Evidence map›Paper›PMID 24986188›Full record

ArticleMolecular diagnosis & therapy2014

Effects of repeated intrathecal triamcinolone-acetonide application on cerebrospinal fluid biomarkers of axonal damage and glial activity in multiple sclerosis patients.

P S Rommer, F Kamin, A Petzold, H Tumani, M Abu-Mugheisib, W Koehler, F Hoffmann, A Winkelmann, R Benecke, U K Zettl

Open access · hybridAbstract readMulticenter Study
In one paragraph

Article in Molecular diagnosis & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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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 at 6 institutions in 3 countries.

P S RommerDepartment of Neurology, Neuroimmunological Section, University of Rostock, Rostock, Germany, paulus.rommer@meduniwien.ac.at.
F Kamin
A Petzold
H Tumani
M Abu-Mugheisib
W Koehler
F Hoffmann
A Winkelmann
R Benecke
U K Zettl
University of Rostock · DEAmsterdam UMC Location VUmc · NLFachkrankenhaus Hubertusburg · DEKlinikum Braunschweig · DEMartha-Maria Hospital · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesMultiple sclerosis (MS) is the most common inflammatory disease of the central nervous system in young adults. Over time, the disease progresses and, with accumulating disability, symptoms such as spasticity may occur. Although several treatment options are available, some patients may not respond to first-line therapeutics. However, some of these patients may benefit from intrathecally administered triamcinolone-acetonide (TCA), a derivative of glucocorticosteroids (GCS). GCS may have neurotoxic effects, and cell apoptosis may occur. The aim of this study was to investigate the effects of TCA on biomarkers in the cerebrospinal fluid (CSF) suggestive of neurodegeneration.

methodsIn order to assess neurotoxic effects of TCA, neurofilament heavy-chain (NfH)(SMI35), tau protein, and S-100B protein levels were determined before and during treatment with TCA in 54 patients with primary progressive MS, as well as relapsing MS (relapsing-remitting and secondary progressive MS).

resultsNfH(SMI35) levels in the CSF of patients treated with TCA intrathecally did not increase significantly during the treatment cycle (p = 0.068). After application of TCA, tau protein levels were increased significantly at day 4 (p = 0.03) and at day 8 (p ≤ 0.001). S-100B protein levels decreased significantly (p ≤ 0.05) during treatment with TCA.

conclusionNfH(SMI35) levels did not change significantly; however, tau protein levels did increase significantly within the reference range. Taking these findings together, the long-term effects of TCA on NfH(SMI35) and tau protein levels need to be investigated further to understand whether levels of both biomarkers will change over repeated TCA applications. Interestingly, S-100B protein levels decreased significantly during the first applications, which may have represented reduced astrocytic activity during TCA treatment.

Indexed as

AdultAnti-Inflammatory AgentsAxonsBiomarkersDisease ProgressionEnzyme-Linked Immunosorbent AssayFemaleFollow-Up StudiesHumansInjections, SpinalMaleMiddle AgedMultiple SclerosisNeurofilament ProteinsNeurogliaPrognosisAnti-Inflammatory AgentsBiomarkersMAPT protein, humanneurofilament protein HNeurofilament ProteinsS100 Calcium Binding Protein beta Subunittau ProteinsTriamcinolone Acetonide

Identifiers

PMID24986188
PMCPMC4245486
OpenAlexW2081160644

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LicenceCC BY-NC
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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.