Effect of Selective COX-2 Inhibition on Ulcer Healing

Condition(s) targeted: Arthritis; Gastric Ulcer

Intervention: celecoxib (Drug); Dologesics (Drug)

Phase: Phase 3

Status: Recruiting

Sponsored by: Chinese University of Hong Kong

Official(s) and/or principal investigator(s):
Francis K Chan, MD, Principal Investigator, Affiliation: Chinese University of Hong Kong

Overall contact:
Francis K Chan, MD, Phone: 85226323143, Email: fklchan@cuhk.edu.hk

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.

Official title: 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)

Study design: Treatment, Randomized, Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Active Control, Parallel Assignment, Safety Study

Primary outcome: ulcer healing

Detailed description: 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.

Minimum age: 18 Years. Maximum age: N/A. Gender(s): Both.

Criteria:

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

Francis K Chan, MD, Phone: 85226323143, Email: fklchan@cuhk.edu.hk

Endoscopy Center, Prince of Wales Hospital, Hong Kong, China; Recruiting
Francis K Chan, MD, Phone: 26323143, Email: fklchan@cuhk.edu.hk
Jessica Y Ching, MPH, Phone: 26323524, Email: jessicaching@cuhk.edu.hk
Francis K Chan, MD, Principal Investigator
Vincent W Wong, MD, Sub-Investigator

Starting date: February 2001
Last updated: March 14, 2008