scholarly journals Incomplete Intestinal Metaplasia as an Indicator for Early Detection of Gastric Carcinoma in The Events of Helicobacter Pylori Positive Chronic Atrophic Gastritis

2006 ◽  
Vol 6 (4) ◽  
pp. 48-53 ◽  
Author(s):  
Zora Vukobrat-Bijedić ◽  
Svjetlana Radović ◽  
Azra Husić-Selimović ◽  
Srđan Gornjaković
Keyword(s):  
Gastric Mucosa ◽  
Gastric Carcinoma ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Risk Group ◽  
Precancerous Lesion ◽  
Chronic Atrophic Gastritis ◽  
Tumor Lesion ◽  
H Pylori ◽  
Lesser Curvature

The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastriccarcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastriccarcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

scholarly journals Helicobacter Pylori as a Promoter of Accelerated Regeneration, Pathological Differentiation and Transformation of Normal Gastric Mucosa into Cancerous Type

2006 ◽  
Vol 6 (3) ◽  
pp. 57-60
Author(s):  
Zora Vukobrat-Bijedić ◽  
Svjetlana Radović ◽  
Azra Husić-Selimović ◽  
Srđan Gornjaković
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Gastric Carcinoma ◽  
Chronic Atrophic Gastritis ◽  
Epithelial Dysplasia ◽  
Control Group ◽  
Tumor Lesion ◽  
Pathological Differentiation ◽  
H Pylori ◽  
Lesser Curvature

The aim of the study was to ascertain presence of Helicobacter pylori in gastric carcinoma as a responsible promoter of inflammatory-regenerative changes, which lead to pathological differentiation and transformation of normal epithelial cells into intestinal type and, in progression, cause epithelial dysplasia that develops into early gastric carcinoma. The paper presents prospective study that includes clinical, pathohistological and microbiological aspects of carcinogenesis initiation in gastric mucosa. The subjects are patients treated at Gastroenterohepatology Clinic divided into two groups. One group included 50 patients with gastric carcinoma while the control group included 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to endoscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the region 1-2 cm removed from tumor lesion. We used HUT test to verify H. pylori presence in biopsy samples. We analyzed the samples for presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in gastric mucosa and evaluated their meaning for the prognosis. Our study confirmed Helicobaster pylori responsibility for inflammatory events in gastric mucosa in patients with gastric carcinoma. Slight and mild epithelial dysplasia with chronic atrophic gastritis grade I and II coupled with intestinal metaplasia may be considered an indicator for early detection of carcinoma. Such patients represent risk group for gastric carcinoma development.

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

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.

Immunohistochemical Detection of Carcinoembryonic Antigen (CEA) in Non-Cancerous and Cancerous Gastric Mucosa

1989 ◽  
Vol 4 (1) ◽  
pp. 8-12 ◽  
Author(s):  
A. Nasierowska-Guttmejer ◽  
A.W. Szawlowski
Keyword(s):  
Gastric Mucosa ◽  
Gastric Carcinoma ◽  
Atrophic Gastritis ◽  
Carcinoembryonic Antigen ◽  
Chronic Atrophic Gastritis ◽  
Immunoperoxidase Method ◽  
Immunohistochemical Detection ◽  
Epithelial Hyperplasia ◽  
Normal Gastric Mucosa ◽  
Localization Pattern

Carcinoembryonic antigen (CEA) was stained by the PAP immunoperoxidase method in cancerous and non-cancerous gastric mucosa of 40 patients (25 non-cancerous dyspeptic patients and 15 patients with gastric carcinoma). The pattern of CEA localization was apical or membranous-cytoplasmic and immuno-reactivity was mild (+), moderate (++) or intensive (+++). No CEA immunoreactivity was detected in normal gastric mucosa whereas it was marked in gastric mucosa of non-cancerous dyspeptic patients with chronic atrophic gastritis and dysplasia (intense). In patients with superficial gastritis and epithelial hyperplasia it was mild or absent. The CEA localization pattern was also apical in non-cancerous dyspeptic patients with microscopic changes, e.g. superficial or chronic atrophic gastritis, epithelial hyperplasia and dysplasia, and in non-cancerous mucosa and cancerous tissue of patients with well (G1) and moderately (G2) differentiated adenocarcinoma.

scholarly journals Review of Research on Routes of Helicobacter pylori Infection

2015 ◽  
Vol 4 (2) ◽  
pp. 45-49
Author(s):  
Hang Li
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Gastric Adenocarcinoma ◽  
Precancerous Lesions ◽  
Natural Environments ◽  
H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

NTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION IN PATIENTS WITH CHRONIC GASTRITIS.

