scholarly journals Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Anna Alakoski ◽  
Teea T. Salmi ◽  
Kaisa Hervonen ◽  
Hannu Kautiainen ◽  
Maarit Salo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Dermatitis Herpetiformis ◽  
Villous Atrophy ◽  
Chronic Atrophic Gastritis ◽  
Controlled Study ◽  
Gastric Corpus ◽  
H Pylori

Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia.Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, andHelicobacter pylori. Duodenal biopsies were taken.Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp.,P<0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%,P=0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P=0.038) andH. pyloriin 17 (18.3%) and 17 (9.3%) (P=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer.Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum.H. pyloriwill partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.

scholarly journals Clinical Recommendations of Russian Gastroenterological Association and RENDO Endoscopic Society on Diagnosis and Treatment of Gastritis and Duodenitis

2021 ◽  
Vol 31 (4) ◽  
pp. 70-99
Author(s):  
V. T. Ivashkin ◽  
I. V. Maev ◽  
T. L. Lapina ◽  
E. D. Fedorov ◽  
A. A. Sheptulin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Eradication Therapy ◽  
Targeted Biopsy ◽  
High Quality ◽  
Familial History ◽  
History Of ◽  
H Pylori

Aim. The clinical guidelines are intended to supplement specialty decision-making for improved aid quality in patients with gastritis and duodenitis though acknowledging the latest clinical evidence and principles of evidencebased medicine.Key points. Gastritis is an inflammatory disease of stomach mucosa, with a separate definition of acute and chronic gastritis. Chronic gastritis is a cohort of chronic diseases uniting a typical morphology of persistent inflammatory infiltration, impaired cellular renewal with emergent intestinal metaplasia, atrophy and epithelial dysplasia of gastric mucosa. Oesophagogastroduodenoscopy (OGDS) or high-resolution OGDS with magnified or non-magnified virtual chromoendoscopy, including targeted biopsy for atrophy and intestinal metaplasia grading and neoplasia detection, are recommended to verify gastritis and duodenitis, precancer states and/or gastric mucosal changes. All chronic gastritis patients positive for H. рylori should undergo eradication therapy as aetiological and subsidiary for gastric cancer prevention. Chronic gastritis patients with symptoms of dyspepsia (epigastric pain, burning and congestion, early satiety), also combined with functional dyspepsia, are recommended proton pump inhibitors, prokinetics, rebamipide and bismuth tripotassium dicitrate in symptomatic treatment. With focal restricted intestinal metaplasia, follow-up is not required in most cases, mainly when advanced atrophic gastritis is ruled out in high-quality endoscopy with biopsy. However, a familial history of gastric cancer, incomplete intestinal metaplasia and persistent H. pylori infection render endoscopy monitoring with chromoendoscopy and targeted biopsy desirable once in three years. Patients with advanced atrophic gastritis should have high-quality endoscopy every 3 years, and once in 1–2 years if complicated with a familial history of gastric cancer.Conclusion. The recommendations condense current knowledge on the aetiology and pathogenesis of gastritis and duodenitis, as well as laboratory and instrumental diagnostic techniques, main approaches to aetiological H. pylori eradication and treatment of dyspeptic states.

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 Proteomics signature of autoimmune atrophic gastritis: towards a link with gastric cancer

2021 ◽  
Author(s):  
Ombretta Repetto ◽  
Valli De Re ◽  
Paolo Giuffrida ◽  
Marco Vincenzo Lenti ◽  
Raffaella Magris ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Tricarboxylic Acid Cycle ◽  
Differential Abundance ◽  
Expression Levels ◽  
2D Dige ◽  
Gastric Corpus ◽  
Gastric Biopsies ◽  
H Pylori ◽  
Autoimmune Atrophic Gastritis

