Evidence map›Paper›PMID 26205715›Full record

ReviewCurrent gastroenterology reports2015

Do We Know What Causes Eosinophilic Esophagitis? A Mechanistic Update.

Thomas M Runge, Evan S Dellon

Open access · greenAbstract readReview
In one paragraph

Review in Current gastroenterology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Inter-institutional variations regarding Barrett's esophagus diagnosis.Esophagus : official journal of the Japan Esophageal Society · 2019
    Article
  10. Monoclonal Antibodies for Treatment of Eosinophilic Esophagitis.Clinical reviews in allergy & immunology · 2018
    Review
  11. Impact of smoking, alcohol consumption, and NSAID use on risk for and phenotypes of eosinophilic esophagitis.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2018
    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

2 authors at 1 institution in 1 country.

Thomas M RungeCenter for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine, CB#7080 Bioinformatics Building, 130 Mason Farm Rd., Chapel Hill, NC, 27599-7080, USA.
Evan S Dellon
University of North Carolina at Chapel Hill · US

Funding

DIGESTIVE DISEASES EPIDEMIOLOGY TRAINING PROGRAMT32DK007634 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1990 to 2026
$7.4M
Budesonide versus fluticasone for treatment of eosinophilic esophagitisR01DK101856 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DELLON, EVAN SAMUEL · 2014 to 2018
$1.7M
Risk Factors and Biomarkers for Diagnosis & Treatment of Eosinophilic EsophagitisK23DK090073 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DELLON, EVAN SAMUEL · 2011 to 2013
$541k
NIDDK NIH HHS K23 DK090073NIDDK NIH HHS K23DK090073NIDDK NIH HHS R01 DK101856NIDDK NIH HHS R01DK101856NIDDK NIH HHS T32 DK007634NIDDK NIH HHS T32DK007634
6 · The paper itself

Abstract

The mechanisms underlying eosinophilic esophagitis (EoE) have been intensely investigated, and significant advances have been made in understanding the pathogenesis of EoE. EoE is defined as a chronic immune/antigen-mediated disease, characterized clinically by symptoms of esophageal dysfunction and histologically by an esophageal eosinophilic infiltrate. In this paper, we will review the current knowledge of EoE pathophysiology based on both animal and human data and discuss possible etiologic mechanisms from the genetic and environmental perspectives. EoE is a Th2-predominant inflammatory process triggered by allergens. Proinflammatory cytokines and chemokines recruit eosinophils and other effector cells, such as mast cells, into the esophageal epithelium, where they cause direct damage and promote esophageal remodeling. The genetic expression profile of EoE has been described, and several single nucleotide polymorphisms have been identified and associated with EoE. While this genetic contribution is important, it is difficult to postulate that EoE is primarily a genetic disease. Given the rapid epidemiologic changes in the incidence and prevalence of EoE over the past two decades, environmental factors may be the driving force. While it is not known what causes EoE in an individual patient at a specific time, the current hypothesis is that there is a complex interaction between genetic factors and environmental exposures that remains to be elucidated.

Indexed as

BiomarkersCytokinesEosinophilic EsophagitisGene-Environment InteractionHumansRisk FactorsBiomarkersCytokines

Identifiers

PMID26205715
PMCPMC4591257
OpenAlexW1030864879

What OpenQuestion holds

Textmetadata
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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.