Evidence map›Paper›PMID 25298190›Full record

ArticleScientific reports2014

Creatine kinase inhibits ADP-induced platelet aggregation.

D L Horjus, R Nieuwland, K B Boateng, M C L Schaap, G A van Montfrans, J F Clark, A Sturk, L M Brewster

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Creatine Kinase and Blood Pressure: A Systematic Review.Medical sciences (Basel, Switzerland) · 2019
    Review
  6. Review
  7. Creatine kinase in ischemic and inflammatory disorders.Clinical and translational medicine · 2016
    Review
  8. 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

8 authors at 3 institutions in 2 countries.

D L HorjusDept. of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
R NieuwlandDept. of Laboratory Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
K B BoatengDept. of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
M C L SchaapDept. of Laboratory Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
G A van Montfrans1] Dept. of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands [2] Dept. of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
J F ClarkDept. of Neurology, Cincinnati Children's Hospital, Cincinnati, Ohio, USA.
A SturkDept. of Laboratory Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
L M Brewster1] Dept. of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands [2] Dept. of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands [3] Dept. of Social Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Academic Medical Center · NLCincinnati Children's Hospital Medical Center · USUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bleeding risk with antiplatelet therapy is an increasing clinical challenge. However, the inter-individual variation in this risk is poorly understood. We assessed whether the level of plasma creatine kinase, the enzyme that utilizes ADP and phosphocreatine to rapidly regenerate ATP, may modulate bleeding risk through a dose-dependent inhibition of ADP-induced platelet activation. Exogenous creatine kinase (500 to 4000 IU/L, phosphocreatine 5 mM) added to human plasma induced a dose-dependent reduction to complete inhibition of ADP-induced platelet aggregation. Accordingly, endogenous plasma creatine kinase, studied in 9 healthy men (mean age 27.9 y, SE 3.3; creatine kinase 115 to 859 IU/L, median 358), was associated with reduced ADP-induced platelet aggregation (Spearman's rank correlation coefficient, -0.6; p < 0.05). After exercise, at an endogenous creatine kinase level of 4664, ADP-induced platelet aggregation was undetectable, normalizing after rest, with a concomitant reduction of creatine kinase to normal values. Thus, creatine kinase reduces ADP-induced platelet activation. This may promote bleeding, in particular when patients use platelet P2Y12 ADP receptor inhibitors.

Indexed as

Adenosine DiphosphateAdultBlood PlateletsCreatine KinaseHemorrhageHumansMalePlatelet AggregationReceptors, Purinergic P2Receptors, Purinergic P2Y12Adenosine DiphosphateCreatine KinaseP2RY12 protein, humanReceptors, Purinergic P2Receptors, Purinergic P2Y12

Identifiers

PMID25298190
PMCPMC4190537
OpenAlexW1973800949

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.