Evidence map›Paper›PMID 40583454›Full record

SynthesisInflammatory bowel diseases2025

Fecal Microbial Community Profiling Allows Discrimination of Phenotype and Treatment Response in Pediatric Crohn's Disease and Ulcerative Colitis-An International Meta-Analysis.

Denise Aldrian, Adam Pollio, Christoph Mayerhofer, Kay Diederen, Jonathan P Jacobs, Nikhil Pai, Jake C Szamosi, Lara Hart, Dan Turner, Federica Del Chierico and 11 more

Erratum issuedAbstract readMeta-Analysis
In one paragraph

Synthesis in Inflammatory bowel diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors.

Denise AldrianDepartment of Paediatrics I, Medical University of Innsbruck, Innsbruck, Austria.
Adam PollioInstitute of Cell Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
Christoph MayerhoferDepartment of Paediatrics I, Medical University of Innsbruck, Innsbruck, Austria.
Kay DiederenDepartment of Pediatric Gastroenterology and Nutrition, Amsterdam UMC, Location AMC & VUmc, Amsterdam, The Netherlands.
Jonathan P JacobsVatche and Tamar Manoukian Division of Digestive Diseases, David Geffen School of Medicin, University of California Los Angeles, Los Angeles, CA, USA.
Nikhil PaiDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, McMaster University, Hamilton, ON, Canada.
Jake C SzamosiDepartment of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada.
Lara HartDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, McMaster University, Hamilton, ON, Canada.ORCID 0000-0003-3819-4317
Dan TurnerShaare Zedek Medical Center, The Hebrew University of Jerusalem, Jerusalem, Israel.
Federica Del ChiericoImmunology, Rheumatology and Infectious Diseases Research Area, Unit of Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.ORCID 0000-0002-4204-4736
Sabrina CardileGastroenterology, Digestive Endoscopy and Nutrition Unit, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
Zoya GrigoryanDivision of Gastroenterology and Hepatology, Rutgers Robert Wood Johnson Medical School, New York, NY, USA.
Lea Ann ChenDivision of Gastroenterology and Hepatology, Rutgers Robert Wood Johnson Medical School, New York, NY, USA.
Jakub HurychDepartment of Medical Microbiology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czechia.ORCID 0000-0002-9813-5290
Ondrej CinekDepartment of Medical Microbiology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czechia.
Carla R TaddeiDepartment of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences Universidade de Sao Paulo (USP), São Paulo, Brazil.
Tobias SchwerdDepartment of Pediatrics, Dr. von Hauner Children's Hospital, University Hospital, LMU Munich, Munich, Germany.
Eytan WineDivision of Pediatric Gastroenterology, Department of Pediatrics, University of Alberta, Edmonton, AB, Canada.ORCID 0000-0002-3458-4142
Anne M GriffithsDivision of Gastroenterology, Hepatology & Nutrition, Department of Pediatrics and IBD Centre, SickKids Hospital, University of Toronto, Toronto, ON, Canada.
Thomas MüllerDepartment of Paediatrics I, Medical University of Innsbruck, Innsbruck, Austria.ORCID 0000-0001-8908-5589
Georg F VogelDepartment of Paediatrics I, Medical University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-2515-4490

Funding

The Study of Families with Heritable Crohn's Disease to Support Rational Design of Microbiota-based TherapiesK23DK119544 · NIDDK · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI CHEN, LEA A · 2020 to 2024
$1.1M
NIDDK NIH HHS K23 DK119544
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe pathophysiology of pediatric inflammatory bowel disease (PIBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is not entirely understood. Dysregulation of the intestinal microbiome is recognized as both a disease-driving and a potential therapeutic target. This study aimed to systematically analyze gut microbiome compositions and its applicability as a biomarker for disease progress and treatment response.

methodsBibliographic and nucleotide databases were searched. Raw 16S-rRNA sequencing reads were subjected to a uniform downstream dada2/phyloseq pipeline to extract taxonomy, community structure, and abundance information. Patient metadata were extracted from publications, and study authors were contacted for further details if required.

resultsTwenty-six studies comprising 3956 stool samples (CD 41%, UC 36%, 23% healthy) were included in the analyses. Median age of individuals was 12 (interquartile range 4). Sex distribution was comparable. Alpha diversity was reduced between the healthy and both UC and CD treatment-naïve groups (P < .001) and further reduced with increasing clinical disease activity. Beta diversity revealed altered community structure in treatment-naïve children with PIBD (P < .001). This alteration remained in patients in clinical remission (P < .001). Machine learning models discriminated between treatment-naïve patients with CD or UC with an area under the receiver operating characteristics curve (AUROC) of 98%. Microbial communities differed between patient responders versus nonresponders to treatment (P < .001). Further, microbial community profiling distinguished treatment response (eg, steroid, nutrition, or TNFα) with AUROCs of 82%-90%.

conclusionsGut microbial community structure is substantially altered in active and inactive PIBD and may be utilized as a biomarker for differentiating PIBD subtype and predicting treatment response.

Indexed as

Colitis, UlcerativeCrohn DiseaseFecesGastrointestinal MicrobiomeAdolescentBiomarkersChildFemaleHumansMalePhenotypeRNA, Ribosomal, 16SBiomarkersRNA, Ribosomal, 16S16S metagenomicsCrohn’s diseasemicrobiometreatment responseulcerative colitis

Identifiers

PMID40583454
PMCPMC12455605

What OpenQuestion holds

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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.