Helicobacter Infection and Gastric Adenoma

Background: We aimed to provide insight into the actual frequencies of gastric adenoma types and their association with gastritis status and associated mucosal changes with a focus on Helicobacter infection and the operative link on gastritis assessment (OLGA)/operative link on gastric intestinal metaplasia assessment (OLGIM) staging. Methods: From the archive of the Institute of Pathology in Bayreuth, we collected a consecutive series of 1058 gastric adenomas diagnosed between 1987 and 2017. Clinicopathological parameters retrieved from diagnostic reports included adenoma type and localization, associated mucosal changes in antrum and corpus (i.e., type of gastritis, the extent of intestinal metaplasia and atrophy), gender, date of birth, and date of diagnosis. Results: Intestinal-type adenoma was the most frequent adenoma (89.1%), followed by foveolar-type adenoma (4.3%), pyloric gland adenoma (3.4%), adenomas associated with hereditary tumor syndromes (2.8%), and oxyntic gland adenoma (0.4%). Adenomas were found in the background of Helicobacter pylori (H. pylori) gastritis in 23.9%, Ex-H. pylori gastritis in 36.0%, autoimmune gastritis in 24.8%, chemical reactive gastritis in 7.4%, and others in 0.1%. More than 70% of patients with gastric adenomas had low-risk stages in OLGA and OLGIM. Conclusions: We found a higher frequency of foveolar-type adenoma than anticipated from the literature. It needs to be questioned whether OLGA/OLGIM staging can be applied to all patients.

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Reduced apoptosis in H. pylori-associated gastric intestinal metaplasia: A factor in gastric carcinogenesis?

Gastroenterology ◽

10.1016/s0016-5085(98)82772-8 ◽

1998 ◽

Vol 114 ◽

pp. A676 ◽

Cited By ~ 2

Author(s):

IA Scotiniotis ◽

T Rokkas ◽

EE Furth ◽

JW Plotkin ◽

B Rigas ◽

...

Keyword(s):

Intestinal Metaplasia ◽

Gastric Carcinogenesis ◽

Gastric Intestinal Metaplasia ◽

H Pylori

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Host Wnt/β-catenin pathway triggered by Helicobacter pylori correlates with regression of gastric intestinal metaplasia after H. pylori eradication

Journal of Medical Microbiology ◽

10.1099/jmm.0.007310-0 ◽

2009 ◽

Vol 58 (5) ◽

pp. 567-576 ◽

Cited By ~ 18

Author(s):

Kuei-Hsiang Hung ◽

Jiunn-Jong Wu ◽

Hsiao-Bai Yang ◽

Li-Ju Su ◽

Bor-Shyang Sheu

Keyword(s):

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Glycogen Synthase ◽

Nucleotide Polymorphisms ◽

Ags Cells ◽

Gastric Intestinal Metaplasia ◽

Before And After ◽

Cox 2 ◽

H Pylori ◽

High Level

Helicobacter pylori eradication can reverse gastric intestinal metaplasia (IM) in some but not all patients. H. pylori induces high levels of nuclear β-catenin staining in IM tissues, as well as overexpression of cyclooxygenase-2 (COX-2). This study investigated whether the Wnt/β-catenin pathway plays a role in IM regression following H. pylori eradication. Sixty-five H. pylori-infected patients with IM who had achieved successful H. pylori eradication provided paired gastric samples before and after eradication to analyse the persistence of IM, and to assess COX-2 and nuclear β-catenin expression. The host genotypes of single nucleotide polymorphisms (SNPs) of the COX-2, β-catenin (CTNNB1) and adenomatous polyposis coli (APC) genes were analysed. In addition, expression of β-catenin, E-cadherin and phosphorylated and unphosphorylated glycogen synthase kinase 3β (GSK-3β) in cell lines challenged with H. pylori isolates from patients with and without IM persistence was compared by immunoanalysis. After a mean 33.9-month follow-up after H. pylori eradication, 44 patients (67.7 %) with IM persistence had a higher rate of high-level nuclear β-catenin expression in IM tissue than those without IM persistence (P=0.008). The patients with IM persistence had a higher rate of AA, GG and AA APC SNP genotypes at positions 4479, 5268 and 5465, respectively, than the patients without IM persistence (P=0.022). The H. pylori isolates from the patients with IM regression after H. pylori eradication induced more phospho-GSK-3β in AGS cells than isolates from patients with IM persistence (P=0.011). It is likely that interactions with H. pylori and the patient's Wnt/β-catenin genetic predisposition determine the outcome of IM persistence following H. pylori eradication.