Abstract Background Autoimmune atrophic gastritis (AAG) is a chronic disease that can progress to gastric cancer (GC). To better understand AAG pathology, this proteomics study investigated gastric proteins whose expression levels are altered in this disease and also in GC. Methods Using two-dimensional difference gel electrophoresis (2D-DIGE), we compared protein maps of gastric corpus biopsies from AAG patients and controls. Differentially abundant spots (|fold change|≥ 1.5, P < 0.01) were selected and identified by LC–MS/MS. The spots were further assessed in gastric antrum biopsies from AAG patients (without and with Helicobacter pylori infection) and from GC patients and unaffected first-degree relatives of GC patients. Results 2D-DIGE identified 67 differentially abundant spots, with 28 more and 39 less abundant in AAG-corpus than controls. LC–MS/MS identified these as 53 distinct proteins. The most significant (adjusted P < 0.01) biological process associated with the less abundant proteins was “tricarboxylic acid cycle”. Of the 67 spots, 57 were similarly differentially abundant in AAG-antrum biopsies irrespective of H. pylori infection status. The differential abundance was also observed in GC biopsies for 14 of 28 more abundant and 35 of 39 less abundant spots, and in normal gastric biopsies of relatives of GC patients for 6 and 25 spots, respectively. Immunoblotting confirmed the different expression levels of two more abundant proteins (PDIA3, GSTP gene products) and four less abundant proteins (ATP5F1A, PGA3, SDHB, PGC). Conclusion This study identified a proteomics signature of AAG. Many differential proteins were shared by GC and may be involved in the progression of AAG to GC.

scholarly journals Trefoil Factor Family in Pre-neoplastic Lesions and Gastric Cancer

2018 ◽  
Vol 4 ◽  
Author(s):  
Zahra Behrooznia ◽  
Pouya Ghaderi ◽  
Narges Jafarzadeh ◽  
Azra Izanloo ◽  
Sepideh Mansoori Majoofardi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastrointestinal Tract ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Suppressor Activity ◽  
Neoplastic Lesions ◽  
Tumor Suppressor Activity ◽  
Trefoil Factor Family

Gastric cancer is the fourth most common cancer and the second leading cause of cancer death worldwide. Although the global incidence of gastric cancer has been decreased dramatically in recent decades, north and northwest of Iran have the highest incidence rate of gastric cancer. Whilst the surgical procedures for gastric cancer have been improved, there is no cure for that. The intestinal type of GC results from pre-neoplastic conditions including atrophic gastritis, intestinal metaplasia and dysplasia. Trefoil Factors Family proteins (TFFs) are small and stable molecules secreted by the mammalian gastrointestinal tract. TFFs constitute a family of three peptides (TFF1, TFF2and TFF3) that are widely expressed in a tissue specific manner in the gastrointestinal tract. Variable TFFs expression in gastric cancer and pre-neoplastic lesions has been found. TFF1 has a tumor suppressor activity and inhibits tumorogenesis in gastric cancer. Its expression decreases in gastritis, gastric atrophy, dysplasia, intestinal metaplasia and gastric cancer.TFF2 has a protective effect on gastrointestinal epithelium. As a prognostic factor, TFF2 expression decreases in gastric ulcer, chronic atrophic gastritis and gastric cancer. TFF3 is considered as an oncogenic factor in gastric tissues. Whilst the normal gastric tissues don’t express TFF3, it increases in intestinal metaplasia. Therefore, more studies are necessary to clarify the role of TFFs in GC and pre-neoplastic conditions. This review has focused on elucidating the important role of TFFs in gastric cancer and pre-neoplastic lesions.

scholarly journals Alterations in mucosa-associated microbiota in the stomach of patients with gastric cancer

2021 ◽  
Author(s):  
Yilin Deng ◽  
Xuewei Ding ◽  
Qingyuan Song ◽  
Gang Zhao ◽  
Lei Han ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Chronic Gastritis ◽  
454 Sequencing ◽  
Alpha Diversity ◽  
Sequencing Platform ◽  
Gastric Corpus ◽  
H Pylori ◽  
Gastric Cancer Progression ◽  
Gastric Microbiota

