Community-based Helicobacter Pylori Eradication
|ClinicalTrials.gov Identifier: NCT00155389|
Recruitment Status : Unknown
Verified July 2012 by National Taiwan University Hospital.
Recruitment status was: Recruiting
First Posted : September 12, 2005
Last Update Posted : November 14, 2012
|Condition or disease||Intervention/treatment||Phase|
|Helicobacter Pylori Infection||Drug: Helicobacter pylori eradication||Phase 4|
Despite the decline of global incidence, gastric cancer still affects public health substantially due to the considerable medical burden in the treatment of disease at the symptomatic stage. This fact has prompted clinicians to extend their attention from the multidisciplinary therapies to the design of preventive strategies. Gastric cancer development follows a carcinogenic process from non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, and eventually to the adenocarcinoma. Helicobacter pylori (H. pylori) infection triggers this carcinogenic cascade and its eradication is currently the most reliable regimen to arrest the histologic progression in order to prevent gastric cancer. Emerging data have suggested that the benefit of H. pylori treatment earlier in the course of infection is larger and cannot be outweighed by a disfavored discount rate as a result of different time horizons between early treatment and later benefit of averting advanced cancer.
In the Asia-Pacific area, however, virulent strains of H. pylori infection are highly prevalent and premalignant gastric lesions may have already developed at the take-off age of active intervention. Our current knowledge remains limited in answering whether H. pylori eradication can regress these premalignant lesions and if so, what determinant can contribute to a positive response is unknown. The concept of "a point of no return" suggests that the benefit of H. pylori eradication may diminish at later stages when many types of molecular damage become irreversible. Several population-based studies, in contrast, found that the premalignant gastric lesions were potentially reversible given a sufficiently long duration free from infection. The inconsistence may reflect the facts that studies with adequate sample size and long enough follow-up are rarely available and that some important factors, such as the variation in host susceptibility to disease and dietary exposure to carcinogens, are difficult to be measured but they are likely to confound the results.
Therefore, the present study was to:
- Determine the efficacy of a novel regimen to treat the H. pylori infection in the general population.
- To address the question whether the premalignant gastric lesion could be reversed following the cure of infection.
- To simulate the cost-effectiveness of this chemoprevention.
- To use individual data to empirically calculate the cost-effectiveness of this intervention.
- To address the host genetic susceptibility to gastric cancer development.
- To follow-up the gastric cancer incidence following the eradication of H. pylori.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||5000 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Community-based Helicobacter Pylori Eradication With Two Sequential Antibiotic Regimens for the Residents and Migrants From a High-risk Area for Gastric Cancer|
|Study Start Date :||January 2004|
|Estimated Primary Completion Date :||December 2015|
|Estimated Study Completion Date :||December 2015|
Active Comparator: H pylori eradication
All enrolled subjects received chemoprevention with Helicobacter pylori eradication
Drug: Helicobacter pylori eradication
For subjects who received the first-line treatment, the costs included the initial 13C-UBT, one-week triple therapy (esomeprazole 40mg once daily, amoxicillin 1g twice daily, and clarithromycin 500mg twice daily), and the confirmatory 13C-UBT. For subjects in whom the initial treatment failed, the costs further included the re-treatment consisting of ten-day triple therapy (esomeprazole 40mg once daily, amoxicillin 1g twice daily, and levofloxacin 500mg once daily), and the confirmatory 13C-UBT.
The first round of study was between 2004 and 2005, the second round was between 2008 and 2009, and the third round was between 2012 and 2013.
Other Name: Chemoprevention
- Successful helicobacter eradication, change in premalignant gastric lesion, and change in gastric cancer incidence rate [ Time Frame: 12 years ]
- Intragastric histologic change [ Time Frame: 12 years ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00155389
|Contact: Pan-Chyr Yang, PHDemail@example.com|
|Taipei, Taiwan, 10015|
|Contact: Yi-Chia Lee, MD, MSc 23123456 ext 63351 firstname.lastname@example.org|
|Principal Investigator: Jaw-Town Lin, MD, PhD|
|Principal Investigator: Tony Hsiu-Hsi Chen, PhD|
|National Taiwan University Hospital||Completed|
|Taipei, Taiwan, 100|
|Study Chair:||Pan-Chyr Yang, PHD||National Taiwan University Hospital|