Evidence map›Paper›PMID 21494615›Full record

Trial reportPloS one2011

Dose effects of oxaliplatin on persistent and transient Na+ conductances and the development of neurotoxicity.

Susanna B Park, Cindy S-Y Lin, Arun V Krishnan, David Goldstein, Michael L Friedlander, Matthew C Kiernan

Open access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. A systematic review on chronic oxaliplatin-induced peripheral neuropathy and the relation with oxaliplatin administration.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2014
    Pooled it
  3. Trial
  4. Trial
  5. Observational
  6. Review
  7. Article
  8. Review
  9. Motor disorders related to oxaliplatin-induced peripheral neuropathy: long-term severity and impact on quality of life.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Early sensory neurophysiological changes in prediabetes.Journal of diabetes investigation · 2020
    Article
  18. Review
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Susanna B ParkPrince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia.
Cindy S-Y Lin
Arun V Krishnan
David Goldstein
Michael L Friedlander
Matthew C Kiernan
UNSW Sydney · AUPrince of Wales Hospital · AUNeuroscience Research Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxaliplatin, a platinum-based chemotherapy utilised in the treatment of colorectal cancer, produces two forms of neurotoxicity--acute sensorimotor neuropathic symptoms and a dose-limiting chronic sensory neuropathy. Given that a Na(+) channelopathy has been proposed as the mechanism underlying acute oxaliplatin-induced neuropathy, the present study aimed to determine specific mechanisms of Na(+) channel dysfunction. METHODOLOGY/PRINCIPAL

findingsSpecifically the function of transient and persistent Na(+) currents were followed during treatment and were investigated in relation to oxaliplatin dose level. Eighteen patients were assessed before and after a single oxaliplatin infusion with motor and sensory axonal excitability studies performed on the median nerve at the wrist. While refractoriness (associated with Na(+) channel inactivation) was significantly altered post-oxaliplatin infusion in both motor (Pre: 31.7±6.4%; Post: 68.8±14.5%; P≤.001) and sensory axons (Pre: 31.4±5.4%; Post: 21.4±5.5%; P<.05), strength-duration time constant (marker of persistent Na(+) conductances) was not significantly altered post-infusion (Motor Pre: 0.395±0.01 ms; Post: 0.394±0.02 ms; NS; Sensory Pre:0.544±0.03 ms; Post: 0.535±0.05 ms; NS). However, changes in strength-duration time constant were significantly correlated with changes in refractoriness in motor and sensory axons (Motor correlation coefficient = -.65; P<.05; Sensory correlation coefficient = .67; P<.05). CONCLUSIONS/SIGNIFICANCE: It is concluded that the predominant effect of acute oxaliplatin exposure in human motor and sensory axons is mediated through changes in transient rather than persistent Na(+) conductances. These findings are likely to have implications for the design and trial of neuroprotective strategies.

Indexed as

AdultAged, 80 and overAxonsDemographyDose-Response Relationship, DrugFemaleHumansInfusions, IntravenousIon Channel GatingMaleMiddle AgedNeurotoxinsOrganoplatinum CompoundsOxaliplatinSodium ChannelsNeurotoxinsOrganoplatinum CompoundsOxaliplatinSodium Channels

Identifiers

PMID21494615
PMCPMC3072981
OpenAlexW1992768230

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.