Evidence map›Paper›PMID 39648597›Full record

Observational studyUnited European gastroenterology journal2025

Serum Neutrophil Biomarkers to Predict Crohn's Disease Progression and Infliximab Treatment Outcomes.

D Magalhaes, M Santiago, M Patita, B Arroja, P Lago, I Rosa, H T Sousa, P Ministro, I Mocanu, A Vieira and 14 more

Abstract readObservational StudyMulticenter Study
In one paragraph

Observational study in United European gastroenterology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
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

24 authors.

D MagalhaesFaculty of Medicine, Department of Biomedicine, Unit of Pharmacology and Therapeutics, University of Porto, Porto, Portugal.
M SantiagoCINTESIS (Center for Health Technology and Services Research), Porto, Portugal.
M PatitaDepartment of Gastroenterology, Garcia da Orta Hospital, Almada, Portugal.
B ArrojaDepartment of Gastroenterology, Braga Hospital, Braga, Portugal.
P LagoDepartment of Gastroenterology, Porto Hospital University Centre, Porto, Portugal.
I RosaDepartment of Gastroenterology, IPOLFG, EPE, Lisbon, Portugal.ORCID 0000-0002-2953-5987
H T SousaDepartment of Gastroenterology, Unidade Local de Saúde do Algarve-Portimão Hospital, Portimão, Portugal.ORCID 0000-0002-6626-205X
P MinistroDepartment of Gastroenterology, Viseu-Tondela Hospital Centre, Viseu, Portugal.
I MocanuDepartment of Gastroenterology, Garcia da Orta Hospital, Almada, Portugal.
A VieiraDepartment of Gastroenterology, Garcia da Orta Hospital, Almada, Portugal.
J CastelaDepartment of Gastroenterology, IPOLFG, EPE, Lisbon, Portugal.
J MoleiroDepartment of Gastroenterology, IPOLFG, EPE, Lisbon, Portugal.
J RoseiraDepartment of Gastroenterology, Unidade Local de Saúde do Algarve-Portimão Hospital, Portimão, Portugal.ORCID 0000-0002-5098-8729
C EugeniaDepartment of Gastroenterology, Viseu-Tondela Hospital Centre, Viseu, Portugal.
P SousaDepartment of Gastroenterology, Viseu-Tondela Hospital Centre, Viseu, Portugal.ORCID 0000-0002-9009-9635
F PortelaDepartment of Gastroenterology, Coimbra Hospital University Centre, Coimbra, Portugal.
L CorreiaDepartment of Gastroenterology, Northern Lisbon University Hospital Centre, Lisbon, Portugal.
S DiasGEDII (Portuguese Inflammatory Bowel Disease Group), Porto, Portugal.
J AfonsoFaculty of Medicine, Department of Biomedicine, Unit of Pharmacology and Therapeutics, University of Porto, Porto, Portugal.
S DaneseDepartment of Biomedical Sciences, Humanitas University, Milan, Italy.ORCID 0000-0001-7341-1351
L Peyrin-BirouletDepartment of Gastroenterology and Inserm NGERE U1256, University Hospital of Nancy, University of Lorraine, Nancy, France.ORCID 0000-0003-2536-6618
C C DiasFaculty of Medicine of the University of Porto (FMUP), Department of Community Medicine, CINTESIS@RISE, Information and Health Decision Sciences (MEDCIDS), Porto, Portugal.
F MagroFaculty of Medicine, Department of Biomedicine, Unit of Pharmacology and Therapeutics, University of Porto, Porto, Portugal.
GEDII

Funding

Grupo de Estudo da Doença Inflamatória Intestinal
6 · The paper itself

Abstract

BACKGROUND AND

aimsPredicting the treatment outcomes of biological therapies is an unmet need in Crohn's Disease. In this study, we explored the potential of serum neutrophil-related biomarkers to predict infliximab therapeutic results and disease progression in Crohn's Disease patients, over a 2-year period, in a real-world setting.

methodsThe study included 100 asymptomatic Crohn's Disease patients in the IFX maintenance phase from the prospective, observational, multicenter DIRECT study. Patients were categorized according to a composite outcome reflecting progression that included surgery, hospitalizations, new fistulae, abscess or stricture, and drug treatment escalation. Serum neutrophil elastase, lipocalin-2, lactoferrin, and resistin (non-neutrophil control) were analyzed via multiplex magnetic bead assays at multiple touchpoints. Fecal calprotectin was assessed by ELISA.

resultsOver up to 2 years of follow-up, serum biomarkers did not differentiate between the composite outcome groups, whereas fecal calprotectin was significantly higher in patients with worse outcomes. During the infliximab maintenance phase, there was a significant, sustained reduction of neutrophil elastase (p < 0.001), lipocalin-2 (p < 0.001), and lactoferrin (p < 0.001), but not of resistin, despite stable neutrophil levels. Correlations between NE and NGAL levels were strong (Pearson correlations 0.75-0.85); all other correlations were of small magnitude.

conclusionOur real-world data do not support using serum neutrophil elastase, lipocalin-2, or lactoferrin concentrations as predictors of treatment outcomes or disease evolution in infliximab -treated Crohn's Disease patients. On the other hand, the sustained decrease in biomarkers over time suggests that neutrophil stabilization might be an additional infliximab mechanism of action.

Indexed as

Crohn DiseaseGastrointestinal AgentsInfliximabNeutrophilsAdultBiomarkersDisease ProgressionFecesFemaleFollow-Up StudiesHumansLactoferrinLeukocyte ElastaseLeukocyte L1 Antigen ComplexLipocalin-2MaleBiomarkersGastrointestinal AgentsInfliximabLactoferrinLCN2 protein, humanLeukocyte ElastaseLeukocyte L1 Antigen ComplexLipocalin-2ResistinRETN protein, humanCrohn's diseasefecal calprotectininfliximablactoferrin’lipocalin‐2neutrophil elastaseresistinserum neutrophil biomarkers

Identifiers

PMID39648597
PMCPMC11975612

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.