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

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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Metaplasia A Transdifferentiatlon Process that Facilitates Cancer Development: The Model of Gastric Intestinal Metaplasia

Critical Reviews™ in Oncogenesis ◽

10.1615/critrevoncog.v12.i1-2.20 ◽

2006 ◽

Vol 12 (1-2) ◽

pp. 3-26 ◽

Cited By ~ 28

Author(s):

Patricia Mesquita ◽

Raquel Almeida ◽

Nuno Lunet ◽

Celso A. Reis ◽

Luis Filipe Santos Silva ◽

...

Keyword(s):

Intestinal Metaplasia ◽

Cancer Development ◽

Gastric Intestinal Metaplasia

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Helicobacter Infection and Gastric Adenoma

Microorganisms ◽

10.3390/microorganisms9010108 ◽

2021 ◽

Vol 9 (1) ◽

pp. 108

Author(s):

Simone Bertz ◽

Miriam Angeloni ◽

Jan Drgac ◽

Christina Falkeis ◽

Corinna Lang-Schwarz ◽

...

Keyword(s):

Intestinal Metaplasia ◽

Clinicopathological Parameters ◽

Consecutive Series ◽

Gastric Adenoma ◽

Gastric Intestinal Metaplasia ◽

Pyloric Gland Adenoma ◽

Hereditary Tumor Syndromes ◽

Mucosal Changes ◽

H Pylori ◽

Insight Into

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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Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori

International Journal of Advances in Medicine ◽

10.18203/2349-3933.ijam20212096 ◽

2021 ◽

Vol 8 (6) ◽

pp. 764

Author(s):

Sultan Nawahir ◽

George Kurian ◽

Thomas Alexander ◽

Susy Kurian

Keyword(s):

Gastric Mucosa ◽

Alcohol Abuse ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Premalignant Lesions ◽

Control Group ◽

Chronic Alcohol ◽

Chronic Alcohol Abuse ◽

High Prevalence ◽

H Pylori

Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

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