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Gastric microbiota eradication for intestinal metaplasia

ABSTRACT: Interventions: After registration, a biopsy will be performed by upper gastrointestinal endoscopy (within 30 days of registration), and if the histological intestinal metaplasia score in the gastric fundus is 2 or higher, treatment will begin (within 30 days of upper gastrointestinal endoscopy). The investigational treatment consists of a 7-day oral administration of vonoprazan 20 mg twice daily (40 mg/day), metronidazole 250 mg twice daily (500 mg/day), and sitafloxacin 100 mg twice daily (200 mg/day). A second upper gastrointestinal endoscopy with biopsy will be performed 1 year +- 3 months after the first one, and the results will be explained (within 30 days of upper gastrointestinal endoscopy).;Gastric microbiota eradication Primary outcome(s): Improvement rate of histological intestinal metaplasia in gastric antrum Definition: In this study, patients with two or more score of intestinal metaplasia score (updated sydney system) in gastric corpus are intervened. After the intervention with berberine group or control group, patients with one or less the score defined as improved. Primary outcome is improvement rate. Study Design: single arm study, open(masking not used), uncontrolled control, single assignment, treatment purpose

DISEASE(S): Intestinal Metaplasia

PROVIDER: 102990 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:Background: Intestinal metaplasia (IM) is a gastric precancerous lesion that precedes the development of gastric cancer in up to 3.77 cases/1000 person-years. It consists in a trans-differentiation process of gastric to intestinal tissue. Two histological subtypes exist, complete (CIM) and incomplete (IIM), the latter having higher progression rates to gastric cancer . Our objective was to identify molecular processes responsible for the tumoral transition from intestinal metaplasia to GC and the initial steps of this lesion Methods: We used expression microarray to compare the transcriptome of intestinal metaplasia subtypes that progress to gastric cancer (IIM-GC and CIM-GC) after a follow-up period with respect to those that do not progress (IIM control and CIM control). Also, IM-NoGC (IM control, comprising both IIM and CIM Control) was compared with healthy gastric mucosa. Differentially expressed genes were obtained and functional analyses (GSEA and IPA softwares) were performed. Some deregulated genes were validated by qPCR. Results: Histological subtypes of intestinal metaplasia that progress or not to GC differ less among them than to healthy mucosa. Incomplete intestinal metaplasia has a higher number of over-expressed carcinogenic genes and molecular processes than the complete subtype. Most relevant molecular processes and genes in this group include antigenic processing, inflammation, activation of cell cycle and cell proliferation, oncogenes and tumor suppressors. When IM-NoGC is compared with healthy gastric mucosa new identified transcripts include TRIM, TMEM, homeobox, transporters and nucleolar RNAs SNORDs116. We confirm previously reported processes such us intestinal differentiation, metabolism of lipids and of xenobiotics and identify new ones such as non tumoral Warburg effect and melatonin degradation. Conclusions: Differentially expressed genes and molecular processes have been identified for the first time in intestinal metaplasia that progress to gastric cancer. New genes and molecular processes have also been identified in intestinal metaplasia in comparison with healthy gastric mucosa.

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Gastric microbiota eradication for intestinal metaplasia

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