Clinical Trial: Immunologic Factors in Reflux Esophagitis and Barrett’s Esophagus

Study Status: Completed
Recruit Status: Unknown status
Study Type: Observational

Official Title: Immunologic Factors Correlating With Cyclooxygenase and Nitric Oxide Synthase in Reflux Esophagitis and Barrett’s Esophagus

Brief Summary: By using combination of the expression of COX-2 and NOS and immunologic reaction in the esophagus with manometry of LES and cruel diaphragm and 24 hr esophageal pH monitoring to investigate the mechanisms and to make a new and more clinically applicable clarification of these reflux diseases will be valuable in the clinical management and prevention. We will perform the following works and complete the objectives: 1) comparing the difference of immuno-inflammatory reactions among NERD, reflux esophagitis and Barrett’s esophagus; 2) the different expression of PGs & COX-2 in functional heartburn, hiatus hernia, NERD, reflux disease and Barrett’s esophagus; determining the subtype of EP receptor (EP1~4); 3) determining and comparing the expression of NOS in the esophagus; 4) investigating the role of ROS in the esophagus; 5) in correlating cytokine, COX-2 and NOS with LESP, TLESR, diaphragm EMG and 24-hour esophageal pH ; 6) the difference of expression of cytokine, atrophic gastritis and Hp in gastric mucosa, in correlating with intragastric acid status, among functional heartburn, hiatus hernia, NERD, erosive esophagitis and Barrett’s esophagus; to determine whether should eradicate Hp in reflux esophageal disease; 7) the effects of lipid peroxidation related immunologic reaction, with relation to COX-2 and NOS, in the inflammatory activity and esophageal carcinogenesis of esophagus; 8) the effects of cytokines, COX-2 and NOS on the apoptosis in these reflux esophageal diseases; 9) integrating immuno-inflamatory reaction, COX-2, NOS with manometry of LES and diaphragm, and 24-hour pH monitoring and intragastric pH to newly clarify GERD into evidence based categories.

Detailed Summary:

It has been commonly accepted that there is considerable geographic variation in the prevalence of gastroesophageal reflux disease (GERD) and much less prevalent in Asia. However, a tendency of increasing the prevalence of GERD has been observed in Taiwan with four folds of growth (attached 1 & 2), Japan and Singapore. GERD is a chronic, relapsing disease, causing a poor quality of life lower than that of CAD and a greater burden with exhausting socioeconomic and medical resource much higher than peptic ulcer disease. Thus, thoroughly elucidating the mechanisms of GERD, in combination of basic science and clinical characteristics, to well and correctly clarify these diseases will be greatly helpful in clinical application.

Reflux of duodenal contents is believed to contribute to esophageal injury, Barrett’s esophagus and esophageal cancer. HCL and bile acid, particularly conjugated form at low pH, has now been considered playing a more important pathogenetic role in the reflux esophagitis; on the contrary, low gastric acid status may increase the risk of dysplasia and carcinogenesis on Barrett’s esophagus due to increased pulse of bile acid. While, only limited reports focusing immune mechanism in the complex populations of GERD. In few preliminary literatures showed that cytokine and tumor necrosis factors are associated with GERD and Barrett’s esophagus; it is worthwhile to further investigate. The effect of benefit or harm of presence of Hp infection in GERD is debated; most are epidemiologic study, lacking evidence- based data; whether need to eradicate Hp in the patients with reflux disease or not is difficult to conclude. The current theory of transient relaxation of LES (TLESRs) as the major pathophysiologic mechanism of GERD has been challenged after pooling mass clinical experiences. Particularly after recent development of endoscopic therap
Sponsor: National Taiwan University Hospital

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Information By: National Taiwan University Hospital

Dates:
Date Received: September 9, 2005
Date Started: February 2004
Date Completion: December 2006
Last Updated: November 25, 2005
Last Verified: February 2004