W1087 A Selective Cyclooxygenase-2 Inhibitor, Etodolac, Suppresses Stomach Carcinogenesis After Eradication Therapy of Helicobacter pylori in Mongolian Gerbils with Intestinal Metaplasia

Background: Helicobacter pylori (H. pylori) eradication therapy may improve gastric atrophy and intestinal metaplasia, but the results of previous studies have not always been consistent. The aim of this study was to compare the histological changes of intestinal metaplasia and gastric atrophy among the use of acid-suppressing drugs after H. pylori eradication. Methods: A cohort of 242 patients who underwent successful eradication therapy for H. pylori gastritis and surveillance endoscopy examination from 1996 to 2015 was analyzed. Changes in the histological scores of intestinal metaplasia and atrophy according to drug use (proton-pump inhibitors (PPIs), H2 receptor antagonists (H2RAs), and non-acid suppressant use) were evaluated in biopsies of the antrum and corpus using a generalized linear mixed model in all patients. Results: The mean follow-up period and number of biopsies were 5.48 ± 4.69 years and 2.62 ± 1.67 times, respectively. Improvement in the atrophy scores of both the antrum (p = 0.042) and corpus (p = 0.020) were significantly superior in patients with non-acid suppressant drug use compared with those of PPI and H2RA use. Metaplasia scores in both the antrum and corpus did not improve in all groups, and no significant differences were observed among groups in the antrum (p = 0.271) and corpus (p = 0.077). Conclusions: Prolonged acid suppression by PPIs or H2RAs may limit the recovery of gastric atrophy following H. pylori eradication.

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Cell Proliferation and Inflammation on Biopsy Samples With Multifocal Atrophic Gastritis Before and 1 Year After Helicobacter pylori Eradication

Archives of Pathology & Laboratory Medicine ◽

10.5858/2005-129-1451-cpaiob ◽

2005 ◽

Vol 129 (11) ◽

pp. 1451-1456

Author(s):

Jeannette Guarner ◽

Jeanine Bartlett ◽

Roslyn Seitz ◽

Toni Whistler ◽

Roberto Herrera-Goepfert ◽

...

Keyword(s):

Cell Proliferation ◽

Helicobacter Pylori ◽

T Lymphocytes ◽

Intestinal Metaplasia ◽

Eradication Therapy ◽

Ki 67 ◽

Proliferation Markers ◽

Helicobacter Pylori Eradication ◽

Biopsy Specimens ◽

H Pylori

Abstract Context.—Results of clinical trials that have assessed whether gastric cancer is preventable with Helicobacter pylori eradication therapy remain inconclusive. These trials have used atrophy, intestinal metaplasia, and dysplasia as histopathologic end points that reflect possible preneoplastic lesions. Trial results would be more compelling if cell proliferation and inflammatory markers improved simultaneously with histopathologic lesions. Objective.—To study the presence of cell proliferation markers and type of inflammatory cells in biopsy specimens with gastritis, atrophy, and intestinal metaplasia before and 1 year after H pylori therapy and to determine if immunohistochemistry can be used to study these. Design.—We evaluated 12 subjects with gastritis and 16 with gastritis and multiple foci of atrophy and intestinal metaplasia by using immunohistochemical assays for tumor suppressor protein p53, proliferation marker Ki-67, cell cycle regulator cyclin D1, T and B lymphocytes, macrophages, and TUNEL (terminal deoxynucleotide transferase deoxyuridine triphosphate nick end labeling) assay for apoptosis. The biopsy specimens were selected from a randomized clinical trial that studied improvement of histopathologic gastric lesions after H pylori eradication. Results.—Groups of surface epithelial cells that expressed p53 and Ki-67 were observed more often in subjects with atrophy and intestinal metaplasia compared with those with gastritis alone. T lymphocytes in the lamina propria were frequently observed 1 year after treatment in subjects with atrophy and intestinal metaplasia. Conclusions.—Immunohistochemical assays for cell proliferation and inflammatory cell markers showed different distribution patterns in these gastric biopsy specimens. The presence of T lymphocytes and groups of cells that expressed proliferation markers in subjects with multiple foci of atrophy and intestinal metaplasia needs further study.