Abstract Purpose The purpose of this study was to characterize alterations in mucosa-associated microbiota in different anatomical locations of the stomach during gastric cancer progression and to identify associations between Helicobacter pylori infection and gastric microbial changes in patients with gastric cancer. Methods Twenty-five H. pylori negative subjects with chronic gastritis and thirty-four subjects with gastric cancer were recruited, including H. pylori negative and positive patients with tumors in the antrum and the corpus. Gastric mucosa-associated microbiota were determined by 16S ribosomal RNA gene sequencing using a 454 sequencing platform. Results We found that individuals with chronic gastritis from three different anatomical sites exhibited different microbiota compositions, although the microbial alpha diversity, richness and beta diversity were similar. Compared to patients with chronic gastritis, the gastric microbiota compositions were significantly different at the order level in the antrum and the corpus of patients with gastric cancer, which was dependent on the H. pylori infection status. Microbial alpha diversity and species richness, however, were similar between chronic gastritis and gastric cancer cases and independent of H. pylori status. The microbial community structure in patients with gastric cancer was distinct from that in patients with chronic gastritis. In addition, we found that the presence of H. pylori markedly altered the structure in gastric corpus cancer, but only mildly affected the antrum. Conclusion Our data revealed distinct niche-specific microbiota alterations during the progression from gastritis to gastric cancer. These alterations may reflect adaptions of the microbiota to the diverse specific environmental habitats in the stomach, and may play an important, as yet undetermined, role in gastric carcinogenesis.

scholarly journals Chronic gastritis and carcinogenesis issues

2019 ◽  
Vol 45 (4) ◽  
pp. 65-70
Author(s):  
M. M. Karimov ◽  
G. N. Sobirova ◽  
U. K. Abdullayeva
Keyword(s):  
Gastric Cancer ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Precancerous Conditions ◽  
Increased Risk ◽  
Operated Stomach ◽  
Increasing Risk ◽  
H Pylori ◽  
Definition Of

Risk factors contributing to the transformation of chronic atrophic gastritis into gastric cancer are analyzed. Detection and monitoring of patients with precancerous conditions/lesions (precancerous changes), proper screening of H. pylori make early diagnosis of gastric cancer real. Features of precancerous conditions are given in order of increasing risk of developing gastric cancer. Adenomatous polyps of the stomach take the first place. Subsequent precancerous conditions include: cancer of the operated stomach, Menetria disease (hypertrophic gastropathy), B12-deficient anemia, and gastric ulcer. A definition of intestinal metaplasia subtypes is proposed as a risk factor for gastric cancer, dividing into complete and incomplete one, taking into account reduction in the expression of gastric mucins MUC1, MUC5AC and MUC6. Currently, the development of gastric cancer (mainly of the “intestinal type”) is considered as a multistage process involving the sequence of mucosal change, such as chronic inflammation, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. Role of the organism’s genetic susceptibility to H. pylori infection, factors of pathogenicity contributing to epithelial metaplasia, are analyzed. Role of Toll-like type 4 receptors (TLR4) involved in the recognition of H. pylori is clarified. It is with this type of receptors that the development of an excessive immune response of the host is associated, resulting in damage to the mucous membrane in H. pylori-infected individuals. In particular, carriers of TLR4+896A> G polymorphism have a more severe atrophy of the stomach and degree of inflammation, as well as an increased risk of non-cardiac gastric cancer.

scholarly journals Evaluation of the lipid peroxidation reactions activity in middle-aged men with chronic gastritis on the background of H. pylori infection

2019 ◽  
Vol 74 (3) ◽  
pp. 149-156
Author(s):  
Marina A. Darenskaya ◽  
Olga V. Smirnova ◽  
Edward V. Kasparov ◽  
Lyudmila A. Grebenkina ◽  
Aleksandr A. Sinyakov ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Atrophic Gastritis ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Chronic Atrophic Gastritis ◽  
Stress Reactions ◽  
Middle Aged ◽  
Glutathione S Transferase ◽  
Group 2 ◽  
H Pylori

