peripheral blood transcriptomes of critically-ill COVID-19 patients obtained at admission in an Intensive Care Unit, to identify two clusters that, in spite of no major clinical differences, have different gene expression profiles that reveal different underlying pathogenetic mechanisms and ultimately have different ICU outcome. A transcriptomic signature was used to identify these clusters in an external validation cohort, yielding a similar result. These results illustrate the potential of transcriptomic profiles to identify patient endotypes and point to relevant pathogenetic mechanisms in COVID-19.
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Project description:Single-cell RNA-sequencing reveals a shift from focused IFN alpha-driven signals in COVID-19 ICU patients who survive to broad pro-inflammatory responses in fatal COVID-19 – a feature not observed in severe influenza. We conclude that fatal COVID-19 infection is driven by uncoordinated inflammatory responses that drive a hierarchy of T cell activation, elements of which can serve as prognostic indicators and potential targets for immune intervention.
2021-06-18 | GSE178404 | GEO
Project description:Sepsis is a frequent complication in critically ill patients and highly heterogeneous that is associated with high morbidity and mortality rates, especially in the elderly population. Utilizing RNA-Sequencing (RNA-Seq) to analysis biological pathways is widely used in clinical and molecular genetics studies, but in elderly patients with sepsis are still lacking. Hence, we aim to investigate the mortality-relevant biological features and transcriptomic features in elderly patients who were admitted to intensive care unit (ICU) for sepsis.
2022-11-03 | GSE216902 | GEO
Project description:ObjectivesTo evaluate the frequency and consequences of prescribing corticosteroids for pneumonia in a biomarker-concordant manner.Patients and methodsThis was a single-center retrospective cohort study of adults with pneumonia admitted to the medical intensive care unit (ICU) at Mayo Clinic in Rochester, Minnesota, between January 1, 2009, and June 30, 2014. Steroid use was "biomarker concordant" if given when C-reactive protein (CRP) was ≥150 mg/L or withheld when CRP was <150 mg/L, and vice versa for biomarker discordant.ResultsOf 3481 ICU admissions with community-acquired pneumonia, 169 (4.9%) had CRPs measured within 48 hours of admission to the ICU. Steroid use in the ICU was biomarker concordant in 88 (52%) patients and biomarker discordant in 81 (48%) patients. Biomarker-concordant steroid use was associated with faster resolution of lung injury: median fraction of inspired oxygen on day 3 (0.4 [0.3, 0.5] vs 0.3 [0.21, 0.4], P=.005), day 4 (0.35 [0.3, 0.5] vs 0.28 [0.21, 0.38], P=<.001), and day 5 (0.30 [0.24, 0.45] vs 0.28 [0.21, 0.40], P=.03), and increased ICU (3.5; 95% CI, 0.5 to 6.4, P=.02), and hospital-free days (3.6; 95% CI, 0.4 to 6.8, P=.03) on multivariate analysis.ConclusionsIn critically ill patients with community-acquired pneumonia, steroid use is rarely biomarker informed and often discordant with inflammatory biomarker levels. Biomarker-concordant steroid use was associated with a faster recovery of hypoxemia and increased ICU- and hospital-free days. Future well-designed prospective studies are justified to test the potential value of biomarker-concordant steroid therapy.
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Project description:Background: Outcomes in patients with severe SARS-CoV-2 infection (COVID-19) are conditioned by viral control and regulation of inflammation. Variants in IFIH1, a gene coding the cytoplasmatic RNA sensor MDA5, regulate the response to viral infections. Methods: Patients admitted to an intensive care unit (ICU) with documented COVID-19 were prospectively included and IFIH1 rs1990760 genotypes determined. Peripheral blood gene expression, cell populations and immune mediators were measured during the first day after ICU admission before steroid therapy. Peripheral blood mononuclear cells from healthy volunteers were exposed ex-vivo to an MDA5 agonist and dexamethasone, and changes in gene expression assessed. ICU discharge and hospital death were modelled using rs1990760 variants and dexamethasone therapy as factors. Findings: 237 patients were studied. Patients with the IFIH1 rs1990760 TT variant showed a decrease in expression of inflammation-related pathways, an anti-inflammatory cell profile and a decrease in pro-inflammatory mediators. Cells with TT variant exposed to an MDA5 agonist ex-vivo showed an increase in FOXO3 and IL6 when dexamethasone was added. All patients with the TT variant not treated with steroids (n=14) survived their ICU stay (HR 2.49 95% confidence interval 1.29 – 4.79). Dexamethasone therapy in this subgroup (N=50) delayed ICU discharge and increased hospital mortality (HR 2.19, 95% confidence interval 1.01 – 4.87) and serum IL-6 concentrations. Interpretation: COVID-19 ICU patients with the IFIH1 rs1990760 TT variant show an ameliorated inflammatory response that results in better outcomes than CC/CT variants. Dexamethasone can reverse this anti-inflammatory phenotype, worsening the outcome. Funding: Instituto de Salud Carlos III.
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Project description:In this study, we aim to evaluate the relation between COVID-19 and bacterial secondary superinfections. We assessed the functional responses of neutrophils and monocytes isolated from acute and recovery COVID-19 patients upon bacterial infection using Flow-cytometry and proteomics based assays. Both neutrophils and monocytes showed impared intracellular microbicidal capacity along with a decreased functional response. Determination of plasma cytokines levels showed a significant association of certain cytokines towards secondary bacterial infection.
2021-12-10 | PXD029547 | Pride