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Cyclooxygenase-2 expression in early gastric cancer, intestinal metaplasia and Helicobacter pylori infection

European Journal of Gastroenterology & Hepatology ◽

10.1097/00042737-200204000-00001 ◽

2002 ◽

Vol 14 (4) ◽

pp. 347-349 ◽

Cited By ~ 15

Author(s):

Marjorie M. Walker

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Early Gastric Cancer ◽

Intestinal Metaplasia ◽

Cyclooxygenase 2 ◽

Helicobacter Pylori Infection

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Over expression of p53 protein in gastric intestinal metaplasia caused by Helicobacter pylori infection in mongolian gerbils

Gastroenterology ◽

10.1016/s0016-5085(98)80617-3 ◽

1998 ◽

Vol 114 ◽

pp. A152

Author(s):

S. Honda ◽

T. Fujioka ◽

M. Tokieda ◽

T. Gotoh ◽

A. Nishizono ◽

...

Keyword(s):

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

P53 Protein ◽

Helicobacter Pylori Infection ◽

Mongolian Gerbils ◽

Gastric Intestinal Metaplasia ◽

Over Expression

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Gastric microbes associated with gastric inflammation, atrophy and intestinal metaplasia 1 year after Helicobacter pylori eradication

Gut ◽

10.1136/gutjnl-2019-319826 ◽

2020 ◽

Vol 69 (9) ◽

pp. 1572-1580 ◽

Cited By ~ 7

Author(s):

Joseph J Y Sung ◽

Olabisi Oluwabukola Coker ◽

Eagle Chu ◽

Chun Ho Szeto ◽

Simson Tsz Yat Luk ◽

...

Keyword(s):

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Inositol Phosphate ◽

Eradication Therapy ◽

Treated Group ◽

Oral Bacteria ◽

Microbial Interactions ◽

Bacterial Taxonomy ◽

Before And After ◽

H Pylori

ObjectiveHelicobacter pylori is associated with gastric inflammation, precancerous gastric atrophy (GA) and intestinal metaplasia (IM). We aimed to identify microbes that are associated with progressive inflammation, GA and IM 1 year after H. pylori eradication.DesignA total of 587 H. pylori–positive patients were randomised to receive H. pylori eradication therapy (295 patients) or placebo (292 patients). Bacterial taxonomy was analysed on 404 gastric biopsy samples comprising 102 pairs before and after 1 year H. pylori eradication and 100 pairs before and after 1 year placebo by 16S rRNA sequencing.ResultsAnalysis of microbial sequences confirmed the eradication of H. pylori in treated group after 1 year. Principal component analysis revealed distinct microbial clusters reflected by increase in bacterial diversity (p<0.00001) after H. pylori eradication. While microbial interactions remained largely unchanged after placebo treatment, microbial co-occurrence was less in treated group. Acinetobacter lwoffii, Streptococcus anginosus and Ralstonia were enriched while Roseburia and Sphingomonas were depleted in patients with persistent inflammation 1 year after H. pylori eradication. A distinct cluster of oral bacteria comprising Peptostreptococcus, Streptococcus, Parvimonas, Prevotella, Rothia and Granulicatella were associated with emergence and persistence of GA and IM. Probiotic Faecalibacterium praustznii was depleted in subjects who developed GA following H. pylori eradication. Functional pathways including amino acid metabolism and inositol phosphate metabolism were enriched while folate biosynthesis and NOD-like receptor signalling decreased in atrophy/IM-associated gastric microbiota.ConclusionThis study identified that gastric microbes contribute to the progression of gastric carcinogenesis after H. pylori eradication.

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