Evidence map›Paper›PMID 40307425›Full record

ArticleScientific reports2025

Untargeted metabolomics reveals key metabolic alterations in pediatric epilepsy with insights into Tryptophan metabolism and the gut-brain axis.

Karol Chojnowski, Mikołaj Opiełka, Krzysztof Urbanowicz, Marta Zawadzka, Karolina Wangin, Ryszard Tomasz Smoleński, Maria Mazurkiewicz-Bełdzińska

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–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

13 citing papers in PubMed.

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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

7 authors.

Karol ChojnowskiDepartment of Developmental Neurology, Medical University of Gdansk, Gdansk, 80-211, Poland. karol.chojnowski@gumed.edu.pl.
Mikołaj OpiełkaDepartment of Biochemistry, Medical University of Gdansk, Gdansk, 80-211, Poland.
Krzysztof UrbanowiczDepartment of Biochemistry, Medical University of Gdansk, Gdansk, 80-211, Poland.
Marta ZawadzkaDepartment of Developmental Neurology, Medical University of Gdansk, Gdansk, 80-211, Poland.
Karolina WanginDepartment of Developmental Neurology, Medical University of Gdansk, Gdansk, 80-211, Poland.
Ryszard Tomasz SmoleńskiDepartment of Biochemistry, Medical University of Gdansk, Gdansk, 80-211, Poland.
Maria Mazurkiewicz-BełdzińskaDepartment of Developmental Neurology, Medical University of Gdansk, Gdansk, 80-211, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biochemical processes of childhood-onset epilepsy remain unclear, with no reliable biomarkers for prognosis or management. Untargeted plasma metabolomics offers a valuable approach to uncover underlying pathomechanisms and identify actionable biomarkers. In this study, plasma samples from 18 pediatric patients with epilepsy and 11 age-matched healthy controls were analyzed using liquid chromatography-mass spectrometry. Data were analyzed using univariate and multivariate statistical methods and pathway enrichment analysis. Multivariate analyses demonstrated separation between the patient and control groups. A total of 19 endogenous metabolites (VIP > 1, adjusted p < 0.05) emerged as key differentiators. Compared with controls, patients exhibited significant reductions in tryptophan (Trp), 5-Hydroxyindoleacetic acid (5-HIAA), several gut microbiota-derived metabolites, including indole, indoxyl sulfate, and p-cresyl sulfate, as well as in niacin metabolism end-products - N1-Methyl-2-pyridone-5-carboxamide (Met2PY) and N1-Methyl-4-pyridone-3-carboxamide (Met4PY). In addition, patients showed decreased levels of tricarboxylic acid (TCA) cycle intermediates, concomitant with an increase in fatty acid derivatives and N-acetylneuraminic acid (Neu5Ac). The most substantially altered metabolic pathways in epilepsy patients involved the TCA cycle, vitamin A and C metabolism, prostaglandin synthesis, and D4/E4-neuroprostane formation. Observed alterations in tryptophan and microbiota-derived metabolites suggest gut dysbiosis may contribute to epilepsy development through the gut-brain axis. Moreover, the circulatory metabolic markers indicating an energy deficit and oxidative stress underscore the systemic impact of seizure activity.

Indexed as

BrainBrain-Gut AxisEpilepsyGastrointestinal MicrobiomeMetabolomicsTryptophanAdolescentBiomarkersCase-Control StudiesChildChild, PreschoolFemaleHumansMaleMetabolic Networks and PathwaysMetabolomeBiomarkersTryptophan

Identifiers

PMID40307425
PMCPMC12044071

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.