Neoplasms

Digestive System Diseases

All Conditions

Rare Diseases

Stomach Neoplasms

Stomach Cancer

Jun-Hyung Jun-Hyung, M.D.

Helicobacter pylori has been recognized as a major pathogen in gastric carcinogenesis. Current guidelines recommend the H. pylori "test-and-treat" strategy for the purpose of primary and secondary gastric cancer prevention. Considering the "point of no return" theory, however, H. pylori eradication cannot reduce the risk of gastric cancer in subjects with gastric atrophy and intestinal metaplasia. The intragastric hypoacidic environment is associated with the risk of intestinal-type gastric cancer development. Recently, the secretory ability of the stomach can be measured using the serum pepsinogen (PG) assay.

This study aimed to evaluate the change of serum PGs after H. pylori eradication success and identify the optimal timing of eradication.

Biospecimen would be obtained for urease test (commercial name: CLOtest).

Serum Pepsinogen After H. Pylori Eradication

Serum Pepsinogen After Helicobacter Pylori Eradication for the Gastric Cancer Prevention

Soonchunhyang University Hospital

Associate Professor

Symptoms and General Pathology

Atrophy

Metaplasia

Gastrointestinal Neoplasms

Digestive System Neoplasms

Gastrointestinal Diseases

Stomach Diseases

Anti-Infective Agents

All Drugs and Chemicals

Gastrointestinal Agents

Anti-Bacterial Agents

Amoxicillin

Rabeprazole

Antibiotics, Antitubercular

Clarithromycin

Omeprazole

Omeprazole 20 mg or Rabeprazole 10 mg bid + clarithromycin 500 mg and amoxicillin 1,000 mg bid for 7 days

Helicobacter pylori eradication

Omeprazole 20 mg or Rabeprazole 10 mg bid + two placebo (for antibiotics) for 7 days

placebo

Il Ju Choi, M.D., Ph.D.

Helicobacter pylori (H. pylori) is associated with gastric cancer in epidemiological studies.Gastric atrophy and intestinal metaplasia caused by H. pylori are considered as precancerous lesions, but whether H. pylori eradication improves these lesions is controversial.The primary objective of this study is to evaluate whether Helicobacter pylori eradication improves glandular atrophy and intestinal metaplasia which are known to be precancerous condition in patients undergoing subtotal gastrectomy for gastric cancer.

Helicobacter pylori (H. pylori) is a primary etiological agent leading to chronic gastritis and peptic ulcer. The organism is also associated with gastric cancer in epidemiological studies. However, detailed mechanism of carcinogenesis remains unknown. Histolopathological studies indicate that chronic H. pylori infection progresses over decades through stages of chronic gastritis, atrophy, intestinal metaplasia, dysplasia and cancer. Gastric atrophy and intestinal metaplasia are considered as precancerous lesions, but whether H. pylori eradication improves these lesions is controversial. And the issue has not been evaluated in gastric cancer patients. However, despite the lack of evidence proven by a well-designed study, current guidelines from Europe and Japan recommend H. pylori eradication treatment in patients who were treated for gastric cancer by surgically or endoscopically. Thus, it is important to evaluate whether H. pylori eradication can improve known precancerous lesion, i.e. glandular atrophy and intestinal metaplasia in gastric cancer patients. Such histological improvement may eventually reduce secondary gastric cancer development and provide evidence for current guidelines. Helicobacter pylori is a primary etiological agent leading to chronic gastritis and peptic ulcer. The organism is also associated with gastric cancer in epidemiological studies. However, detailed mechanism of carcinogenesis remains unknown. Histolopathological studies indicate that chronic H. pylori infection progresses over decades through stages of chronic gastritis, atrophy, intestinal metaplasia, dysplasia and cancer. Gastric atrophy and intestinal metaplasia are considered as precancerous lesions, but whether H. pylori eradication improves these lesions is controversial. And the issue has not been evaluated in gastric cancer patients. However, despite the lack of evidence proven by a well-designed study, current guidelines from Europe and Japan recommend H. pylori eradication treatment in patients who were treated for gastric cancer by surgically or endoscopically. Thus, it is important to evaluate whether H. pylori eradication can improve known precancerous lesion, i.e. glandular atrophy and intestinal metaplasia in gastric cancer patients. Such histological improvement may eventually reduce secondary gastric cancer development and provide evidence for current guidelines.

Efficacy Study of Helicobacter Pylori Eradication in Patients Undergoing Subtotal Gastrectomy for Gastric Cancer

Effect of Helicobacter Pylori Eradication on Glandular Atrophy and Intestinal Metaplasia in Patients Undergoing Subtotal Gastrectomy for Gastric Cancer

National Cancer Center, Korea

Infections

Communicable Diseases

Antineoplastic Agents

Esomeprazole

Levofloxacin

Ofloxacin

All enrolled subjects received chemoprevention with 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.

Pan-Chyr Yang, PHD

Yi-Chia Lee, MD, MSc

Jaw-Town Lin, MD, PhD

Tony Hsiu-Hsi Chen, PhD

Based on a universal eradication of H. pylori in an offshore island (Matsu) with a high prevalence of gastric cancer as well as premalignant gastric lesion, we first examined the infection rate of H. pylori. Secondly, we evaluated the efficacy of clarithromycin-based triple therapy with a levofloxacin-based rescue treatment. And thirdly, we tested the hypothesis that whether the cure of H. pylori can reverse the premalignant gastric lesion. Fourth, we determine the cost-effectiveness of this intervention. The gene-environment interaction will be addressed regarding gastric cancer carcinogenesis. Finally, the incident rate of gastric cancer would be followed in this cohort.