Background: There is not enough information about the course of the processes of lipid peroxidation-antioxidant defense in middle-aged men who are at risk of developing gastric cancer on the Correa cascade. Aims: To analyze of the processes of lipid peroxidation activity and antioxidant defense in men with chronic gastritis and chronic atrophic gastritis in combination with and without the presence of Helicobacter pylori. Materials and methods: 173 middle-aged men with an established diagnosis of chronic gastritis were examined, which were divided into 4 groups: group 1 ― patients with chronic gastritis without H. pylori (n=58), group 2 ― patients with chronic gastritis in combination with H. pylori (n=61), group 3 ― patients with chronic atrophic gastritis without H. pylori (n=28), group 4 ― patients with chronic atrophic gastritis in combination with H. pylori (n=26). Evaluation of the content of parameters of the lipid peroxidation system and the antioxidant components activity using spectrophotometric research methods was carried out. For statistical analysis, the software package Statistica 7.0 (Stat Soft, USA) was used. The study was conducted during 20132015. Results: Infection H. pylori with chronic and chronic atrophic gastritis accompanied by significant changes in the system of lipid peroxidation, and antioxidant defense components in the form of primary and accumulation of end products, insufficient activity of antioxidant enzymes ― superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and reducing content of reduced glutathione. The use of an integrating factor to assess the severity of prooxidant activity confirms the development of antioxidant deficiency in patients of these groups. Conclusions: In patients with chronic and chronic atrophic gastritis, combined with H. Pylori infection, a more pronounced progression of oxidative stress reactions and a significant lack of antioxidant factors were found in comparison with patients with these forms of gastritis without H. pylori.

scholarly journals Pathways of Gastric Carcinogenesis, Helicobacter pylori Virulence and Interactions with Antioxidant Systems, Vitamin C and Phytochemicals

2020 ◽  
Vol 21 (17) ◽  
pp. 6451 ◽  
Author(s):  
James W. T. Toh ◽  
Robert B. Wilson
Keyword(s):  
Gastric Cancer ◽  
Ascorbic Acid ◽  
Helicobacter Pylori ◽  
Vitamin C ◽  
Atrophic Gastritis ◽  
Chronic Atrophic Gastritis ◽  
Gastric Carcinogenesis ◽  
Antioxidant Systems ◽  
H Pylori

Helicobacter pylori is a class one carcinogen which causes chronic atrophic gastritis, gastric intestinal metaplasia, dysplasia and adenocarcinoma. The mechanisms by which H. pylori interacts with other risk and protective factors, particularly vitamin C in gastric carcinogenesis are complex. Gastric carcinogenesis includes metabolic, environmental, epigenetic, genomic, infective, inflammatory and oncogenic pathways. The molecular classification of gastric cancer subtypes has revolutionized the understanding of gastric carcinogenesis. This includes the tumour microenvironment, germline mutations, and the role of Helicobacter pylori bacteria, Epstein Barr virus and epigenetics in somatic mutations. There is evidence that ascorbic acid, phytochemicals and endogenous antioxidant systems can modify the risk of gastric cancer. Gastric juice ascorbate levels depend on dietary intake of ascorbic acid but can also be decreased by H. pylori infection, H. pylori CagA secretion, tobacco smoking, achlorhydria and chronic atrophic gastritis. Ascorbic acid may be protective against gastric cancer by its antioxidant effect in gastric cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosation, reducing toxic effects of ingested nitrosodimethylamines and heterocyclic amines, and preventing H. pylori infection. The effectiveness of such cytoprotection is related to H. pylori strain virulence, particularly CagA expression. The role of vitamin C in epigenetic reprogramming in gastric cancer is still evolving. Other factors in conjunction with vitamin C also play a role in gastric carcinogenesis. Eradication of H. pylori may lead to recovery of vitamin C secretion by gastric epithelium and enable regression of premalignant gastric lesions, thereby interrupting the Correa cascade of gastric carcinogenesis.

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