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

This study is ongoing, but not recruiting participants.
Sponsor:
Collaborator:
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Information provided by (Responsible Party):
Stuart Spechler, Dallas VA Medical Center
ClinicalTrials.gov Identifier:
NCT01733810
First received: November 16, 2012
Last updated: August 1, 2016
Last verified: August 2016

November 16, 2012
August 1, 2016
February 2013
January 2017   (final data collection date for primary outcome measure)
change in esophageal inflammation from baseline to 14 days [ Time Frame: day 0 and day 14 ] [ Designated as safety issue: No ]
inflammation of the squamous esophageal mucosa will be measured at baseline and at 14 days
Same as current
Complete list of historical versions of study NCT01733810 on ClinicalTrials.gov Archive Site
change in HIF-2a levels from baseline to 14 days [ Time Frame: day 0 and day 14 ] [ Designated as safety issue: No ]
Amount of HIF-2a present will be measured at baseline and at 14 days
Same as current
Not Provided
Not Provided
 
The Role of HIF-2a in the Pathogenesis of Reflux Esophagitis
The Role of HIF-2a in the Pathogenesis of Reflux Esophagitis
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.
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.
Interventional
Not Provided
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Basic Science
  • Esophagitis
  • Reflux Esophagitis
  • Gastroesophageal Reflux Disease
Other: Cessation of Acid Suppressing Medications
Acid-suppressing medications are stopped for all participants the day after baseline assessment. Subsequent evaluations performed while participant is not on acid-suppressing medications.
Experimental: Reflux Patients
Patients with reflux and a prior history of reflux esophagitis are being enrolled. The intervention is cessation of acid-suppressing medications.
Intervention: Other: Cessation of Acid Suppressing Medications
Dunbar KB, Agoston AT, Odze RD, Huo X, Pham TH, Cipher DJ, Castell DO, Genta RM, Souza RF, Spechler SJ. Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes. JAMA. 2016 May 17;315(19):2104-12. doi: 10.1001/jama.2016.5657.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Active, not recruiting
15
March 2017
January 2017   (final data collection date for primary outcome measure)

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
Both
18 Years and older   (Adult, Senior)
No
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT01733810
2R01DK063621-11, R01DK063621
No
Not Provided
Not Provided
Stuart Spechler, Dallas VA Medical Center
Dallas VA Medical Center
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Principal Investigator: Stuart J Spechler, MD Dallas VA Medical Center
Dallas VA Medical Center
August 2016

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP