Topographic association of Ki-67 and Bcl-2 expression with H. pylori infection, gastric atrophy, intestinal metaplasia: A role for antralization in gastric carcinogenesis?

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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Precancerous gastric conditions in high Helicobacter pylori prevalence areas: comparison between Eastern European (Lithuanian, Latvian) and Asian (Taiwanese) patients

Medicina ◽

10.3390/medicina43080080 ◽

2007 ◽

Vol 43 (8) ◽

pp. 623 ◽

Cited By ~ 3

Author(s):

Laimas Jonaitis ◽

Audrius Ivanauskas ◽

Dainius Jančiauskas ◽

Konrads Funka ◽

Agnese Sudraba ◽

...

Keyword(s):

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

The Elderly ◽

Gastric Atrophy ◽

Eastern European ◽

Urease Test ◽

Gastric Biopsies ◽

The Mean ◽

H Pylori ◽

Positive Results

The aim of the study was to compare the prevalence and severity of precancerous condition – gastric atrophy and intestinal metaplasia (IM) between Eastern European (Lithuania and Latvia) and Asian (Taiwan) countries in population older than 55 years. Methods. Patients aged 55 years and older, referred for upper endoscopy due to dyspeptic symptoms, were included in the study. Gastric biopsies were histological investigated according modified Sydney classification. Helicobacter pylori (H. pylori) was detected if any two of three methods (urease test, histology, and serology) were positive. Results. Overall 322 patients included: 52 from Taiwan (TW), 171 from Latvia (LV) and 99 from Lithuania (LT). There were 227 (70%) females and 95 (30%) males. The mean age of TW patients was significantly lower (61.0±5.8 years), than of LV (68.1±7.3 years) and LT (66.5±7.5 years) patients. H. pylori was established in 224 (69.6%) patients. H. pylori positivity was established in 43 (82.7%) TW patients, in 112 (65.5%) LV patients, and in 69 (69.7%) LT patients (P>0.05). In H. pylori-infected patients, any atrophy either in the corpus or in the antrum of the stomach was detected in 26 (60.5%) TW patients, in 40 (35.7%) LV patients, and in 36 (52.2%) LT patients (between TW and LV patients P<0.005). Severe atrophy (grade 2 or 3) detected in 8 (18.6%) TW patients, in 17 (15.2%) LV patients, and in 18 (26.1%) LT patients (P>0.05). Intestinal metaplasia was detected in 22 (51.2%) TW patients, in 37 (33.0%) LV patients and in 31 (44.9%) LT patients among countries (P>0.05). There were no significant differences in proportions of different degrees of both atrophy and intestinal metaplasia among countries. Intestinal metaplasia was found in 79 (77.5%) of 102 patients with any degree of atrophy and in 11 (9.0%) of 122 patients without atrophy (P<0.0001). We found strong statistically significant correlations between atrophy and intestinal metaplasia in antrum (r=0.89), P<0.01, and corpus (r= 0.73), P<0.01. Conclusions. The prevalence of H. pylori in the elderly population is still high in LT, LV, and TW. There are no significant differences in prevalence of gastric atrophy and intestinal metaplasia among TW, LT, and LV. There is a strong correlation between gastric atrophy and intestinal metaplasia.

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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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The Prevalence ofHelicobacter pyloriInfection Decreases with Older Age in Atrophic Gastritis

Gastroenterology Research and Practice ◽

10.1155/2013/494783 ◽

2013 ◽

Vol 2013 ◽

pp. 1-7 ◽

Cited By ~ 6

Author(s):

Shaohua Chen ◽

Lixiong Ying ◽

Mei Kong ◽

Yu Zhang ◽

Youming Li

Keyword(s):

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Prospective Studies ◽

Large Population ◽

Chronic Atrophic Gastritis ◽

Population Based ◽

Gastric Atrophy ◽

Inflammatory Activity ◽

Pathological Characteristics ◽

H Pylori

The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however,H. pyloripositivity and inflammatory activity decreased significantly with increased age.H. pyloriinfection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects withH. pyloriinfection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence ofH. pyloriinfection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG.

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Oxidative DNA damage accumulation in gastric carcinogenesis

Gut ◽

10.1136/gut.42.3.351 ◽

1998 ◽

Vol 42 (3) ◽

pp. 351-356 ◽

Cited By ~ 182

Author(s):

F Farinati ◽

R Cardin ◽

P Degan ◽

M Rugge ◽

F Di Mario ◽

...

Keyword(s):

Dna Damage ◽

Free Radical ◽

Disease Activity ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Oxidative Dna Damage ◽

Multiple Logistic Regression Analysis ◽

Gastric Carcinogenesis ◽

Indirect Measure ◽

H Pylori

Background—Gastric carcinogenesis is a multifactorial, multistep process, in which chronic inflammation plays a major role.Aims—In order to ascertain whether free radical mediated oxidative DNA damage is involved in such a process, concentrations of 8-hydroxydeoxyguanosine (8OHdG), a mutagenic/carcinogenic adduct, and thiobarbituric acid reactive substances (TBARS), as an indirect measure of free radical mediated damage, were determined in biopsy specimens from patients undergoing endoscopy.Patients—Eighty eight patients were divided into histological subgroups as follows: 27 with chronic non-atrophic gastritis, 41 with atrophic gastritis, six with gastric cancer, and 14 unaffected controls.Methods—Intestinal metaplasia,Helicobacter pylori infection, and disease activity were semiquantitatively scored. 8OHdG concentrations were assessed by HPLC with electrochemical detection, and TBARS concentrations were fluorimetrically assayed.Results—8OHdG concentrations (mean number of adducts/105 dG residues) were significantly higher in chronic atrophic gastritis (p=0.0009). Significantly higher concentrations were also detected in the presence of severe disease activity (p=0.02), intestinal metaplasia (p=0.035), and H pylori infection (p=0.001). TBARS concentrations were also higher in atrophic gastritis, though not significantly so. In a multiple logistic regression analysis, 8OHdG concentrations correlated best with the presence and severity of H pylori infection (r=0.53, p=0.002).Conclusions—Chronic gastritis is characterised by the accumulation of oxidative DNA damage with mutagenic and carcinogenic potential. H pylori infection is the major determinant for DNA adduct formation.

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Prospects for intervention in gastric carcinogenesis: reversibility of gastric atrophy and intestinal metaplasia

Gut ◽

10.1136/gut.49.1.2 ◽

2001 ◽

Vol 49 (1) ◽

pp. 2-4 ◽

Cited By ~ 55

Author(s):

M F DIXON

Keyword(s):

Intestinal Metaplasia ◽

Gastric Carcinogenesis ◽

Gastric Atrophy

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Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

BioMed Research International ◽

10.1155/2015/737621 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 18

Author(s):

Soichiro Sue ◽

Wataru Shibata ◽

Shin Maeda

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Signaling Pathways ◽

Intracellular Signaling ◽

Gastric Carcinogenesis ◽

Dependent Manner ◽

Intracellular Signaling Pathways ◽

H Pylori

Helicobacter pylori(H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated.H. pyloriinduces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner.H. pylorieventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.

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