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Topographic study of H. pylori and gastric intestinal metaplasia in patients with dyspepsia in a tertiary health care setting

Tropical Journal of Pathology and Microbiology ◽

10.17511/jopm.2019.i05.05 ◽

2019 ◽

Vol 5 (5) ◽

pp. 281-286

Author(s):

Dr. Jawahar R. ◽

◽

Dr. Renu G’Boy Varghese ◽

Dr. Thomas Alexander ◽

Dr. George Kurian ◽

...

Keyword(s):

Health Care ◽

Intestinal Metaplasia ◽

Care Setting ◽

Health Care Setting ◽

Gastric Intestinal Metaplasia ◽

H Pylori

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H. pylori Eradication Prevents the Progression of Gastric Intestinal Metaplasia in Reflux Esophagitis Patients Using Long-Term Esomeprazole

The American Journal of Gastroenterology ◽

10.1038/ajg.2009.172 ◽

2009 ◽

Vol 104 (7) ◽

pp. 1642-1649 ◽

Cited By ~ 32

Author(s):

Hsiao-Bai Yang ◽

Bor-Shyang Sheu ◽

Shin-Tar Wang ◽

Hsiu-Chi Cheng ◽

Wei-Lun Chang ◽

...

Keyword(s):

Intestinal Metaplasia ◽

Reflux Esophagitis ◽

Gastric Intestinal Metaplasia ◽

H Pylori

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H. pylori Eradication Prevents the Progression of Gastric Intestinal Metaplasia in Reflux Esophagitis Patients Using Long-Term Esomeprazole

Yearbook of Gastroenterology ◽

10.1016/s0739-5930(10)79438-1 ◽

2010 ◽

Vol 2010 ◽

pp. 24-25

Author(s):

N.J. Talley

Keyword(s):

Intestinal Metaplasia ◽

Reflux Esophagitis ◽

Gastric Intestinal Metaplasia ◽

H Pylori

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Short segment Barrett's esophagus and distal gastric intestinal metaplasia

Arquivos de Gastroenterologia ◽

10.1590/s0004-28032006000200011 ◽

2006 ◽

Vol 43 (2) ◽

pp. 117-120

Author(s):

Judite Dietz ◽

Sílvia Chaves-e-Silva ◽

Luíse Meurer ◽

Setsuo Sekine ◽

Andréa Ribeiro de Souza ◽

...

Keyword(s):

Gastroesophageal Reflux Disease ◽

Gastroesophageal Reflux ◽

Intestinal Metaplasia ◽

Barrett’S Esophagus ◽

Reflux Disease ◽

Barrett's Esophagus ◽

Short Segment ◽

Disease Symptoms ◽

Gastric Intestinal Metaplasia ◽

H Pylori

BACKGROUND: Short segment Barrett's esophagus is defined by the presence of <3 cm of columnar-appearing mucosa in the distal esophagus with intestinal metaplasia on histophatological examination. Barrett's esophagus is a risk factor to develop adenocarcinoma of the esophagus. While Barrett's esophagus develops as a result of chronic gastroesophageal reflux disease, intestinal metaplasia in the gastric cardia is a consequence of chronic Helicobacter pylori infection and is associated with distal gastric intestinal metaplasia. It can be difficult to determine whether short-segment columnar epithelium with intestinal metaplasia are lining the esophagus (a condition called short segment Barrett's esophagus) or the proximal stomach (a condition called intestinal metaplasia of the gastric cardia). AIMS: To study the association of short segment Barrett's esophagus (length <3 cm) with gastric intestinal metaplasia (antrum or body) and infection by H. pylori. PATIENTS AND METHODS: Eight-nine patients with short segment columnar-appearing mucosa in the esophagus, length <3 cm, were studied. Symptoms of gastroesophageal reflux disease were recorded. Biopsies were obtained immediately below the squamous-columnar lining, from gastric antrum and gastric corpus for investigation of intestinal metaplasia and H. pylori. RESULTS: Forty-two from 89 (47.2%) patients were diagnosed with esophageal intestinal metaplasia by histopathology. The mean-age was significantly higher in the group with esophageal intestinal metaplasia. The two groups were similar in terms of gender (male: female), gastroesophageal reflux disease symptoms and H. pylori infection. Gastric intestinal metaplasia (antrum or body) was diagnosed in 21 from 42 (50.0%) patients in the group with esophageal intestinal metaplasia and 7 from 47 (14.9%) patients in the group with esophageal columnar appearing mucosa but without intestinal metaplasia. CONCLUSION: Intestinal metaplasia is a frequent finding in patients with <3 cm of columnar-appearing mucosa in the distal esophagus. In the present study, short segment intestinal metaplasia in the esophagus is associated with distal gastric intestinal metaplasia. Gastroesophageal reflux disease symptoms and H. pylori infection did not differ among the two groups studied.

