Evidence map›Paper›PMID 28721978›Full record

ArticleSaudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association

Noninvasive biomarkers as surrogate predictors of clinical and endoscopic remission after infliximab induction in patients with refractory ulcerative colitis.

Elham A Hassan, Haidi K Ramadan, Ali A Ismael, Khaled F Mohamed, Madiha M El-Attar, Ihab Alhelali

Registry-linked trialOpen access · diamondAbstract readComparative Study
In one paragraph

Article in Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03885713 (Identification of Predictive Biomarkers for Response to Biologic Therapies and Tofacitinib in Inflammatory Bowel Disease by Proteomic and Mass Cytometry Approaches), which is not on this map. Cited by 12 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 12% 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.

NCT03885713 phase4completednot on this map

Identification of Predictive Biomarkers for Response to Biologic Therapies and Tofacitinib in Inflammatory Bowel Disease by Proteomic and Mass Cytometry Approaches

TypeinterventionalSponsorFundación de Investigación Biomédica - Hospital Universitario de La PrincesaRan2019 to 2024Enrolled180ConditionsInflammatory Bowel Diseases, Crohn Disease, Ulcerative ColitisArmsInfliximab or adalimumab or golimumab or vedolizumab or ustekinumab or tofacitinib
3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 3 syntheses or guidelines pooled it, 21 citations in OpenAlex.

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  11. Observational
  12. Barbaloin Attenuates Mucosal Damage in Experimental Models of Rat Colitis by Regulating Inflammation and the AMPK Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019
    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

6 authors at 3 institutions in 2 countries.

Elham A HassanDepartment of Tropical Medicine and Gastroenterology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Haidi K RamadanDepartment of Tropical Medicine and Gastroenterology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Ali A IsmaelDepartment of Internal Medicine, Faculty of Medicine, Zagazig University, Sharqia, Egypt; Gastroenterology Unit, Farwaniya Hospital, Kuwait.
Khaled F MohamedGastroenterology Unit, Farwaniya Hospital, Kuwait.
Madiha M El-AttarDepartment of Tropical Medicine and Gastroenterology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Ihab AlhelaliDepartment of Clinical Biochemistry, Ministry of Health, Kuwait.
Assiut University · EGFarwaniya Hospital · KWMinistry of Health · KW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsTreatment of refractory ulcerative colitis (UC) is a clinical challenge, and after biological therapy, monitoring clinical and endoscopic responses is fundamental. We aimed to investigate and compare the predictive power of different noninvasive parameters for clinical remission and mucosal healing after infliximab induction therapy in refractory UC patients. PATIENTS AND

methodsSerum and fecal biomarkers, including hemoglobin, white blood cells, erythrocyte sedimentation rate, C-reactive protein (CRP), and fecal calprotectin (FC), and colonoscopy were assessed in 44 patients with refractory UC before and after (week 12) infliximab induction. Clinical and endoscopic responses were measured by clinical Mayo score and endoscopic Mayo subscore, respectively.

resultsAfter infliximab induction, 54.5% and 65.9% had clinical remission and mucosal healing, respectively. Post-induction CRP and FC were significantly lower in clinical responders versus nonresponders (P = 0.01 and 0.001, respectively) and in patients with mucosal healing than without (P < 0.001). Among all the parameters tested, FC had the best predictive value of clinical remission [Area under the curve (AUC = 0.826)] and mucosal healing (AUC = 0.949). Post-induction FC had 87.5% sensitivity and 89% specificity (cut-off <100 μg/g) for predicting clinical remission and 89.7% sensitivity and 93.3% specificity (cut-off <58 μg/g) for predicting mucosal healing.

conclusionsPost-infliximab induction FC can be used as a surrogate marker for predicting clinical remission and mucosal healing in refractory UC patients.

Indexed as

Administration, IntravenousAdultBiomarkersColitis, UlcerativeColonoscopyC-Reactive ProteinEndoscopy, GastrointestinalFecesFemaleHumansInfliximabIntestinal MucosaKuwaitLeukocyte L1 Antigen ComplexMalePredictive Value of TestsBiomarkersC-Reactive ProteinInfliximabLeukocyte L1 Antigen ComplexTumor Necrosis Factor-alpha

Identifiers

PMID28721978
PMCPMC5539678
OpenAlexW2949240786

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.