Evidence map›Paper›PMID 15153236›Full record

ReviewCritical care (London, England)2004

Bench-to-bedside review: understanding genetic predisposition to sepsis.

Jesús Villar, Nicole Maca-Meyer, Lina Pérez-Méndez, Carlos Flores

Abstract readReview
In one paragraph

Review in Critical care (London, England), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Stroke-induced immunodepression and dysphagia independently predict stroke-associated pneumonia - The PREDICT study.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Trial
  3. Review
  4. Association ofInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Review
  7. Risk Factors for Maternal Readmission with Sepsis.American journal of perinatology · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Interleukin-6, -7, -8 and -10 predict outcome in acute myocardial infarction complicated by cardiogenic shock.Clinical research in cardiology : official journal of the German Cardiac Society · 2012
    Article
  19. Article
  20. Management and outcome of colorectal anastomotic leaks.International journal of colorectal disease · 2011
    Article
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

4 authors.

Jesús VillarDivision Critical Care Research, Research Institute, Hospital Universitario NS de Candelaria, Tenerife, Canary Islands, Spain. jesus.villar@canarias.org
Nicole Maca-Meyer
Lina Pérez-Méndez
Carlos Flores

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a complex syndrome that develops when the initial, appropriate host response to an infection becomes amplified, and is then dysregulated. Among other factors, the innate immune system is of central importance to the early containment of infection. Death from infection is strongly heritable in human populations. Hence, genetic variations that disrupt innate immune sensing of infectious organisms could explain the ability of the immune system to respond to infection, the diversity of the clinical presentation of sepsis, the response to current medical treatment, and the genetic predisposition to infection in each individual patient. Such genetic variations may identify patients at high risk for the development of sepsis and organ dysfunction during severe infections. Single base variations, known as single nucleotide polymorphisms (SNPs), are the most commonly used variants. There has been great interest in exploring SNP in those genes involved in the inflammatory cascade resulting from the systemic inflammatory response to micro organisms. The rationale for studying gene SNPs in critical illnesses seeks to identify potential markers of susceptibility, severity, and clinical outcome; seeks to identify potential markers for responders and non-responders in clinical trials, and seeks to identify targets for therapeutic intervention. In this review, we focus on the current state of association studies of those genes governing the powerful bacterial infection-induced inflammation and provide guidelines for future studies describing disease associations with genetic variations based on current recommendations. We envision a time in the near future when genotyping will be include in the standard evaluation of critically ill patients and will help to prioritize a therapeutic option.

Indexed as

Genetic MarkersGenetic Predisposition to DiseaseHaplotypesHumansInflammationInterleukin-10Multiple Organ FailurePolymorphism, Single NucleotideRisk AssessmentSepsisGenetic MarkersInterleukin-10

Identifiers

PMID15153236
PMCPMC468916

What OpenQuestion holds

Textmetadata
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.