Evidence map›Paper›PMID 19439056›Full record

ReviewCritical care (London, England)2009

Bench-to-bedside review: Association of genetic variation with sepsis.

Ainsley M Sutherland, Keith R Walley

Open access · goldAbstract readReview
In one paragraph

Review in Critical care (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% of its field
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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Genetic associations in sepsis and ARDS.Frontiers in pharmacology · 2026
    Review
  6. Article
  7. Review
  8. Genetic differences in hippocampus of mice susceptible to sepsis-associated encephalopathy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  9. The Global Burden of Sepsis and Septic Shock.Epidemiologia (Basel, Switzerland) · 2024
    Review
  10. Article
  11. Discovering Causal Mechanistic Pathways in Sepsis-associated Acute Respiratory Distress Syndrome.American journal of respiratory and critical care medicine · 2020
    Article
  12. Genetic Polymorphisms and Cytokine Profile of Different Ethnicities inSeptic Shock Patients and their Association with Mortality.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2019
    Article
  13. Article
  14. Article
  15. Cytokine storm and sepsis disease pathogenesis.Seminars in immunopathology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Variants in the Mannose-binding Lectin Gene MBL2 do not Associate With Sepsis Susceptibility or Survival in a Large European Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Ainsley M SutherlandFaculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Keith R Walley
University of British Columbia · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease.

Indexed as

Genetic VariationGene DosageGene ExpressionGenetic TestingHaplotypesHumansPolymorphism, Single NucleotideSepsis

Identifiers

PMID19439056
PMCPMC2689454
OpenAlexW2079941677

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.