Evidence map›Paper›PMID 19074762›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2009

Hepatotoxic interaction of sulindac with lipopolysaccharide: role of the hemostatic system.

Wei Zou, Sachin S Devi, Erica Sparkenbaugh, Husam S Younis, Robert A Roth, Patricia E Ganey

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.5field-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

23 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Roles of Cofactors in Drug-Induced Liver Injury: Drug Metabolism and Beyond.Drug metabolism and disposition: the biological fate of chemicals · 2022
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Molecular mechanisms of hepatocellular apoptosis induced by trovafloxacin-tumor necrosis factor-alpha interaction.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  9. Roles of the hemostatic system and neutrophils in liver injury from co-exposure to amiodarone and lipopolysaccharide.Toxicological sciences : an official journal of the Society of Toxicology · 2013
    Article
  10. Article
  11. Article
  12. Article
  13. Hypoxia sensitization of hepatocytes to neutrophil elastase-mediated cell death depends on MAPKs and HIF-1α.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Intrinsic versus idiosyncratic drug-induced hepatotoxicity--two villains or one?The Journal of pharmacology and experimental therapeutics · 2010
    Article
  20. 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

6 authors at 2 institutions in 1 country.

Wei ZouDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824, USA.
Sachin S Devi
Erica Sparkenbaugh
Husam S Younis
Robert A Roth
Patricia E Ganey
Michigan State University · USPfizer (United States) · US

Funding

Gene Expression in Drug-inflammation Models as Predictive of Idiosyncratic ADRSR21GM075865 · NIGMS · MICHIGAN STATE UNIVERSITY · PI GANEY, PATRICIA E · 2005 to 2008
$1.5M
NIGMS NIH HHS GM075865
6 · The paper itself

Abstract

Sulindac (SLD) is a nonsteroidal anti-inflammatory drug (NSAID) that has been associated with a greater incidence of idiosyncratic hepatotoxicity in human patients than other NSAIDs. One hypothesis regarding idiosyncratic adverse drug reactions is that interaction of a drug with a modest inflammatory episode precipitates liver injury. In this study, we tested the hypothesis that lipopolysaccharide (LPS) interacts with SLD to cause liver injury in rats. SLD (50 mg/kg) or its vehicle was administered to rats by gavage 15.5 h before LPS (8.3 x 10(5) endotoxin unit/kg) or its saline vehicle (i.v.). Thirty minutes after LPS treatment, SLD or vehicle administration was repeated. Rats were killed at various times after treatment, and serum, plasma, and liver samples were taken. Neither SLD nor LPS alone caused liver injury. Cotreatment with SLD/LPS led to increases in serum biomarkers of both hepatocellular injury and cholestasis. Histological evidence of liver damage was found only after SLD/LPS cotreatment. As a result of activation of hemostasis induced by SLD/LPS cotreatment, fibrin and hypoxia were present in liver tissue before the onset of hepatotoxicity. Heparin treatment reduced hepatic fibrin deposition and hypoxia and protected against liver injury induced by SLD/LPS cotreatment. These results indicate that cotreatment with nontoxic doses of LPS and SLD causes liver injury in rats, and this could serve as a model of human idiosyncratic liver injury. The hemostatic system is activated by SLD/LPS cotreatment and plays an important role in the development of SLD/LPS-induced liver injury.

Indexed as

Chemical and Drug Induced Liver InjuryAnalysis of VarianceAnimalsCholestasisDose-Response Relationship, DrugFibrinHemostasisHeparinHypoxiaLipopolysaccharidesLiverMaleRatsSulindacTumor Necrosis Factor-alphaFibrinHeparinLipopolysaccharidesSulindacTumor Necrosis Factor-alpha

Identifiers

PMID19074762
PMCPMC2644401
OpenAlexW2124723131

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.