Evidence map›Paper›PMID 24151376›Full record

ReviewWorld journal of gastroenterology2013

Gastroesophageal reflux disease: Update on inflammation and symptom perception.

Annamaria Altomare, Michele Pier Luca Guarino, Silvia Cocca, Sara Emerenziani, Michele Cicala

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06564246 (Clinical Study Evaluating The Role of Vonoprazan Versus Pantoprazole in Patients With Gastroesophageal Reflux Disease), which is not on this map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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.

NCT06564246 phase4recruitingnot on this mapstarted 2024, after this paper: background citation

Clinical Study Evaluating The Role of Vonoprazan Versus Pantoprazole in Patients With Gastroesophageal Reflux Disease

TypeinterventionalSponsorTanta UniversityRan2024 to 2026Enrolled44ConditionsGastroesophageal Reflux Disease (GERD)ArmsVonoprazan 20 mg versus Pantoprazole 40 mg
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

5 authors at 1 institution in 1 country.

Annamaria AltomareAnnamaria Altomare, Michele Pier Luca Guarino, Silvia Cocca, Sara Emerenziani, Michele Cicala, Unit of Digestive Disease, Campus Bio Medico University of Rome, 00128 Rome, Italy.
Michele Pier Luca Guarino
Silvia Cocca
Sara Emerenziani
Michele Cicala
Università Campus Bio-Medico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although gastroesophageal reflux disease (GERD) is a common disorder in Western countries, with a significant impact on quality of life and healthcare costs, the mechanisms involved in the pathogenesis of symptoms remain to be fully elucidated. GERD symptoms and complications may result from a multifactorial mechanism, in which acid and acid-pepsin are the important noxious factors involved. Prolonged contact of the esophageal mucosa with the refluxed content, probably caused by a defective anti-reflux barrier and luminal clearance mechanisms, would appear to be responsible for macroscopically detectable injury to the esophageal squamous epithelium. Receptors on acid-sensitive nerve endings may play a role in nociception and esophageal sensitivity, as suggested in animal models of chronic acid exposure. Meanwhile, specific cytokine and chemokine profiles would appear to underlie the various esophageal phenotypes of GERD, explaining, in part, the genesis of esophagitis in a subset of patients. Despite these findings, which show a significant production of inflammatory mediators and neurotransmitters in the pathogenesis of GERD, the relationship between the hypersensitivity and esophageal inflammation is not clear. Moreover, the large majority of GERD patients (up to 70%) do not develop esophageal erosions, a variant of the condition called non-erosive reflux disease. This summary aims to explore the inflammatory pathway involved in GERD pathogenesis, to better understand the possible distinction between erosive and non-erosive reflux disease patients and to provide new therapeutic approaches.

Indexed as

EsophagusPerceptionAnimalsCytokinesEsophagitisGastroesophageal RefluxHumansHyperalgesiaInflammation MediatorsPain PerceptionPrognosisRisk FactorsSignal TransductionCytokinesInflammation MediatorsEsophagitisGastroesophageal reflux diseaseHeartburnHypersensitivityMucosal inflammation

Identifiers

PMID24151376
PMCPMC3801363
OpenAlexW2130703669

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.