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The Role of HIF-2a in the Pathogenesis of Reflux Esophagitis

D

Dallas VA Medical Center

Status

Completed

Conditions

Esophagitis
Reflux Esophagitis
Gastroesophageal Reflux Disease

Treatments

Other: Cessation of Acid Suppressing Medications

Study type

Interventional

Funder types

Other U.S. Federal agency
NIH

Identifiers

NCT01733810
2R01DK063621-11
R01DK063621 (U.S. NIH Grant/Contract)

Details and patient eligibility

About

The purpose of this study is to determine the role of hypoxia inducible factor (HIF)-2a on the production of inflammatory cytokines that lead to reflux esophagitis.

Full description

Reflux esophagitis is thought to be caused by gastric acid that refluxes into the esophagus, causing injury. Newer data suggest that reflux of gastric juice into the esophagus stimulates HIF-2a, which increases production of inflammatory cytokines. These cytokines are thought to lead to reflux esophagitis. The investigators plan to study the relationship of HIF-2a to inflammatory cytokines in patients with known gastroesophageal reflux disease and reflux esophagitis.

Enrollment

12 patients

Sex

All

Ages

18+ years old

Volunteers

No Healthy Volunteers

Inclusion criteria

  • U.S Veteran
  • History of Los Angeles Grade C erosive esophagitis

Exclusion criteria

  • Inability to provide informed consent
  • Esophageal varices
  • Warfarin use
  • Coagulopathy that precludes safe biopsy of the esophagus
  • Comorbidity that precludes safe participation in the study
  • Allergy to fluorescein sodium
  • Pregnancy

Trial design

Primary purpose

Basic Science

Allocation

N/A

Interventional model

Single Group Assignment

Masking

None (Open label)

12 participants in 1 patient group

Reflux Patients
Experimental group
Description:
Patients with reflux and a prior history of reflux esophagitis are being enrolled. The intervention is cessation of acid-suppressing medications.
Treatment:
Other: Cessation of Acid Suppressing Medications

Trial contacts and locations

1

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Data sourced from clinicaltrials.gov

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