Evidence map›Paper›PMID 32612493›Full record

ArticleFrontiers in neuroscience2020

Bridging the Gap Between Vessels and Nerves in Fabry Disease.

Julia Forstenpointner, Manon Sendel, Paul Moeller, Maren Reimer, Sima Canaan-Kühl, Jens Gaedeke, Stefanie Rehm, Philipp Hüllemann, Janne Gierthmühlen, Ralf Baron

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In one paragraph

Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Cold-evoked potentials in Fabry disease and polyneuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Platelet and myeloid cell phenotypes in a rat model of Fabry disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Review
  16. 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

10 authors.

Julia ForstenpointnerDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Manon SendelDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Paul MoellerDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Maren ReimerDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Sima Canaan-KühlDepartment of Medicine, Division of Nephrology, Charité, Berlin, Germany.
Jens GaedekeDepartment of Medicine, Division of Nephrology, Charité, Berlin, Germany.
Stefanie RehmDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Philipp HüllemannDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Janne GierthmühlenDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Ralf BaronDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeFabry disease frequently includes pain as an early disease feature, which was characterized as a dysfunctional processing of somatosensory information in various studies. The pathomechanism involves the mutation in the x-chromosomal GLA-gene and a consequent reduction of the α-galactosidase. This results in an insufficient reduction of globotriaosylceramide (GL3). Interestingly, an accumulation of GL3 was shown in both vascular endothelial cells and nerve tissue. This implicates that both an endothelial and nerve-dependent dysfunction may be considered as prominent mechanisms in pain pathogeneses. PATIENTS AND

methodsThe exploration of endothelial and C-fiber-dependent microcirculatory changes was conducted in a healthy cohort (

resultsThe results indicated a characteristic perfusion profile in the control group as well as both patient groups. Fabry patients had the smallest increase of endothelial-dependent perfusion as compared to the others [% increase as compared to Fabry: control + 129% (

conclusionOur results point to both an endothelial and a nerve-dependent dysfunction in Fabry disease. Therefore, not only direct changes in nerve fiber tissue may contribute to an altered sensory processing. Indeed, evidence of a perfusion change in vasa nervorum could also contribute to the dysfunctional processing of sensory information, which likely occurs under physical stress.

Indexed as

LASCAlaser speckle contrast analysislysosomal storage diseaseQSTQuantitative Sensory Testing

Identifiers

PMID32612493
PMCPMC7308469

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Registered trials

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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.