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:

1. Determine the efficacy of a novel regimen to treat the H. pylori infection in the general population.
2. To address the question whether the premalignant gastric lesion could be reversed following the cure of infection.
3. To simulate the cost-effectiveness of this chemoprevention.
4. To use individual data to empirically calculate the cost-effectiveness of this intervention.
5. To address the host genetic susceptibility to gastric cancer development.
6. To follow-up the gastric cancer incidence following the eradication of H. pylori.

Community-based Helicobacter Pylori Eradication

Community-based Helicobacter Pylori Eradication With Two Sequential Antibiotic Regimens for the Residents and Migrants From a High-risk Area for Gastric Cancer

National Taiwan University Hospital

Polyps

Adenomatous Polyps

Pathological Conditions, Anatomical

Adenoma

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

Enzyme Inhibitors

Cytochrome P-450 CYP3A Inhibitors

Cytochrome P-450 Enzyme Inhibitors

H. pylori eradication (Triple Therapy) as first line treatment if eradication failure, quadruple therpy will be provided as 2nd line treatment

H. pylori eradication (Amoxaxillin, Lanston, Clarithromycin)

Su Youn Y Nam, MD, PhD

Evaluation of the effect of H. pylori eradication on regression of H. pylori-related gastric polyp (Ranomized controlled trial)

1. Study design: open labeled RCT
2. Study group H. pylori eradication group (N=17), non-eradication group (N=15)
3. Treatment plan

   1. Baseline EGD

      : 0.3-1cm sized polyp - bx \& CLO test (antrum \& body)

      ==\> if H. pylori positive and eligible patients, randomization
   2. Triple therapy
   3. UBT (4week after eradication)
   4. Follow-up EGD: gross finding, CLO test
4. Evaluation of polyp regression

   1. disappear
   2. regression over 50% (size, number)
   3. no change or increase (size, number)

(A) Study population

1. inclusion HP-realetd polyp polyp size with 0.3cm-1cm 20 yr - 70yr
2. exclusion peptic ulcer, healing stage or acute stage recent use of PPI within 4weeks Liver cirrhosis, renal insufficiency, other serious chronic or acute disease current infection of other bacteria, virus, or fungus cancer, psychologic disease heavy drinker drug abuser pregnant women, Penicillin allergy, digoxin, antifungal, wafarin previosu H. pylori eradication enroll gastric polyp with bleeding or malignant transformation tiny polyp less than 3mm.

(B) Study method

1. Study design: open labeled RCT
2. Study group H. pylori eradication group (N=17), non-eradication group (N=15)
3. Treatment plan

   1. Baseline EGD: 0.3-1cm sized polyp - bx \& CLO test (antrum \& body) ==\> if H. pylori positive and eligible patients, randomization
   2. Triple therapy
   3. UBT (4week after eradication) if eradication failure in triple therapy, 2nd line treatment (metroniazole based quadraple therpay) and the UBT (4week after eradication)
   4. Follow-up EGD (3-9M): gross finding, CLO test
4. Evaluation of polyp regression

   1. disappear
   2. regression over 50% (size, number)
   3. no change or increase (size, number)
5. Statistical analysis

   1. Chi-square test to compare polyp regression between treatment \& control group.
   2. t-test to compare continuous variables between treatment \& control group.
   3. Paired T-test to compare the size between baseline and follow-up EGD.
   4. Regression analysis: univariate \& multivariate analysis.

open labelled randomized controlled trial. randomization : 2015 September

Effect of H. Pylori Eradication on the Fate of H. Pylori-associated Gastric Polyp

Effect of H. Pylori Eradication on the Fate of H. Pylori-associated Gastric Polyp (Randomized Controlled Study)

Evaluation of the effect of H. pylori eradication on the regression of H. pylori associated gastric polyp

Study group

1. H. pylori eradication
2. H. pylori non-eradication

Definition of gastric polyp change:

1. Disappearance of gastric polyp
2. Reduction of polyp size over 50%
3. No change of size or increased size

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Serum Pepsinogen After H. Pylori Eradication	NCT03924375	Helicobacter Py...		20 Years - 70 Years	Soonchunhyang University Hospital
Efficacy Study of Helicobacter Pylori Eradication in Patients Undergoing Subtotal Gastrectomy for Gastric Cancer	NCT01002443	Gastric Cancer	Helicobacter py... placebo	18 Years - 70 Years	National Cancer Center, Korea
Community-based Helicobacter Pylori Eradication	NCT00155389	Helicobacter Py...	Helicobacter py...	30 Years -	National Taiwan University Hospital
Community-based Helicobacter Pylori Eradication	NCT00155389	Helicobacter Py...	Helicobacter py...	30 Years -	National Taiwan University Hospital
Effect of H. Pylori Eradication on the Fate of H. Pylori-associated Gastric Polyp	NCT03065868	Gastric Polyp Helicobacter Py...	H. pylori eradi...	20 Years - 70 Years	Kyungpook National University Hospital
Serum Pepsinogen After H. Pylori Eradication	NCT03924375	Helicobacter Py...		20 Years - 70 Years	Soonchunhyang University Hospital
Efficacy Study of Helicobacter Pylori Eradication in Patients Undergoing Subtotal Gastrectomy for Gastric Cancer	NCT01002443	Gastric Cancer	Helicobacter py... placebo	18 Years - 70 Years	National Cancer Center, Korea

Spots Global Cancer Trial Database for helicobacter pylori eradication