Evidence map›Paper›PMID 40634451›Full record

ArticleScientific reports2025

Impact of glucocorticoid receptor polymorphism rs6198 on sepsis survival in a prospective multicenter cohort.

Christoph Sombetzki, Lars Palmowski, Dominik Ziehe, Hartmuth Nowak, Tim Rahmel, Stefan Felix Ehrentraut, Patrick Thon, Jennifer Orlowski, Lars Bergmann, Michael Adamzik and 3 more

Abstract readMulticenter Study
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Precision medicine in sepsis: reappraising glucocorticoid therapy through the lens of molecular endotypes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Christoph Sombetzki *Department of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Lars Palmowski *Department of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Dominik ZieheDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Hartmuth NowakDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Tim RahmelDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Stefan Felix EhrentrautDepartment of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Bonn, Germany.
Patrick ThonDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Jennifer OrlowskiDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Lars BergmannDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Michael AdamzikDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Björn KoosDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany.
Katharina RumpDepartment of Anesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum, Bochum, Germany. katharina.k.rump@rub.de.
SepsisDataNet.NRW research group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The glucocorticoid receptor (GR), particularly its isoforms GRα and GRβ, plays a crucial role in modulating inflammatory responses. The rs6198 single nucleotide polymorphism (SNP) in the NR3C1 gene, which encodes GR, has been associated with adverse outcomes in various diseases due to its potential effect on GR isoform expression. This study aims to explore the impact of the rs6198 SNP in sepsis. Specifically, we tested the hypothesis that the presence of a particular genotype of the rs6198 SNP is associated with an increased 30-day mortality rate in patients with sepsis. This prospective, multicenter study included 204 ICU patients diagnosed with sepsis, as part of the Sepsis.Data.Net NRW cohort. Genotyping for rs6198 and immunofluorescence as well as quantification of GR expression were performed. Statistical analyses included Hardy-Weinberg equilibrium, Kaplan-Meier survival analysis, log-rank tests, multivariate Cox regression, and logistic regression. Genotyping for the rs6198 SNP identified 137 patients (67%) with the TT- and 67 (33%) with CC/CT-genotype. Patients with the TT-genotype had a 30-day survival rate of 65% (89 of 137 patients), which was significantly lower than the 82% survival rate (55 of 67 patients) observed in the patients with the CC/CT-genotype (p = 0.006). A multivariate Cox regression analysis, adjusted for age, SOFA and SAPS2 score, and selected laboratory values, revealed that the TT-genotype was independently associated with an increased risk of death (HR 3.56, 95% CI 1.22-10.38, p = 0.02). Subgroup analysis demonstrated a particularly pronounced impact among patients with initially high disease severity (HR 6.16, 95% CI 1.66-22.80, p = 0.007). In addition, expression analysis revealed a significantly higher presence of GRα in patients with the TT-genotype compared to those with CC/CT genotype (p = 0.023). Increased GRα expression was also associated with higher 30-day mortality (HR 2.38, 95% CI 1.48-3.82, p < 0.001). The rs6198 SNP in the NR3C1 gene is associated with 30-day mortality in sepsis patients and correlates with increased expression of the GRα isoform. These results highlight the TT-genotype as a potential risk marker. Further research is needed to clarify the causal mechanisms and explore personalized therapeutic implications in sepsis management.

Indexed as

Polymorphism, Single NucleotideReceptors, GlucocorticoidSepsisAgedFemaleGenetic Predisposition to DiseaseGenotypeHumansKaplan-Meier EstimateMaleMiddle AgedProspective StudiesSurvival RateNR3C1 protein, humanReceptors, GlucocorticoidBiomarkerGlucocorticoid receptor isoformsGlucocorticoidsNR3C1rs6198SepsisSepsis survival

Identifiers

PMID40634451
PMCPMC12241491

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.