Evidence map›Paper›PMID 30212252›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2018

Eosinophilic esophagitis: pathophysiology and its clinical implications.

Eisuke Inage, Glenn T Furuta, Calies Menard-Katcher, Joanne C Masterson

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Observational
  3. Cow milk protein allergy mimics in infancy.World journal of clinical pediatrics · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Sleep in children with eosinophilic esophagitis.World journal of pediatrics : WJP · 2021
    Article
  13. Review
  14. Review
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

4 authors at 3 institutions in 3 countries.

Eisuke InageDepartment of Pediatrics and Adolescent Medicine, Juntendo University Graduate School of Medicine , Tokyo , Japan.
Glenn T FurutaDigestive Health Institute, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Hospital Colorado, Gastrointestinal Eosinophilic Diseases Program, Department of Pediatrics, Mucosal Inflammation Program, University of Colorado School of Medicine , Aurora, Colorado.
Calies Menard-KatcherDigestive Health Institute, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Hospital Colorado, Gastrointestinal Eosinophilic Diseases Program, Department of Pediatrics, Mucosal Inflammation Program, University of Colorado School of Medicine , Aurora, Colorado.
Joanne C MastersonDigestive Health Institute, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Hospital Colorado, Gastrointestinal Eosinophilic Diseases Program, Department of Pediatrics, Mucosal Inflammation Program, University of Colorado School of Medicine , Aurora, Colorado.
Children's Hospital Colorado · USNational University of Ireland, Maynooth · IEUniversity of Colorado Denver · US

Funding

TRAINING (CAREER DEVELOPMENT) COMPONENTU54AI117804 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI Marc E. Rothenberg · 2014 to 2026
$18.5M
Hypoxia Inducible Factor Control of Epithelial Regeneration in Eosinophilic EsophagitisK01DK106315 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MASTERSON, JOANNE CAROL · 2015 to 2017
$415k
NIAID NIH HHS U54 AI117804NIDDK NIH HHS K01 DK106315
6 · The paper itself

Abstract

Classically, eosinophilic esophagitis is an antigen-mediated chronic disease distinct from gastroesophageal reflux disease. Eosinophilic esophagitis is an emerging clinical problem that is growing in recognition. It is characterized clinically by feeding dysfunction, dysphagia, and reflux-like symptoms. Histologically, eosinophilic esophagitis is identifiable by a dense epithelial eosinophilic infiltrate. Experimental modeling and clinical studies over the last decade have greatly improved mechanistic insights and led to improvements in clinical understanding and the assessment of therapeutic options for patients and their clinicians who manage this disease. Here, we review the clinicopathologic diagnostic criteria and our understanding of eosinophilic esophagitis as an allergic disease with genetic and immunological components. We present studies defining the importance of the epithelial barrier and the concept of barrier dysfunction as an initiating or perpetuating factor for this disease. We discuss the relationship between the symptoms of dysphagia and feeding dysfunction, our current knowledge of the underlying pathophysiologic mechanisms, and advances in clinical assessment of esophageal distensibility and narrowing in eosinophilic esophagitis patients. Finally, therapeutic implications relating to the advances that have led to our current understanding of the pathophysiology of eosinophilic esophagitis are explored.

Indexed as

AnimalsEosinophilic EsophagitisEosinophilsEpithelial CellsHumansImmunoglobulin GImmunoglobulin Gbarrierdysphagiaeosinophilic oesophagitisfeeding dysfunction

Identifiers

PMID30212252
PMCPMC6293259
OpenAlexW2891288898

What OpenQuestion holds

Textmetadata
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.