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The Prevalence of Gastric Intestinal Metaplasia and Distribution ofHelicobacter pyloriInfection, Atrophy, Dysplasia, and Cancer in Its Subtypes

Gastroenterology Research and Practice ◽

10.1155/2015/434039 ◽

2015 ◽

Vol 2015 ◽

pp. 1-6 ◽

Cited By ~ 14

Author(s):

Sehmus Olmez ◽

Mehmet Aslan ◽

Remzi Erten ◽

Suleyman Sayar ◽

Irfan Bayram

Keyword(s):

Intestinal Metaplasia ◽

Gastric Adenocarcinoma ◽

Cancer Development ◽

Common Finding ◽

Gastric Intestinal Metaplasia ◽

Type Iii ◽

High Prevalence ◽

H Pylori ◽

Clinical Records ◽

Main Factor

Objectives. Gastric intestinal metaplasia (IM) is frequently encountered and is considered a precursor of gastric adenocarcinoma. In the Van region of Turkey, gastric adenocarcinoma incidence is high but the prevalence of gastric IM is not known.Helicobacter pylori(H. pylori) infection is a main factor leading to atrophy, IM, and cancer development in the stomach. The aim of the current study was to investigate the prevalence of IM and its subtypes and the prevalence ofH. pyloriinfection, atrophy, dysplasia, and cancer in gastric IM subtypes.Materials and Methods. This retrospective study was conducted on 560 IM among the 4050 consecutive patients who were undergoing esophagogastroduodenoscopy (EGD) with biopsy between June 2010 and October 2014. Clinical records and endoscopic and histopathologic reports of patients with IM were analyzed.Results. The prevalence of gastric IM was 13.8%. The prevalence of incomplete IM was statistically significantly higher than complete IM. Type III IM was the most frequent subtype.Conclusions. Gastric IM is a common finding in patients undergoing EGD with biopsy in this region. High prevalence of incomplete type IM, especially type III, can be associated with the high prevalence of gastric cancer in our region.

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Does eradication of H. pylori reverse gastric intestinal metaplasia? Long-term follow-up utilizing methylene blue staining

Gastroenterology ◽

10.1016/s0016-5085(98)82643-7 ◽

1998 ◽

Vol 114 ◽

pp. A646

Author(s):

TG Morales ◽

RE Sampliner ◽

HS Garewal ◽

E Camargo ◽

MB Fennerty

Keyword(s):

Methylene Blue ◽

Intestinal Metaplasia ◽

Blue Staining ◽

Gastric Intestinal Metaplasia ◽

Long Term Follow Up ◽

H Pylori

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Prevalence of intestinal metaplasia and its relation to Helicobacter pylori infection in Iraq

Iraq Medical Journal ◽

10.22317/imj.v5i1.1025 ◽

2021 ◽

Vol 5 (1) ◽

Keyword(s):

Intestinal Metaplasia ◽

Gastrointestinal Symptoms ◽

Gastric Biopsy ◽

Gastric Atrophy ◽

Gastric Intestinal Metaplasia ◽

Medical City ◽

Upper Gastrointestinal Symptoms ◽

Male Patients ◽

And Gender ◽

H Pylori

Objectives: The aim of this study was to investigate the prevalence of intestinal metaplasia and its relation to H. Pylori infection, gastric atrophy, ulcer, age and gender in patients underwent esophagogastroduodenoscopy and gastric biopsy for upper gastrointestinal symptoms. Method: 200 gastric biopsy blocks examined for patients underwent esophagogastroduodenoscopy (EGD) and gastric biopsy, between January 2019 October 2020 at Gastroenterology and hepatology Hospital / Medical city / Baghdad / Iraq. Result: (67.5%) of patients examined in the study had H. pylori infection, while (20.5%) of the total number patients in the study had gastric intestinal metaplasia. There was significant association between Intestinal metaplasia with both active chronic inflammation and intestinal atrophy but there was no significant association between Intestinal metaplasia with both ulcer and H. pylori infection. Conclusion: gastric intestinal metaplasia encountered more in old age male patients with gastric atrophy and it is not solely related to h pylori, other risk factors could be responsible for it.

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