Effect of Selective COX-2 Inhibition on Ulcer Healing

The recruitment status of this study is unknown because the information has not been verified recently.
Verified March 2010 by Chinese University of Hong Kong.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
Chinese University of Hong Kong
ClinicalTrials.gov Identifier:
NCT00153673
First received: September 8, 2005
Last updated: March 25, 2010
Last verified: March 2010

September 8, 2005
March 25, 2010
February 2001
December 2010   (final data collection date for primary outcome measure)
ulcer healing [ Time Frame: 8 weeks ] [ Designated as safety issue: No ]
ulcer healing at week 8
Complete list of historical versions of study NCT00153673 on ClinicalTrials.gov Archive Site
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Effect of Selective COX-2 Inhibition on Ulcer Healing
Phase III Study of a Double-Blind Randomized Comparison of Famotidine Plus Celecoxib Versus Dologesics for Gastric Ulcer Healing in Arthritis Patients (NSAID#5A Study)

The purpose of this study is to compare the effect of Famotidine plus a COX-2 inhibitor (celecoxib) with Famotidine plus dologesics in ulcer healing in arthritis patients.

For many years the integrity of the stomach mucosal barrier is thought to be maintained by mucosal prostaglandins (PG) synthesized by COX-1. However, the notion that COX-1 protects the stomach and COX-2 induces inflammation may be over-simplistic. In animal studies, COX-2, but not COX-1, is expressed in experimental gastric ulcer. Inhibition of COX-2 delays ulcer healing, indicating that PG derived from COX-2 contributes to restoring the mucosal barrier [1]. Whether this animal observation can be generalized to the human stomach is unknown. To date the biological functions of COX-1 and COX-2 in the healing of human gastric ulcer healing is unclear. Unlike experimental ulcers that only express COX-2, recently we have shown that both COX-1 and COX-2 are up-regulated in human gastric ulcers [2]. Furthermore, our preliminary results suggest that inhibition of COX-2 alone may not lead to a clinically significant delay in ulcer healing (refer to progress report). These observations suggest that peptic ulcer healing is more complex in the human stomach - both COX isoforms may be involved in the healing process. Inhibition of COX-2 alone may have less adverse effect than non-selective inhibition of both COX isoforms in ulcer healing. The current study aims to resolve the functional significance of COX-2 in human gastric ulcer from a biological and clinical perspective.

Interventional
Phase 3
Allocation: Randomized
Endpoint Classification: Safety Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
  • Arthritis
  • Gastric Ulcer
  • Drug: celecoxib
    Celecoxib 200mg bd
  • Drug: Dologesics
    Dologesics 2 tablets bd
  • Active Comparator: 1
    Celecoxib + Famotidine
    Intervention: Drug: celecoxib
  • Active Comparator: 2
    Dologesics + Famotidine
    Intervention: Drug: Dologesics
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
200
Not Provided
December 2010   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Gastric ulcers confirmed by endoscopy
  • Stop taking NSAIDs for 1 week prior to endoscopy
  • Age 18
  • H. pylori negative
  • Informed written consent

Exclusion Criteria:

  • Actively bleeding ulcers
  • Ulcers showing dysplasia or malignancy
  • Renal failure (serum creatinine >200umol/l)
  • Previous gastric surgery
  • Moribund or terminal malignancy
  • Concomitant use of proton pump inhibitor, misoprostol, aspirin, steroid or anticoagulant
Both
18 Years and older
No
Contact: Francis K Chan, MD 85226323143 fklchan@cuhk.edu.hk
Contact: Jessica Y Ching, MPH 85226323524 jessicaching@cuhk.edu.hk
China
 
NCT00153673
5NA study
Not Provided
Francis K CHAN, Chinese University of Hong Kong
Chinese University of Hong Kong
Not Provided
Principal Investigator: Francis K Chan, MD Chinese University of Hong Kong
Chinese University of Hong Kong
March 2010

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