Browse
Submit Data
Databases
API
Help

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Antibiotic Use and Fatal Outcomes among Critically Ill Patients with COVID-19 in Tacna, Peru.

ABSTRACT: Overuse of antibiotics during the Coronavirus Disease 2019 (COVID-19) pandemic could increase the selection of extensively resistant bacteria (XDR). However, it is unknown what impact they could have on the evolution of patients, particularly critically ill patients. This study aimed to evaluate the characteristics and impact of ICU-acquired infections in patients with COVID-19. A retrospective cohort study was conducted, evaluating all patients with critical COVID-19 admitted to the intensive care unit (ICU) of a hospital in Southern Peru from 28 March 2020 to 1 March 2021. Of the 124 patients evaluated, 50 (40.32%) developed a healthcare-associated infection (HAI), which occurred at a median of 8 days (IQR 6-17) after ICU admission. The proportion of patients with HAI that required ceftriaxone was significantly higher; the same was true for the use of dexamethasone. Forty bacteria isolations (80%) were classified as XDR to antibiotics, with the most common organisms being Acinetobacter baumannii (54%) and Pseudomonas aeruginosa (22%); 33% (41/124) died at the ICU during the follow-up. In the adjusted analysis, healthcare-associated infection was associated with an increased risk of mortality (aHR= 2.7; 95% CI: 1.33-5.60) and of developing acute renal failure (aRR = 3.1; 95% CI: 1.42-6.72). The incidence of healthcare infection mainly by XDR pathogens is high in critically ill patients with COVID-19 and is associated with an increased risk of complications or death.

SUBMITTER: Copaja-Corzo C

PROVIDER: S-EPMC8388967 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients

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

Transcriptomic clustering of critically-ill COVID-19 patients

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-28 | GSE197259 | GEO

Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients.

Project description:Prior studies have demonstrated that immunologic dysfunction underpins severe illness in COVID-19 patients, but have lacked an in-depth analysis of the immunologic drivers of death in the most critically ill patients. We performed immunophenotyping of viral antigen-specific and unconventional T cell responses, neutralizing antibodies, and serum proteins in critically ill patients with SARS-CoV-2 infection, using influenza infection, SARS-CoV-2-convalescent health care workers, and healthy adults as controls. We identify mucosal-associated invariant T (MAIT) cell activation as an independent and significant predictor of death in COVID-19 (HR = 5.92, 95% CI = 2.49-14.1). MAIT cell activation correlates with several other mortality-associated immunologic measures including broad activation of CD8+ T cells and non-Vδ2 γδT cells, and elevated levels of cytokines and chemokines, including GM-CSF, CXCL10, CCL2, and IL-6. MAIT cell activation is also a predictor of disease severity in influenza (ECMO/death HR = 4.43, 95% CI = 1.08-18.2). Single-cell RNA-sequencing reveals a shift from focused IFNα-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.

| S-EPMC8445447 | biostudies-literature

Transcriptomic clustering of critically-ill COVID-19 patients [Day 4 RNAseq]

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.

2023-04-29 | GSE206264 | GEO

Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients

Project description:Identification of immune correlates of fatal outcomes in critically ill COVID-19 patients

| PRJNA738888 | ENA

Glycosylation signature of plasma IgA of critically ill COVID-19 patients

Project description:Total plasma IgA glycosylation was compared between healthy volunteers and volunteers suffering fromo infections with either the influenza A virus or the severe acute respiratory syndrome corona virus 2. Data from functional assays of the same plasma samples, such as neutrophil extracellular trap formation is also available.

2024-10-22 | PXD057019 | Pride

Transcriptomic clustering of critically-ill COVID-19 patients [Day 1-miRNA-Seq]

2022-02-28 | GSE197258 | GEO

Transcriptomic clustering of critically-ill COVID-19 patients [Day 1-RNA-Seq]

2022-02-28 | GSE197204 | GEO

Steroid use in elderly critically ill COVID-19 patients.

Project description: Not available

| S-EPMC8246007 | biostudies-literature

Peripheral blood gene expression according to IFIH1 rs1990760 variants in critically-ill COVID-19 patients

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.

2021-07-03 | GSE168400 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data