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Hiatal Hernia clinical trials

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NCT ID: NCT00260585 Recruiting - Esophageal Cancer Clinical Trials

Esophageal Cancer Risk Registry

Start date: June 1999
Phase:
Study type: Observational

The purpose of this study is to identify markers in the blood and tissue that could indicate risk factors for the development and progression of esophagus cancer. This research aims to collect medical history, blood, and tissue samples from patients who present with an esophageal disorder. Identifying genetic and behavioral risk factors involved in the development of esophageal cancer might allow for early detection and prevention. Survival and an opportunity for a cure with esophageal cancer will depend greatly on the stage of diagnosis. Tumors can develop changes in their genetic (hereditary) make-up, and these changes can sometimes be seen in normal tissues before the development of cancer. These genetic (hereditary) changes can serve as tumor markers and can be detected using methods that study changes in genetic material like DNA and RNA. The analysis of proteins can provide additional information. By identifying changes in these molecules that are different or altered in cancer, the investigators can use methods and tests for the detection of these changes.

NCT ID: NCT00155805 Recruiting - Hiatal Hernia Clinical Trials

Immunologic Factors in Reflux Esophagitis and Barrett’s Esophagus

Start date: February 2004
Phase: N/A
Study type: Observational

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.