Role of Statin on the Gastric Inflammation in Patients at High Risk of Gastric Cancer
The recruitment status of this study is unknown. The completion date has passed and the status has not been verified in more than two years.
Verified February 2014 by Yonsei University.
Recruitment status was: Recruiting
Information provided by (Responsible Party):
First received: March 7, 2013
Last updated: May 26, 2014
Last verified: February 2014
Statins are commonly used as cholesterol-lowering medications and have shown effectiveness in the primary and secondary prevention of heart attack and stroke. In addition, several recent studies of human cancer cell lines and animal tumor models indicate that statins may have chemopreventive properties through the arresting of cell-cycle progression. The chemopreventive effect of statins was demonstrated in some kind of human tumors including colorectal cancer. In addition, recent one large epidemiologic study showed that statins decreased risk of gastric cancer. On the other hands, it has been well known that Helicobacter pylori infection induces gastric atrophy and intestinal metaplasia, which are premalignant lesions of gastric cancer. Progression of these premalignant lesions could be limited by H. pylori eradication. In addition, a recent double blind randomization study revealed that simvastatin as adjuvant to standard therapy improves significantly the H. pylori eradication rate. Therefore, investigators conjecture that statins may have an adjuvant role for inhibition of gastric carcinogenesis. investigators aim to evaluate the role of statins in gastric carcinogenesis by observing the changes of gastric inflammation under statins.
Early Gastric Cancer or Gastric Adenoma
Drug: Arm1: Statin
Drug: Arm2: Placebo
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
Primary Outcome Measures:
| Estimated Enrollment:
| Study Start Date:
| Estimated Study Completion Date:
| Estimated Primary Completion Date:
||December 2015 (Final data collection date for primary outcome measure)
Placebo Comparator: Control group
Drug: Arm1: Statin
Study1 (only H. pylori infected patients) Arm1: All patients undergo H. pylori eradication therapy after 2 weeks from the endoscopic submucosal dissection. In this arm2, all patients take statins for 6 months. Then, follow-up endoscopy for gastric biopsy and CLO test will be performed after 6.5 months from the endoscopic submucosal dissection.
Study2 (only H. pylori non-infected patients) Arm1: In this arm2, all patients start taking statins after 2 weeks from the endoscopic submucosal dissection. Follow-up endoscopy for gastric biopsy will be performed after 6.5 months from the endoscopic submucosal dissection.
Placebo Comparator: Statin group
Drug: Arm2: Placebo
Study1 (only H. pylori infected patients) Arm2: All patients undergo H. pylori eradication therapy after 2 weeks from the endoscopic submucosal dissection. In this arm2, all patients take placebos for 6 months. Then, follow-up endoscopy for gastric biopsy and CLO test will be performed after 6.5 months from the endoscopic submucosal dissection.
Study2 (only H. pylori non-infected patients) Arm2: In this arm2, all patients start taking placebos after 2 weeks from the endoscopic submucosal dissection. Follow-up endoscopy for gastric biopsy will be performed after 6.5 months from the endoscopic submucosal dissection.
Other Name: C10AA-Hmg coa reductase inhibitors
|Ages Eligible for Study:
||20 Years to 70 Years (Adult, Senior)
|Genders Eligible for Study:
|Accepts Healthy Volunteers:
- Age, between 20 and 70
- Early gastric cancer or adenoma which is achieved curative resection by endoscopic submucosal dissection
- ECOG performance status 0 or 1
- Previous subtotal gastrectomy or gastrostomy
- Repeated endoscopic submucosal dissection
- Two or more synchronous lesions
- Presence of gastric or duodenal ulcer except artificial ulcer due to endoscopic submucosal dissection
- History of drugs which are able to induce gastric ulcer including aspirin, NSAIDs, and steroid (30 days or more, within 1 year at the time of screening
- Indication of statins, including dyslipidemia, myocardial infarction, and heart failure.
- Develop of complications caused by endoscopic submucosal dissection, including bleeding, perforation, and pneumonia
- LDL < 70 mg/dL
- Allergy to statins
- Pregnancy or breast milk feeding
- Active infection
- Significant cardiopulmonary disease
- Active hepatitis or severe hepatic dysfunction
- Severe renal dysfunction
- Severe bone marrow dysfunction
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Please refer to this study by its ClinicalTrials.gov identifier: NCT01813994
|Seoul, Korea, Republic of, 120-752 |
History of Changes
|Other Study ID Numbers:
|Study First Received:
||March 7, 2013
||May 26, 2014
||Korea: Institutional Review Board
Keywords provided by Yonsei University:
Statin; Gastric inflammation; Gastric cancer
Additional relevant MeSH terms:
ClinicalTrials.gov processed this record on January 18, 2017
Digestive System Neoplasms
Neoplasms by Site
Digestive System Diseases
Neoplasms, Glandular and Epithelial
Neoplasms by Histologic Type
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Molecular Mechanisms of Pharmacological Action
Lipid Regulating Agents