Evidence map›Paper›PMID 35606704›Full record

ArticleBMC gastroenterology2022

Intestinal fatty acid binding protein is a disease biomarker in paediatric coeliac disease and Crohn's disease.

Michael Logan, Mary MacKinder, Clare Martha Clark, Aikaterini Kountouri, Mwansa Jere, Umer Zeeshan Ijaz, Richard Hansen, Paraic McGrogan, Richard K Russell, Konstantinos Gerasimidis

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02341248 (Gut Microbial Taxonomy and Metabolism in Paediatric Crohn's Disease During Exclusive and Supplementary Enteral Nutrition Using -Omics Technologies), which is not on this map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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.

NCT02341248 unknown statusnot on this map

Gut Microbial Taxonomy and Metabolism in Paediatric Crohn's Disease During Exclusive and Supplementary Enteral Nutrition Using -Omics Technologies

TypeobservationalSponsorNHS Greater Glasgow and ClydeRan2014 to 2018Enrolled200ConditionsCrohn DiseaseArmsExclusive Enteral Nutrition (EEN)
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Prebiotic BimunoExperimental physiology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Recent advances in the diagnosis of celiac disease.World journal of gastroenterology · 2025
    Article
  9. Article
  10. Article
  11. The follow-up of patients with celiac disease.Journal of translational autoimmunity · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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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 3 institutions in 1 country.

Michael LoganHuman Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, G31 2ER, UK.ORCID http://orcid.org/0000-0003-3967-6123
Mary MacKinderHuman Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, G31 2ER, UK.
Clare Martha ClarkHuman Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, G31 2ER, UK.
Aikaterini KountouriHuman Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, G31 2ER, UK.
Mwansa JereDepartment of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, UK.
Umer Zeeshan IjazCivil Engineering, School of Engineering, University of Glasgow, Oakfield Avenue, Glasgow, UK.ORCID http://orcid.org/0000-0001-5780-8551
Richard HansenDepartment of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, UK.ORCID http://orcid.org/0000-0002-3944-6646
Paraic McGroganDepartment of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, UK.
Richard K RussellDepartment of Paediatric Gastroenterology, Royal Hospital for Sick Children, 9 Sciennes, Road, Edinburgh, EH9 1LF, UK.ORCID http://orcid.org/0000-0001-7398-4926
Konstantinos GerasimidisHuman Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, G31 2ER, UK. Konstantinos.gerasimidis@glasgow.ac.uk.ORCID http://orcid.org/0000-0001-9432-2200
Glasgow Royal Infirmary · GBRoyal Hospital for Children · GBUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is a clinical need to develop biomarkers of small bowel damage in coeliac disease and Crohn's disease. This study evaluated intestinal fatty acid binding protein (iFABP), a potential biomarker of small bowel damage, in children with coeliac disease and Crohn's disease.

methodsThe concentration iFABP was measured in plasma and urine of children with ulcerative colitis, coeliac disease, and Crohn's disease at diagnosis and from the latter two groups after treatment with gluten free diet (GFD) or exclusive enteral nutrition (EEN), respectively. Healthy children (Controls) were also recruited.

results138 children were recruited. Plasma but not urinary iFABP was higher in patients with newly diagnosed coeliac disease than Controls (median [Q1, Q3] coeliac disease: 2104 pg/mL 1493, 2457] vs Controls: 938 pg/mL [616, 1140], p = 0.001). Plasma or urinary iFABP did not differ between patients with coeliac on GFD and Controls. Baseline iFABP in plasma decreased by 6 months on GFD (6mo GFD: 1238 pg/mL [952, 1618], p = 0.045). By 12 months this effect was lost, at which point 25% of patients with coeliac disease had detectable gluten in faeces, whilst tissue transglutaminase IgA antibodies (TGA) continued to decrease. At diagnosis, patients with Crohn's disease had higher plasma iFABP levels than Controls (EEN Start: 1339 pg/mL [895, 1969] vs Controls: 938 pg/mL [616, 1140], p = 0.008). iFABP did not differ according to Crohn's disease phenotype. Induction treatment with EEN tended to decrease (p = 0.072) iFABP in plasma which was no longer different to Controls (EEN End: 1114 pg/mL [689, 1400] vs Controls: 938 pg/mL [616, 1140], p = 0.164). Plasma or urinary iFABP did not differ in patients with ulcerative colitis from Controls (plasma iFABP, ulcerative colitis: 1309 pg/mL [1005, 1458] vs Controls: 938 pg/mL [616, 1140], p = 0.301; urinary iFABP ulcerative colitis: 38 pg/mg [29, 81] vs Controls: 53 pg/mg [27, 109], p = 0.605).

conclusionsPlasma, but not urinary iFABP is a candidate biomarker with better fidelity in monitoring compliance during GFD than TGA. The role of plasma iFABP in Crohn's disease is promising but warrants further investigation.

trial registrationClinical Trials.gov, NCT02341248. Registered on 19/01/2015.

Indexed as

Celiac DiseaseColitis, UlcerativeCrohn DiseaseEnteral NutritionFatty Acid-Binding ProteinsHumansFatty Acid-Binding ProteinsBiomarkersCoeliac diseaseCrohn’s diseaseInflammatory bowel diseasePaediatricUlcerative colitis

Identifiers

PMID35606704
PMCPMC9125891
OpenAlexW4281390208

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.