Evidence map›Paper›PMID 29333082›Full record

ArticleInternational journal of medical sciences2018

A

Patricia Romero-Cara, Daniel Torres-Moreno, José Pedregosa, Juan Antonio Vílchez, María Sergia García-Simón, Guadalupe Ruiz-Merino, Senador Morán-Sanchez, Pablo Conesa-Zamora

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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.

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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Translating IBD Genomics into Clinical Practice.Digestive diseases and sciences · 2026
    Review
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Assessing Immunogenicity of Biologic Drugs in Inflammatory Joint Diseases: Progress Towards Personalized Medicine.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

8 authors at 2 institutions in 1 country.

Patricia Romero-CaraGastroenterology Department, Santa Lucía General University Hospital (HGUSL), C/ Mezquita sn, 30202 Cartagena, Spain.
Daniel Torres-MorenoPathology Department, HGUSL, Cartagena, Spain.
José PedregosaClinical Analysis Department, HGUSL. Instituto Murciano de Investigaciones Biosanitarias (IMIB-Arrixaca), Murcia, Spain.
Juan Antonio VílchezClinical Analysis Department, HGUSL. Instituto Murciano de Investigaciones Biosanitarias (IMIB-Arrixaca), Murcia, Spain.
María Sergia García-SimónPharmacy Department, HGUSL, Cartagena, Spain.
Guadalupe Ruiz-MerinoInstitute for Biohealth Research from Murcia (IMIB), Cartagena, Spain.
Senador Morán-SanchezGastroenterology Department, Santa Lucía General University Hospital (HGUSL), C/ Mezquita sn, 30202 Cartagena, Spain.
Pablo Conesa-ZamoraInstitute for Biohealth Research from Murcia (IMIB), Cartagena, Spain.
Instituto Murciano de Investigación Biosanitaria · ESSanta Lucía University General Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe production of anti-drug antibodies (ADAs) against IgG monoclonal antibodies (mAbs) targeting tumour necrosis factor (TNF) is an important cause of loss of response to anti-TNF mAbs in patients with inflammatory bowel diseases (IBD) such as Crohn's disease (CD) and ulcerative colitis (UC). Since receptors for the Fc portion of IgG (FCGRs) are involved in the degradation of IgG complexes, we hypothesised that a polymorphism in MATERIAL AND

methodsA cohort of 103 IBD patients (80 CD, 23 UC) were genotyped and serum level of both anti-TNFs (infliximab or adalimumab) and ADA against them were measured.

resultsNo significant differences were observed between ADA occurrence or V158F genotype and type of disease or the kind of anti-TNF administrated. Interestingly, VV genotype correlated with patients producing ADA (VV: 37.5% vs. FV: 10.6% or FF: 5%; p=0.004) and was an independent predictor of this event after multivariate analysis. Moreover, VV genotype also correlated with those patients receiving anti-TNF dose intensification (p=0.03).

conclusion

Indexed as

AdalimumabAdultAntibodies, Anti-IdiotypicCohort StudiesColitis, UlcerativeCrohn DiseaseFemaleGastrointestinal AgentsHumansInfliximabMaleMiddle AgedPolymorphism, GeneticReceptors, IgGTumor Necrosis Factor-alphaAdalimumabAntibodies, Anti-IdiotypicFCGR3A protein, humanGastrointestinal AgentsInfliximabReceptors, IgGTNF protein, humanTumor Necrosis Factor-alphaadalimumabanti-drug antibodyCrohn's Diseaseinfliximabpharmacogenetics.ulcerative colitis

Identifiers

PMID29333082
PMCPMC5765734
OpenAlexW2774965460

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.