2011 ◽  
pp. 63-71
Author(s):  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Significant Relationship ◽  
Precancerous Lesion ◽  
Chronic Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Antral Gastritis

Background: Intestinal metaplasia is a precancerous lesion. Helicobacter pylori is identified as an important cause of gastric cancer. This study is aimed at assessing the intestinal metaplasia and Helicobacter pylori infection and their relation in patients with chronic gastritis. Patients and methods: Study includes 75 patients with chronic gastritis diagnosed by clinical, endoscopic and histopathological criteria. Intestinal metaplasia is diagnosed by HE stain. Hp infection is tested by CLO-test from Viet A Ltd. Results: Hp infecton rate in this study is 66.67% and is highest in patients with antral gastritis. Intestinal metaplasia is found in 29.33% of patients with chronic gastritis with the predominance of complete intestinal metaplasia. The rate of intestinal metaplasia is the highest in the group with chronic atrophic gastritis. There is a significant relationship between intestinal metaplasia and Hp ìnfection. Conclusion: Hp and intestinal metaplasia are found at significant rates in chronic gastritis. The rate of intestinal metaplasia is clearly higher in the group with Hp-positive chronic gastritis.

scholarly journals Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

2016 ◽  
Vol 2 (3) ◽  
pp. 173
Author(s):  
Sergii Vernygorodskyi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Gastric Epithelium ◽  
Number Of Genes ◽  
Activating Transcription Factor ◽  
H Pylori ◽  
Gene Inhibition

<p class="BodyText1"><em>Helicobacter pylori</em> (<em>H. pylori</em>) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). <em>H. pylori</em> infection persistence leads to the formation of gastrointestinal phenotype of IM. <em>H. pylori</em> can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to <em>MUC5AC</em> gene inhibition and <em>MUC2</em> gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of <em>H. pylori</em> in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (<em>e.g.</em>, <em>SHH</em>, <em>SOX2</em>, and <em>RUNX3</em>) responsible for gastric differentiation, was identified to cause the appearance of IM. </p>

scholarly journals Pathological Diversity of Gastric Cancer from the Viewpoint of Background Condition

Digestion ◽  
2021 ◽  
pp. 1-9
Author(s):  
Hiroyuki Abe ◽  
Tetsuo Ushiku
Keyword(s):  
Gastric Cancer ◽  
Gastric Carcinoma ◽  
Atrophic Gastritis ◽  
Gastric Adenocarcinoma ◽  
Chronic Atrophic Gastritis ◽  
Signet Ring Cell ◽  
Diffuse Gastric Cancer ◽  
Fundic Gland ◽  
Histological Characteristics ◽  
H Pylori

<b><i>Background:</i></b> The prevalence of <i>Helicobacter pylori</i> infection and chronic atrophic gastritis is decreasing in Japan, which has led to a decline in the incidence of gastric cancer. However, there are various subtypes of gastric cancer that arise from the background mucosa without <i>H. pylori</i> infection, and their histological characteristics are distinct from those of gastric cancer with chronic atrophic gastritis. <b><i>Summary:</i></b> In this review, after a brief overview of conventional gastric carcinoma with <i>H. pylori</i> infection, including its molecular classification, histological characteristics of gastric cancer after eradicating <i>H. pylori</i> are described. The clinicopathological characteristics of gastric cancer independent of <i>H. pylori</i> infection are then explained. Autoimmune gastritis (type A gastritis) increases the risk of gastric adenocarcinoma and neuroendocrine tumors. Gastric carcinoma without <i>H. pylori</i> infection has various histological subtypes, including fundic gland-type adenocarcinoma (oxyntic gland adenoma), foveolar-type adenocarcinoma/adenoma, signet ring cell carcinoma, and adenocarcinoma of the esophagogastric junction. In addition, some familial gastric cancer syndromes, including hereditary diffuse gastric cancer, familial adenomatous polyposis, and gastric adenocarcinoma and proximal polyposis of the stomach, are also discussed. <b><i>Key Messages:</i></b> Although the incidence of gastric cancer will decrease in the near future, the diversity of gastric cancer pathology will be enhanced because <i>H. pylori</i>-negative gastric cancer will have a significant impact on the clinical practice guidelines for gastric cancer. Gastroenterologists and pathologists should be aware of the morphological diversity of <i>H. pylori</i>-negative gastric cancer, and attention should be paid to the status of the background gastric mucosa while examining gastric cancer.

Study on the Mechanism of Olfactomedin 4-shRNA Plasmid Chitosan Magnetic Nanoparticles in Intestinal Metaplasia of Chronic Atrophic Gastritis

2020 ◽  
Vol 20 (12) ◽  
pp. 7324-7332
Author(s):  
Haiwen Li ◽  
Jingwei Li ◽  
Peiwu Li ◽  
Weijian Zhang ◽  
Weiqin Yang ◽  
...  
Keyword(s):  
Magnetic Nanoparticles ◽  
Epithelial Cells ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Differentially Expressed Gene ◽  
Precancerous Lesion ◽  
Chronic Atrophic Gastritis ◽  
Incidence Rates ◽  
Pathological Process ◽  
Shrna Plasmid

Intestinal metaplasia (IM) refers to the replacement of gastric epithelial cells by intestinal epithelial cells. This is often accompanied by chronic atrophic gastritis (CAG), which is a precancerous lesion of gastric cancer. The incidence rates of CAG and IM are increasing gradually, which generates an enormous economic burden to individuals and society. To explore the pathogenesis of CAG with IM, we screened out the differentially expressed gene olfactomedin 4 (OLFM4) by bioinformatics and constructed OLFM4-shRNA plasmid chitosan magnetic nanoparticles to knockdown this gene. This caused a downregulation of caudal type homeobox 2 (CDX2), a marker of IM, suggesting that knocking down OLFM4 may slow the pathological process of IM, thus providing putative relevant targets for the treatment of CAG with IM.

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